Neuroendocrine factors regulate retinoic acid receptors in normal and hypoplastic lung development
Key points Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associat...
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Published in | The Journal of physiology Vol. 593; no. 15; pp. 3301 - 3311 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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England
Wiley Subscription Services, Inc
01.08.2015
John Wiley & Sons, Ltd |
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Abstract | Key points
Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model.
In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model.
The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors α and γ. Moreover bombesin and ghrelin supplementation, in vitro, to normal lungs increased RA receptor α/γ expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it.
These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation.
Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague–Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post‐conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up‐regulation of RARα and RARγ. |
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AbstractList | Key points * Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model. * In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model. * The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors alpha and gamma . Moreover bombesin and ghrelin supplementation, in vitro, to normal lungs increased RA receptor alpha / gamma expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it. * These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation. Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague-Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) alpha , beta and gamma expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post-conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RAR alpha / gamma expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RAR alpha / gamma expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RAR alpha / gamma expression levels, whereas the bombesin and ghrelin antagonists decreased RAR alpha / gamma expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up-regulation of RAR alpha and RAR gamma . KEY POINTSRetinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model. In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model. The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors α and γ. Moreover bombesin and ghrelin supplementation, in vitro, to normal lungs increased RA receptor α/γ expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it. These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation.ABSTRACTCongenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague-Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post-conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up-regulation of RARα and RARγ. Key points Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model. In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model. The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors α and γ. Moreover bombesin and ghrelin supplementation, in vitro , to normal lungs increased RA receptor α/γ expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it. These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation. Abstract Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague–Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post‐conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up‐regulation of RARα and RARγ. Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague–Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post-conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up-regulation of RARα and RARγ. Key points Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model. In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model. The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors α and γ. Moreover bombesin and ghrelin supplementation, in vitro, to normal lungs increased RA receptor α/γ expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it. These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation. Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague–Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post‐conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up‐regulation of RARα and RARγ. Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained about RA, ghrelin and bombesin in the congenital diaphragmatic hernia (CDH) rat model, neuroendocrine factors have never been associated with the RA signalling pathway in this animal model. In this study, the interaction between neuroendocrine factors and RA was explored in the CDH rat model. The authors found that normal fetal lung explants treated with RA, bombesin and ghrelin showed an increase in lung growth. Hypoplastic lungs presented higher expression levels of the RA receptors α and γ. Moreover bombesin and ghrelin supplementation, in vitro, to normal lungs increased RA receptor α/γ expression whereas administration of bombesin and ghrelin antagonists to normal and hypoplastic lungs decreased it. These data reveal for the first time that there is a link between neuroendocrine factors and RA, and that neuroendocrine factors sensitise the lung to the RA action through RA receptor modulation. Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and mortality rates. Moreover, CDH has been associated with an increase in the levels of pulmonary neuroendocrine factors, such as bombesin and ghrelin, and a decrease in the action of retinoic acid (RA). The present study aimed to elucidate the interaction between neuroendocrine factors and RA. In vitro analyses were performed on Sprague-Dawley rat embryos. Normal lung explants were treated with bombesin, ghrelin, a bombesin antagonist, a ghrelin antagonist, dimethylsulfoxide (DMSO), RA dissolved in DMSO, bombesin plus RA and ghrelin plus RA. Hypoplastic lung explants (nitrofen model) were cultured with bombesin, ghrelin, bombesin antagonist or ghrelin antagonist. The lung explants were analysed morphometrically, and retinoic acid receptor (RAR) α, β and γ expression levels were assessed via Western blotting. Immunohistochemistry analysis of RAR was performed in normal and hypoplastic lungs 17.5 days post-conception (dpc). Compared with the controls, hypoplastic lungs exhibited significantly higher RARα/γ expression levels. Furthermore considering hypoplastic lungs, bombesin and ghrelin antagonists decreased RARα/γ expression. Normal lung explants (13.5 dpc) treated with RA, bombesin plus RA, ghrelin plus RA, bombesin or ghrelin exhibited increased lung growth. Moreover, bombesin and ghrelin increased RARα/γ expression levels, whereas the bombesin and ghrelin antagonists decreased RARα/γ expression. This study demonstrates for the first time that neuroendocrine factors function as lung growth regulators, sensitising the lung to the action of RA through up-regulation of RARα and RARγ. |
Author | Moura, Rute S. Nogueira‐Silva, Cristina Correia‐Pinto, Jorge Pereira‐Terra, Patrícia |
Author_xml | – sequence: 1 givenname: Patrícia surname: Pereira‐Terra fullname: Pereira‐Terra, Patrícia organization: Life and Health Sciences Research Institute/3B's – PT Government Associate Laboratory – sequence: 2 givenname: Rute S. surname: Moura fullname: Moura, Rute S. organization: Life and Health Sciences Research Institute/3B's – PT Government Associate Laboratory – sequence: 3 givenname: Cristina surname: Nogueira‐Silva fullname: Nogueira‐Silva, Cristina organization: Hospital de Braga – sequence: 4 givenname: Jorge surname: Correia‐Pinto fullname: Correia‐Pinto, Jorge organization: Hospital de Braga |
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Cites_doi | 10.1002/neu.20242 10.1136/adc.2004.057547 10.1007/s00383-009-2425-8 10.1159/000209850 10.1016/S0002-9440(10)63861-8 10.1007/s00383-010-2833-9 10.1177/002215540205000803 10.1074/jbc.M307977200 10.1002/bdra.20370 10.2119/molmed.2011.00210 10.1002/ajmg.c.30126 10.1152/ajplung.00403.2003 10.1016/0304-3940(93)90367-T 10.1007/BF02483031 10.1097/SLA.0000000000001054 10.1016/j.jpedsurg.2005.01.034 10.1002/ppul.20252 10.1016/j.peptides.2008.08.012 10.1203/01.pdr.0000246245.05530.02 10.1152/ajplung.1999.277.2.L423 10.1242/dev.120.10.2749 10.1203/01.pdr.0000202748.66359.a9 10.1007/PL00007644 10.1007/s00383-015-3703-2 10.1152/ajplung.1998.275.6.L1184 10.1111/j.1753-4887.2009.00247.x 10.2350/07-04-0267.1 10.1016/j.peptides.2011.10.010 10.1007/s00383-010-2654-x 10.1007/s003830050399 10.1371/journal.pone.0067607 10.1016/j.amjsurg.2005.05.035 10.1016/j.jpedsurg.2007.10.050 10.1164/rccm.200907-1126OC 10.1093/ajcn/71.5.1325s 10.1159/000068932 10.1111/jpc.12508 10.1164/ajrccm.164.6.2010115 10.1371/journal.pone.0030517 |
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References | 1941; 62 2009; 67 2005; 190 2004; 286 2009; 25 2001; 164 2002; 50 1999; 29 2005; 90 2015; 31 2006; 59 2005; 40 1993; 163 2000; 71 2011; 32 2010; 182 1998; 275 2007; 10 2013; 8 2003; 278 2011; 18 2007; 79 2006; 60 2009; 96 2010; 26 2006; 66 2008; 29 1994; 120 2003; 162 2008; 43 2015 1999; 177 1999; 277 2007; 145C 2003; 83 2012; 7 2011; 27 2014; 50 1998; 13 22015267 - Peptides. 2011 Dec;32(12):2474-83 18280292 - J Pediatr Surg. 2008 Feb;43(2):367-72 10444537 - Am J Physiol. 1999 Aug;277(2 Pt 1):L423-9 17436298 - Am J Med Genet C Semin Med Genet. 2007 May 15;145C(2):158-71 18001162 - Pediatr Dev Pathol. 2007 Nov-Dec;10(6):419-35 22113494 - Mol Med. 2012;18:231-43 16549524 - Pediatr Res. 2006 Apr;59(4 Pt 1):531-7 12947094 - J Biol Chem. 2003 Nov 21;278(47):46911-8 14729516 - Am J Physiol Lung Cell Mol Physiol. 2004 May;286(5):L970-3 12660430 - Biol Neonate. 2003;83(3):157-61 21258935 - Pediatr Surg Int. 2011 Jun;27(6):573-7 10333410 - Surg Today. 1999;29(5):407-12 15852274 - J Pediatr Surg. 2005 Apr;40(4):658-65 23826327 - PLoS One. 2013;8(6):e67607 10799410 - Am J Clin Nutr. 2000 May;71(5 Suppl):1325S-33S 7607068 - Development. 1994 Oct;120(10):2749-71 12133904 - J Histochem Cytochem. 2002 Aug;50(8):1013-21 10384062 - Lung. 1999;177(4):241-51 25862168 - Pediatr Surg Int. 2015 Jul;31(7):659-63 9799371 - Pediatr Surg Int. 1998 Oct;13(8):547-9 19669650 - Pediatr Surg Int. 2009 Sep;25(9):733-43 16688755 - J Neurobiol. 2006 Jun;66(7):606-30 11588001 - Am J Respir Crit Care Med. 2001 Sep 15;164(6):1083-9 22291973 - PLoS One. 2012;7(1):e30517 17469205 - Birth Defects Res A Clin Mol Teratol. 2007 Aug;79(8):565-72 20623292 - Pediatr Surg Int. 2010 Oct;26(10):1011-5 18789988 - Peptides. 2008 Dec;29(12):2150-8 20413632 - Am J Respir Crit Care Med. 2010 Aug 15;182(4):555-61 12547725 - Am J Pathol. 2003 Feb;162(2):673-9 24528549 - J Paediatr Child Health. 2014 Sep;50(9):667-73 16023454 - Am J Surg. 2005 Aug;190(2):324-32 15724031 - Arch Dis Child Fetal Neonatal Ed. 2005 Mar;90(2):F103-8 19941617 - Nutr Rev. 2009 Dec;67(12):719-30 17065567 - Pediatr Res. 2006 Dec;60(6):693-8 8309621 - Neurosci Lett. 1993 Dec 12;163(2):145-7 15965895 - Pediatr Pulmonol. 2005 Aug;40(2):113-34 25563880 - Ann Surg. 2015 Dec;262(6):1130-40 19325248 - Neonatology. 2009;96(3):137-49 9843856 - Am J Physiol. 1998 Dec;275(6 Pt 1):L1184-91 e_1_2_6_32_1 e_1_2_6_10_1 e_1_2_6_31_1 e_1_2_6_30_1 Nogueira‐Silva C (e_1_2_6_23_1) 2011; 18 e_1_2_6_19_1 e_1_2_6_13_1 e_1_2_6_36_1 e_1_2_6_14_1 e_1_2_6_35_1 e_1_2_6_11_1 e_1_2_6_34_1 e_1_2_6_12_1 e_1_2_6_33_1 e_1_2_6_17_1 e_1_2_6_18_1 e_1_2_6_39_1 e_1_2_6_15_1 e_1_2_6_38_1 e_1_2_6_16_1 e_1_2_6_37_1 Mendelsohn C (e_1_2_6_21_1) 1994; 120 e_1_2_6_20_1 e_1_2_6_41_1 e_1_2_6_40_1 e_1_2_6_9_1 e_1_2_6_8_1 Andersen DH (e_1_2_6_2_1) 1941; 62 e_1_2_6_5_1 e_1_2_6_4_1 e_1_2_6_7_1 e_1_2_6_6_1 e_1_2_6_25_1 e_1_2_6_24_1 e_1_2_6_3_1 e_1_2_6_22_1 e_1_2_6_29_1 e_1_2_6_28_1 e_1_2_6_27_1 e_1_2_6_26_1 |
References_xml | – volume: 18 start-page: 231 year: 2011 end-page: 243 article-title: Local fetal lung renin‐angiotensin system as a target to treat congenital diaphragmatic hernia publication-title: Mol Med – volume: 177 start-page: 241 year: 1999 end-page: 251 article-title: Bombesin inhibits apoptosis in developing fetal rat lung publication-title: Lung – volume: 120 start-page: 2749 year: 1994 end-page: 2771 article-title: Function of the retinoic acid receptors (RARs) during development. (II) Multiple abnormalities at various stages of organogenesis in RAR double mutants publication-title: Development – volume: 83 start-page: 157 year: 2003 end-page: 161 article-title: The activation of the retinoic acid response element is inhibited in an animal model of congenital diaphragmatic hernia publication-title: Biol Neonate – volume: 7 start-page: e30517 year: 2012 article-title: Leukemia inhibitory factor in rat fetal lung development: expression and functional studies publication-title: PLoS One – volume: 67 start-page: 719 year: 2009 end-page: 730 article-title: Role of nutrition, lifestyle factors, and genes in the pathogenesis of congenital diaphragmatic hernia: human and animal studies publication-title: Nutr Rev – volume: 59 start-page: 531 year: 2006 end-page: 537 article-title: Ghrelin expression in human and rat fetal lungs and the effect of ghrelin administration in nitrofen‐induced congenital diaphragmatic hernia publication-title: Pediatr Res – volume: 8 start-page: e67607 year: 2013 article-title: The role of glycoprotein 130 family of cytokines in fetal rat lung development publication-title: PLoS One – volume: 163 start-page: 145 year: 1993 end-page: 147 article-title: Electrophysiological evidence for the presence of receptors for cholecystokinin and bombesin on cultured astrocytes of rat central nervous system publication-title: Neurosci Lett – volume: 40 start-page: 658 year: 2005 end-page: 665 article-title: Antenatal vitamin A administration attenuates lung hypoplasia by interfering with early instead of late determinants of lung underdevelopment in congenital diaphragmatic hernia publication-title: J Pediatr Surg – volume: 40 start-page: 113 year: 2005 end-page: 134 article-title: Similarities and dissimilarities of branching and septation during lung development publication-title: Pediatr Pulmonol – volume: 29 start-page: 2150 year: 2008 end-page: 2158 article-title: Ghrelin and obestatin: Different role in fetal lung development? publication-title: Peptides – volume: 182 start-page: 555 year: 2010 end-page: 561 article-title: Congenital diaphragmatic hernia: endothelin‐1, pulmonary hypertension, and disease severity publication-title: Am J Respir Crit Care Med – volume: 145C start-page: 158 year: 2007 end-page: 171 article-title: Overview of epidemiology, genetics, birth defects, and chromosome abnormalities associated with CDH publication-title: Am J Med Genet C Semin Med Genet – volume: 26 start-page: 1011 year: 2010 end-page: 1015 article-title: Prenatal retinoic acid upregulates pulmonary gene expression of PI3K and AKT in nitrofen‐induced pulmonary hypoplasia publication-title: Pediatr Surg Int – volume: 32 start-page: 2474 year: 2011 end-page: 2483 article-title: The apelinergic system in the developing lung: expression and signalling publication-title: Peptides – volume: 286 start-page: L970 year: 2004 end-page: L973 article-title: Reductions in the incidence of nitrofen‐induced diaphragmatic hernia by vitamin A and retinoic acid publication-title: Am J Physiol Lung Cell Mol Physiol – volume: 10 start-page: 419 year: 2007 end-page: 435 article-title: Pulmonary neuroendocrine cell system in pediatric lung disease – recent advances publication-title: Pediatr Dev Pathol – year: 2015 article-title: Unique tracheal fluid microRNA signature predicts response to FETO in patients with congenital diaphragmatic hernia publication-title: Ann Surg – volume: 50 start-page: 667 year: 2014 end-page: 673 article-title: Congenital diaphragmatic hernia publication-title: J Paediatr Child Health – volume: 190 start-page: 324 year: 2005 end-page: 332 article-title: Congenital diaphragmatic hernia: searching for answers publication-title: Am J Surg – volume: 43 start-page: 367 year: 2008 end-page: 372 article-title: Prenatal treatment with retinoic acid accelerates type 1 alveolar cell proliferation of the hypoplastic lung in the nitrofen model of congenital diaphragmatic hernia publication-title: J Pediatr Surg – volume: 96 start-page: 137 year: 2009 end-page: 149 article-title: Congenital diaphragmatic hernia: comparison of animal models and relevance to the human situation publication-title: Neonatology – volume: 275 start-page: 1184 year: 1998 end-page: 1191 article-title: Effects of maternal vitamin A status on fetal heart and lung: changes in expression of key developmental genes publication-title: Am J Physiol Lung Cell Mol Physiol – volume: 27 start-page: 573 year: 2011 end-page: 577 article-title: Prenatal administration of retinoic acid upregulates connective tissue growth factor in the nitrofen CDH model publication-title: Pediatr Surg Int – volume: 66 start-page: 606 year: 2006 end-page: 630 article-title: Overview of retinoid metabolism and function publication-title: J Neurobiol – volume: 90 start-page: 103 year: 2005 end-page: 108 article-title: Vitamin A and preterm infants: what we know, what we don't know, and what we need to know publication-title: Arch Dis Child Fetal Neonatal Ed – volume: 50 start-page: 1013 year: 2002 end-page: 1021 article-title: Ghrelin expression in fetal, infant, and adult human lung publication-title: J Histochem Cytochem – volume: 13 start-page: 547 year: 1998 end-page: 549 article-title: Retinol status of newborn infants with congenital diaphragmatic hernia publication-title: Pediatr Surg Int – volume: 278 start-page: 46911 year: 2003 end-page: 46918 article-title: Down‐regulation of retinoic acid receptor αsignalling is required for sacculation and type I cell formation in the developing lung publication-title: J Biol Chem – volume: 29 start-page: 407 year: 1999 end-page: 412 article-title: Immunohistochemical distribution of bombesin‐positive pulmonary neuroendocrine cells in a congenital diaphragmatic hernia publication-title: Surg Today – volume: 60 start-page: 693 year: 2006 end-page: 698 article-title: Spatial and temporal expression of glucocorticoid, retinoid, and thyroid hormone receptors is not altered in lungs of congenital diaphragmatic hernia publication-title: Pediatr Res – volume: 31 start-page: 659 year: 2015 end-page: 663 article-title: Lower NPAS3 expression during the later stages of abnormal lung development in rat congenital diaphragmatic hernia publication-title: Pediatr Surg Int – volume: 25 start-page: 733 year: 2009 end-page: 743 article-title: Can we improve outcome of congenital diaphragmatic hernia? publication-title: Pediatr Surg Int – volume: 71 start-page: 1325S year: 2000 end-page: 1333S article-title: Vitamin A in pregnancy: requirements and safety limits publication-title: Am J Clin Nutr – volume: 79 start-page: 565 year: 2007 end-page: 572 article-title: Linking animal models to human congenital diaphragmatic hernia publication-title: Birth Defects Res A Clin Mol Teratol – volume: 62 start-page: 888 year: 1941 end-page: 889 article-title: Incidence of congenital diaphragmatic hernia in the young of rats bred on a diet deficient in vitamin A publication-title: Am J Dis Child – volume: 277 start-page: 423 year: 1999 end-page: 429 article-title: Vitamin A decreases the incidence and severity of nitrofen‐induced congenital diaphragmatic hernia in rats publication-title: Am J Physiol Lung Cell Mol Physiol – volume: 162 start-page: 673 year: 2003 end-page: 679 article-title: Retinal dehydrogenase‐2 is inhibited by compounds that induce congenital diaphragmatic hernias in rodents publication-title: Am J Pathol – volume: 164 start-page: 1083 year: 2001 end-page: 1089 article-title: Restoring effects of vitamin A on surfactant synthesis in nitrofen‐induced congenital diaphragmatic hernia in rats publication-title: Am J Respir Crit Care Med – ident: e_1_2_6_10_1 doi: 10.1002/neu.20242 – ident: e_1_2_6_19_1 doi: 10.1136/adc.2004.057547 – ident: e_1_2_6_38_1 doi: 10.1007/s00383-009-2425-8 – ident: e_1_2_6_39_1 doi: 10.1159/000209850 – ident: e_1_2_6_22_1 doi: 10.1016/S0002-9440(10)63861-8 – ident: e_1_2_6_33_1 doi: 10.1007/s00383-010-2833-9 – ident: e_1_2_6_40_1 doi: 10.1177/002215540205000803 – ident: e_1_2_6_41_1 doi: 10.1074/jbc.M307977200 – ident: e_1_2_6_8_1 doi: 10.1002/bdra.20370 – volume: 18 start-page: 231 year: 2011 ident: e_1_2_6_23_1 article-title: Local fetal lung renin‐angiotensin system as a target to treat congenital diaphragmatic hernia publication-title: Mol Med doi: 10.2119/molmed.2011.00210 contributor: fullname: Nogueira‐Silva C – ident: e_1_2_6_30_1 doi: 10.1002/ajmg.c.30126 – ident: e_1_2_6_6_1 doi: 10.1152/ajplung.00403.2003 – ident: e_1_2_6_15_1 doi: 10.1016/0304-3940(93)90367-T – ident: e_1_2_6_4_1 doi: 10.1007/BF02483031 – ident: e_1_2_6_27_1 doi: 10.1097/SLA.0000000000001054 – ident: e_1_2_6_7_1 doi: 10.1016/j.jpedsurg.2005.01.034 – ident: e_1_2_6_32_1 doi: 10.1002/ppul.20252 – ident: e_1_2_6_26_1 doi: 10.1016/j.peptides.2008.08.012 – ident: e_1_2_6_31_1 doi: 10.1203/01.pdr.0000246245.05530.02 – ident: e_1_2_6_37_1 doi: 10.1152/ajplung.1999.277.2.L423 – volume: 120 start-page: 2749 year: 1994 ident: e_1_2_6_21_1 article-title: Function of the retinoic acid receptors (RARs) during development. (II) Multiple abnormalities at various stages of organogenesis in RAR double mutants publication-title: Development doi: 10.1242/dev.120.10.2749 contributor: fullname: Mendelsohn C – ident: e_1_2_6_34_1 doi: 10.1203/01.pdr.0000202748.66359.a9 – ident: e_1_2_6_17_1 doi: 10.1007/PL00007644 – ident: e_1_2_6_28_1 doi: 10.1007/s00383-015-3703-2 – volume: 62 start-page: 888 year: 1941 ident: e_1_2_6_2_1 article-title: Incidence of congenital diaphragmatic hernia in the young of rats bred on a diet deficient in vitamin A publication-title: Am J Dis Child contributor: fullname: Andersen DH – ident: e_1_2_6_3_1 doi: 10.1152/ajplung.1998.275.6.L1184 – ident: e_1_2_6_9_1 doi: 10.1111/j.1753-4887.2009.00247.x – ident: e_1_2_6_12_1 doi: 10.2350/07-04-0267.1 – ident: e_1_2_6_29_1 doi: 10.1016/j.peptides.2011.10.010 – ident: e_1_2_6_13_1 doi: 10.1007/s00383-010-2654-x – ident: e_1_2_6_20_1 doi: 10.1007/s003830050399 – ident: e_1_2_6_25_1 doi: 10.1371/journal.pone.0067607 – ident: e_1_2_6_14_1 doi: 10.1016/j.amjsurg.2005.05.035 – ident: e_1_2_6_35_1 doi: 10.1016/j.jpedsurg.2007.10.050 – ident: e_1_2_6_16_1 doi: 10.1164/rccm.200907-1126OC – ident: e_1_2_6_5_1 doi: 10.1093/ajcn/71.5.1325s – ident: e_1_2_6_11_1 doi: 10.1159/000068932 – ident: e_1_2_6_18_1 doi: 10.1111/jpc.12508 – ident: e_1_2_6_36_1 doi: 10.1164/ajrccm.164.6.2010115 – ident: e_1_2_6_24_1 doi: 10.1371/journal.pone.0030517 |
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Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been... Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been obtained... Key points Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been... KEY POINTSRetinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been... Key points * Retinoic acid (RA) and ghrelin levels are altered in human hypoplastic lungs when compared to healthy lungs. Although considerable data have been... Congenital diaphragmatic hernia (CDH) is characterised by a spectrum of lung hypoplasia and consequent pulmonary hypertension, leading to high morbidity and... |
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SubjectTerms | Animals Bombesin - antagonists & inhibitors Bombesin - pharmacology Ghrelin - antagonists & inhibitors Ghrelin - pharmacology Hernias, Diaphragmatic, Congenital - metabolism Lung - drug effects Lung - embryology Lung - metabolism Rats Rats, Sprague-Dawley Respiratory Retinoid X Receptor alpha - genetics Retinoid X Receptor alpha - metabolism Retinoid X Receptor gamma - genetics Retinoid X Receptor gamma - metabolism |
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Title | Neuroendocrine factors regulate retinoic acid receptors in normal and hypoplastic lung development |
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