Upregulation of KAT2B and ESCO2 gene expression level in patients with rheumatoid arthritis
Background Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 ( KAT1 ; HAT1 ) and ly...
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Published in | Clinical rheumatology Vol. 42; no. 1; pp. 253 - 259 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Cham
Springer International Publishing
01.01.2023
Springer Nature B.V |
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Abstract | Background
Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 (
KAT1
;
HAT1
) and lysine acetyltransferase 2B (
KAT2B
;
PCAF
), and the establishment of sister chromatid cohesion N-acetyltransferase 2 (
ESCO2
) in peripheral blood mononuclear cells (PBMCs) from RA patients.
Method and material
In this case–control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of
KAT1
,
KAT2B
, and
ESCO2
were determined using SYBR green real-time quantitative PCR.
Results
Our results exhibited a significant upregulation in the expression levels of
ESCO2
and
KAT2B
genes in patients with RA compared to normal individuals (
P-
value < 0.0001). Similarly, we observed higher expression of
KAT1
in the patients’ group when compared to the healthy controls, although the difference in expression level failed to show any significant changes (
P-
value = 0.485). Also, we found a positive correlation between
ESCO2
and the level of erythrocyte sedimentation rate (ESR) in patients.
Conclusion
Collectively, our results suggest that upregulated expression of
KAT2B
and
ESCO2
genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA.
Key Points
• Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients.
• The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects.
• The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group.
• There was a positive correlation between ESCO2 expression and the ESR level in patients. |
---|---|
AbstractList | Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 (KAT1; HAT1) and lysine acetyltransferase 2B (KAT2B; PCAF), and the establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) in peripheral blood mononuclear cells (PBMCs) from RA patients.
In this case-control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of KAT1, KAT2B, and ESCO2 were determined using SYBR green real-time quantitative PCR.
Our results exhibited a significant upregulation in the expression levels of ESCO2 and KAT2B genes in patients with RA compared to normal individuals (P-value < 0.0001). Similarly, we observed higher expression of KAT1 in the patients' group when compared to the healthy controls, although the difference in expression level failed to show any significant changes (P-value = 0.485). Also, we found a positive correlation between ESCO2 and the level of erythrocyte sedimentation rate (ESR) in patients.
Collectively, our results suggest that upregulated expression of KAT2B and ESCO2 genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA. Key Points • Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients. • The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects. • The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group. • There was a positive correlation between ESCO2 expression and the ESR level in patients. BackgroundRheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 (KAT1; HAT1) and lysine acetyltransferase 2B (KAT2B; PCAF), and the establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) in peripheral blood mononuclear cells (PBMCs) from RA patients.Method and materialIn this case–control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of KAT1, KAT2B, and ESCO2 were determined using SYBR green real-time quantitative PCR.ResultsOur results exhibited a significant upregulation in the expression levels of ESCO2 and KAT2B genes in patients with RA compared to normal individuals (P-value < 0.0001). Similarly, we observed higher expression of KAT1 in the patients’ group when compared to the healthy controls, although the difference in expression level failed to show any significant changes (P-value = 0.485). Also, we found a positive correlation between ESCO2 and the level of erythrocyte sedimentation rate (ESR) in patients.ConclusionCollectively, our results suggest that upregulated expression of KAT2B and ESCO2 genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA. Key Points• Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients. • The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects. • The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group.• There was a positive correlation between ESCO2 expression and the ESR level in patients. Background Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 ( KAT1 ; HAT1 ) and lysine acetyltransferase 2B ( KAT2B ; PCAF ), and the establishment of sister chromatid cohesion N-acetyltransferase 2 ( ESCO2 ) in peripheral blood mononuclear cells (PBMCs) from RA patients. Method and material In this case–control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of KAT1 , KAT2B , and ESCO2 were determined using SYBR green real-time quantitative PCR. Results Our results exhibited a significant upregulation in the expression levels of ESCO2 and KAT2B genes in patients with RA compared to normal individuals ( P- value < 0.0001). Similarly, we observed higher expression of KAT1 in the patients’ group when compared to the healthy controls, although the difference in expression level failed to show any significant changes ( P- value = 0.485). Also, we found a positive correlation between ESCO2 and the level of erythrocyte sedimentation rate (ESR) in patients. Conclusion Collectively, our results suggest that upregulated expression of KAT2B and ESCO2 genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA. Key Points • Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients. • The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects. • The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group. • There was a positive correlation between ESCO2 expression and the ESR level in patients. Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 (KAT1; HAT1) and lysine acetyltransferase 2B (KAT2B; PCAF), and the establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) in peripheral blood mononuclear cells (PBMCs) from RA patients.BACKGROUNDRheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 (KAT1; HAT1) and lysine acetyltransferase 2B (KAT2B; PCAF), and the establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) in peripheral blood mononuclear cells (PBMCs) from RA patients.In this case-control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of KAT1, KAT2B, and ESCO2 were determined using SYBR green real-time quantitative PCR.METHOD AND MATERIALIn this case-control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of KAT1, KAT2B, and ESCO2 were determined using SYBR green real-time quantitative PCR.Our results exhibited a significant upregulation in the expression levels of ESCO2 and KAT2B genes in patients with RA compared to normal individuals (P-value < 0.0001). Similarly, we observed higher expression of KAT1 in the patients' group when compared to the healthy controls, although the difference in expression level failed to show any significant changes (P-value = 0.485). Also, we found a positive correlation between ESCO2 and the level of erythrocyte sedimentation rate (ESR) in patients.RESULTSOur results exhibited a significant upregulation in the expression levels of ESCO2 and KAT2B genes in patients with RA compared to normal individuals (P-value < 0.0001). Similarly, we observed higher expression of KAT1 in the patients' group when compared to the healthy controls, although the difference in expression level failed to show any significant changes (P-value = 0.485). Also, we found a positive correlation between ESCO2 and the level of erythrocyte sedimentation rate (ESR) in patients.Collectively, our results suggest that upregulated expression of KAT2B and ESCO2 genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA. Key Points • Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients. • The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects. • The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group. • There was a positive correlation between ESCO2 expression and the ESR level in patients.CONCLUSIONCollectively, our results suggest that upregulated expression of KAT2B and ESCO2 genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA. Key Points • Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients. • The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects. • The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group. • There was a positive correlation between ESCO2 expression and the ESR level in patients. BACKGROUND: Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to RA development. The present study aimed to assess the expression pattern of K (lysine) acetyltransferase 1 (KAT1; HAT1) and lysine acetyltransferase 2B (KAT2B; PCAF), and the establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) in peripheral blood mononuclear cells (PBMCs) from RA patients. METHOD AND MATERIAL: In this case–control study, we studied 50 cases with RA in comparison to 50 age- and gender-matched healthy subjects. Separation of PBMCs samples from whole blood, extraction of RNA, and reverse transcription were performed. Gene transcript levels of KAT1, KAT2B, and ESCO2 were determined using SYBR green real-time quantitative PCR. RESULTS: Our results exhibited a significant upregulation in the expression levels of ESCO2 and KAT2B genes in patients with RA compared to normal individuals (P-value < 0.0001). Similarly, we observed higher expression of KAT1 in the patients’ group when compared to the healthy controls, although the difference in expression level failed to show any significant changes (P-value = 0.485). Also, we found a positive correlation between ESCO2 and the level of erythrocyte sedimentation rate (ESR) in patients. CONCLUSION: Collectively, our results suggest that upregulated expression of KAT2B and ESCO2 genes may be correlated to RA development. Further studies with larger sample sizes are required for understanding the potential contribution of these enzymes in the pathology of RA. Key Points • Dysregulated expression level of epigenetics enzymes was observed in PBMCs from RA patients. • The expression of KAT2B was 2.44 times higher in the PBMCs of RA patients than in the healthy subjects. • The expression of ESCO2 was upregulated (2.75 times) in the PBMCs of RA patients compared to the control group. • There was a positive correlation between ESCO2 expression and the ESR level in patients. |
Author | Farazmand, Ali Soltani, Samaneh Akhtari, Maryam Farhadi, Elham Ghasemi, Alaleh Akhlaghi, Maassoumeh Hassanzadeh, Vahideh Poursani, Shiva Jamshidi, Ahmadreza Mahmoudi, Mahdi |
Author_xml | – sequence: 1 givenname: Alaleh surname: Ghasemi fullname: Ghasemi, Alaleh organization: Department of Cell & Molecular Biology, School of Biology, College of Science, University of Tehran – sequence: 2 givenname: Ali surname: Farazmand fullname: Farazmand, Ali email: afarazmand@ut.ac.ir organization: Department of Cell & Molecular Biology, School of Biology, College of Science, University of Tehran – sequence: 3 givenname: Vahideh surname: Hassanzadeh fullname: Hassanzadeh, Vahideh organization: Department of Cell & Molecular Biology, School of Biology, College of Science, University of Tehran – sequence: 4 givenname: Shiva surname: Poursani fullname: Poursani, Shiva organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital – sequence: 5 givenname: Samaneh surname: Soltani fullname: Soltani, Samaneh organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital – sequence: 6 givenname: Maryam surname: Akhtari fullname: Akhtari, Maryam organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital, Inflammation Research Center, Tehran University of Medical Sciences – sequence: 7 givenname: Maassoumeh surname: Akhlaghi fullname: Akhlaghi, Maassoumeh organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital – sequence: 8 givenname: Elham surname: Farhadi fullname: Farhadi, Elham organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital, Inflammation Research Center, Tehran University of Medical Sciences – sequence: 9 givenname: Ahmadreza surname: Jamshidi fullname: Jamshidi, Ahmadreza organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital – sequence: 10 givenname: Mahdi orcidid: 0000-0002-8164-8831 surname: Mahmoudi fullname: Mahmoudi, Mahdi email: mahmoudim@tums.ac.ir organization: Rheumatology Research Center, Tehran University of Medical Sciences, Shariati Hospital, Inflammation Research Center, Tehran University of Medical Sciences |
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Copyright | The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. 2022. The Author(s), under exclusive licence to International League of Associations for Rheumatology (ILAR). |
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Keywords | Gene expression Rheumatoid arthritis Epigenetic KAT1 KAT2B ESCO2 |
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References | SadlerAJSulimanBAYuLYuanXWangDIrvingATThe acetyltransferase HAT1 moderates the NF-κB response by regulating the transcription factor PLZFNat Commun2015611110.1038/ncomms7795 NemtsovaMVZaletaevDVBureIVMikhaylenkoDSKuznetsovaEBAlekseevaEAEpigenetic changes in the pathogenesis of rheumatoid arthritisFront Genet20191057010.3389/fgene.2019.00570 GohES-YLiCHorsburghSKasaiYKolomietzEMorelCFThe Roberts syndrome/SC phocomelia spectrum—a case report of an adult with review of the literatureAm J Med Genet A2010152A47247810.1002/ajmg.a.33261 de JongRCMEwingMMde VriesMRKarperJCBastiaansenAJNMPetersHABThe epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia developmentPLoS One201712e0185820e018582010.1371/journal.pone.0185820 Trisciuoglio D, Di Martile M, Del Bufalo D (2018) Emerging role of histone acetyltransferase in stem cells and cancer. Stem Cells Int 2018:8908751 MiaoFGonzaloIGLantingLNatarajanRIn vivo chromatin remodeling events leading to inflammatory gene transcription under diabetic conditionsJ Biol Chem2004279180911809710.1074/jbc.M311786200 FournierMOrpinellMGrauffelCScheerEGarnierJ-MYeTKAT2A/KAT2B-targeted acetylome reveals a role for PLK4 acetylation in preventing centrosome amplificationNat Commun2016711610.1038/ncomms13227 HuberLCBrockMHemmatazadHGigerOTMoritzFTrenkmannMHistone deacetylase/acetylase activity in total synovial tissue derived from rheumatoid arthritis and osteoarthritis patientsArthritis Rheum2007561087109310.1002/art.22512 Nemtsova MV, Zaletaev DV, Bure IV, Mikhaylenko DS, Kuznetsova EB, Alekseeva EA et al (2019) Epigenetic changes in the pathogenesis of rheumatoid arthritis. Front Genet 10:570. https://doi.org/10.3389/fgene.2019.00570 SuzukiAMinamideRIwataJThe role of acetyltransferases for the temporal-specific accessibility of β-catenin to the myogenic gene locusSci Rep20188150571505710.1038/s41598-018-32888-z Rivera-ColónYMaguireALiszczakGPOliaASMarmorsteinRMolecular basis for cohesin acetylation by establishment of sister chromatid cohesion N-acetyltransferase ESCO1J Biol Chem2016291264682647710.1074/jbc.M116.752220 NejatbakhshSamimiLFarhadiETahmasebiMNJamshidiASharafatVaziriAMahmoudiMNF-κB signaling in rheumatoid arthritis with focus on fibroblast-like synoviocytesAutoimmun Highlights2020111110.1186/s13317-020-00135-z ToussirotEAbbasWKhanKATissotMJeudyABaudLImbalance between HAT and HDAC activities in the PBMCs of patients with ankylosing spondylitis or rheumatoid arthritis and influence of HDAC inhibitors on TNF alpha productionPLoS One20138e7093910.1371/journal.pone.0070939 FiorentinoFMaiARotiliDLysine acetyltransferase inhibitors: structure–activity relationships and potential therapeutic implicationsFuture Med Chem2018101067109110.4155/fmc-2017-0244 WadaTTArakiYSatoKAizakiYYokotaKKimYTAberrant histone acetylation contributes to elevated interleukin-6 production in rheumatoid arthritis synovial fibroblastsBiochem Biophys Res Commun201444468268610.1016/j.bbrc.2014.01.195 ChenHZhangLHeWLiuTZhaoYChenHESCO2 knockdown inhibits cell proliferation and induces apoptosis in human gastric cancer cellsBiochem Biophys Res Commun201849647548110.1016/j.bbrc.2018.01.048 SheikhBNAkhtarAThe many lives of KATs—detectors, integrators and modulators of the cellular environmentNat Rev Genet20192072310.1038/s41576-018-0072-4 PercivalSMThomasHRAmsterdamACarrollAJLeesJAYostHJVariations in dysfunction of sister chromatid cohesion in esco2 mutant zebrafish reflect the phenotypic diversity of Roberts syndromeDis Model Mech20158941955 BaierAMeineckelIGaySPapTApoptosis in rheumatoid arthritisCurr Opin Rheumatol20031527427910.1097/00002281-200305000-00015 GlantTTBesenyeiTKádárAKurkóJTryniszewskaBGálJDifferentially expressed epigenome modifiers, including aurora kinases A and B, in immune cells in rheumatoid arthritis in humans and mouse modelsArthritis Rheum2013651725173510.1002/art.37986 KleinKOspeltCGaySEpigenetic contributions in the development of rheumatoid arthritisArthritis Res Ther20121422710.1186/ar4074 KimBJKangKMJungSYChoiHKSeoJHChaeJHEsco2 is a novel corepressor that associates with various chromatin modifying enzymesBiochem Biophys Res Commun200837229830410.1016/j.bbrc.2008.05.056 MorinobuABiaoWTanakaSHoriuchiMJunLTsujiG(−)-Epigallocatechin-3-gallate suppresses osteoclast differentiation and ameliorates experimental arthritis in miceArthritis Rheum2008582012201810.1002/art.23594 SheppardKARoseDWHaqueZKKurokawaRMcInerneyEWestinSTranscriptional activation by NF-kappaB requires multiple coactivatorsMol Cell Biol1999196367637810.1128/mcb.19.9.6367 HouY-SWangJ-ZShiSHanYZhangYZhiJ-XIdentification of epigenetic factor KAT2B gene variants for possible roles in congenital heart diseasesBiosci Rep202040BSR2019177910.1042/BSR20191779 Viatte S, Plant D, Raychaudhuri S (2013) Genetics and epigenetics of rheumatoid arthritis. Nat Rev Rheumatol 9:141–153. https://doi.org/10.1038/nrrheum.2012.237 ManzoFTambaroFPMaiAAltucciLHistone acetyltransferase inhibitors and preclinical studiesExpert Opin Ther Pat20091976177410.1517/13543770902895727 Li Y, Zhou M, Lv X, Song L, Zhang D, He Y et al (2018) Reduced activity of HDAC3 and increased acetylation of histones H3 in peripheral blood mononuclear cells of patients with rheumatoid arthritis. J Immunol Res 2018:7313515 ArnettFCEdworthySMBlochDAMcshaneDJFriesJFCooperNSThe American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritisArthritis Rheum Off J Am Coll Rheumatol19883131532410.1002/art.1780310302 K Klein (6351_CR18) 2012; 14 FC Arnett (6351_CR16) 1988; 31 KA Sheppard (6351_CR25) 1999; 19 L NejatbakhshSamimi (6351_CR21) 2020; 11 Y-S Hou (6351_CR29) 2020; 40 6351_CR1 TT Wada (6351_CR15) 2014; 444 6351_CR2 F Miao (6351_CR24) 2004; 279 6351_CR3 BN Sheikh (6351_CR8) 2019; 20 RCM de Jong (6351_CR23) 2017; 12 H Chen (6351_CR27) 2018; 496 F Manzo (6351_CR13) 2009; 19 TT Glant (6351_CR26) 2013; 65 6351_CR12 ES-Y Goh (6351_CR11) 2010; 152A MV Nemtsova (6351_CR17) 2019; 10 A Baier (6351_CR28) 2003; 15 Y Rivera-Colón (6351_CR7) 2016; 291 M Fournier (6351_CR4) 2016; 7 A Suzuki (6351_CR6) 2018; 8 LC Huber (6351_CR19) 2007; 56 SM Percival (6351_CR9) 2015; 8 BJ Kim (6351_CR10) 2008; 372 E Toussirot (6351_CR20) 2013; 8 AJ Sadler (6351_CR22) 2015; 6 F Fiorentino (6351_CR5) 2018; 10 A Morinobu (6351_CR14) 2008; 58 |
References_xml | – reference: PercivalSMThomasHRAmsterdamACarrollAJLeesJAYostHJVariations in dysfunction of sister chromatid cohesion in esco2 mutant zebrafish reflect the phenotypic diversity of Roberts syndromeDis Model Mech20158941955 – reference: NejatbakhshSamimiLFarhadiETahmasebiMNJamshidiASharafatVaziriAMahmoudiMNF-κB signaling in rheumatoid arthritis with focus on fibroblast-like synoviocytesAutoimmun Highlights2020111110.1186/s13317-020-00135-z – reference: ChenHZhangLHeWLiuTZhaoYChenHESCO2 knockdown inhibits cell proliferation and induces apoptosis in human gastric cancer cellsBiochem Biophys Res Commun201849647548110.1016/j.bbrc.2018.01.048 – reference: ManzoFTambaroFPMaiAAltucciLHistone acetyltransferase inhibitors and preclinical studiesExpert Opin Ther Pat20091976177410.1517/13543770902895727 – reference: SadlerAJSulimanBAYuLYuanXWangDIrvingATThe acetyltransferase HAT1 moderates the NF-κB response by regulating the transcription factor PLZFNat Commun2015611110.1038/ncomms7795 – reference: KleinKOspeltCGaySEpigenetic contributions in the development of rheumatoid arthritisArthritis Res Ther20121422710.1186/ar4074 – reference: MiaoFGonzaloIGLantingLNatarajanRIn vivo chromatin remodeling events leading to inflammatory gene transcription under diabetic conditionsJ Biol Chem2004279180911809710.1074/jbc.M311786200 – reference: SuzukiAMinamideRIwataJThe role of acetyltransferases for the temporal-specific accessibility of β-catenin to the myogenic gene locusSci Rep20188150571505710.1038/s41598-018-32888-z – reference: KimBJKangKMJungSYChoiHKSeoJHChaeJHEsco2 is a novel corepressor that associates with various chromatin modifying enzymesBiochem Biophys Res Commun200837229830410.1016/j.bbrc.2008.05.056 – reference: de JongRCMEwingMMde VriesMRKarperJCBastiaansenAJNMPetersHABThe epigenetic factor PCAF regulates vascular inflammation and is essential for intimal hyperplasia developmentPLoS One201712e0185820e018582010.1371/journal.pone.0185820 – reference: Rivera-ColónYMaguireALiszczakGPOliaASMarmorsteinRMolecular basis for cohesin acetylation by establishment of sister chromatid cohesion N-acetyltransferase ESCO1J Biol Chem2016291264682647710.1074/jbc.M116.752220 – reference: GohES-YLiCHorsburghSKasaiYKolomietzEMorelCFThe Roberts syndrome/SC phocomelia spectrum—a case report of an adult with review of the literatureAm J Med Genet A2010152A47247810.1002/ajmg.a.33261 – reference: ArnettFCEdworthySMBlochDAMcshaneDJFriesJFCooperNSThe American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritisArthritis Rheum Off J Am Coll Rheumatol19883131532410.1002/art.1780310302 – reference: WadaTTArakiYSatoKAizakiYYokotaKKimYTAberrant histone acetylation contributes to elevated interleukin-6 production in rheumatoid arthritis synovial fibroblastsBiochem Biophys Res Commun201444468268610.1016/j.bbrc.2014.01.195 – reference: NemtsovaMVZaletaevDVBureIVMikhaylenkoDSKuznetsovaEBAlekseevaEAEpigenetic changes in the pathogenesis of rheumatoid arthritisFront Genet20191057010.3389/fgene.2019.00570 – reference: FiorentinoFMaiARotiliDLysine acetyltransferase inhibitors: structure–activity relationships and potential therapeutic implicationsFuture Med Chem2018101067109110.4155/fmc-2017-0244 – reference: HuberLCBrockMHemmatazadHGigerOTMoritzFTrenkmannMHistone deacetylase/acetylase activity in total synovial tissue derived from rheumatoid arthritis and osteoarthritis patientsArthritis Rheum2007561087109310.1002/art.22512 – reference: Li Y, Zhou M, Lv X, Song L, Zhang D, He Y et al (2018) Reduced activity of HDAC3 and increased acetylation of histones H3 in peripheral blood mononuclear cells of patients with rheumatoid arthritis. J Immunol Res 2018:7313515 – reference: BaierAMeineckelIGaySPapTApoptosis in rheumatoid arthritisCurr Opin Rheumatol20031527427910.1097/00002281-200305000-00015 – reference: GlantTTBesenyeiTKádárAKurkóJTryniszewskaBGálJDifferentially expressed epigenome modifiers, including aurora kinases A and B, in immune cells in rheumatoid arthritis in humans and mouse modelsArthritis Rheum2013651725173510.1002/art.37986 – reference: Viatte S, Plant D, Raychaudhuri S (2013) Genetics and epigenetics of rheumatoid arthritis. Nat Rev Rheumatol 9:141–153. https://doi.org/10.1038/nrrheum.2012.237 – reference: Nemtsova MV, Zaletaev DV, Bure IV, Mikhaylenko DS, Kuznetsova EB, Alekseeva EA et al (2019) Epigenetic changes in the pathogenesis of rheumatoid arthritis. Front Genet 10:570. https://doi.org/10.3389/fgene.2019.00570 – reference: MorinobuABiaoWTanakaSHoriuchiMJunLTsujiG(−)-Epigallocatechin-3-gallate suppresses osteoclast differentiation and ameliorates experimental arthritis in miceArthritis Rheum2008582012201810.1002/art.23594 – reference: SheikhBNAkhtarAThe many lives of KATs—detectors, integrators and modulators of the cellular environmentNat Rev Genet20192072310.1038/s41576-018-0072-4 – reference: Trisciuoglio D, Di Martile M, Del Bufalo D (2018) Emerging role of histone acetyltransferase in stem cells and cancer. Stem Cells Int 2018:8908751 – reference: FournierMOrpinellMGrauffelCScheerEGarnierJ-MYeTKAT2A/KAT2B-targeted acetylome reveals a role for PLK4 acetylation in preventing centrosome amplificationNat Commun2016711610.1038/ncomms13227 – reference: ToussirotEAbbasWKhanKATissotMJeudyABaudLImbalance between HAT and HDAC activities in the PBMCs of patients with ankylosing spondylitis or rheumatoid arthritis and influence of HDAC inhibitors on TNF alpha productionPLoS One20138e7093910.1371/journal.pone.0070939 – reference: SheppardKARoseDWHaqueZKKurokawaRMcInerneyEWestinSTranscriptional activation by NF-kappaB requires multiple coactivatorsMol Cell Biol1999196367637810.1128/mcb.19.9.6367 – reference: HouY-SWangJ-ZShiSHanYZhangYZhiJ-XIdentification of epigenetic factor KAT2B gene variants for possible roles in congenital heart diseasesBiosci Rep202040BSR2019177910.1042/BSR20191779 – ident: 6351_CR12 doi: 10.1155/2018/7313515 – volume: 14 start-page: 227 year: 2012 ident: 6351_CR18 publication-title: Arthritis Res Ther doi: 10.1186/ar4074 – volume: 10 start-page: 1067 year: 2018 ident: 6351_CR5 publication-title: Future Med Chem doi: 10.4155/fmc-2017-0244 – volume: 291 start-page: 26468 year: 2016 ident: 6351_CR7 publication-title: J Biol Chem doi: 10.1074/jbc.M116.752220 – ident: 6351_CR3 doi: 10.1155/2018/8908751 – volume: 56 start-page: 1087 year: 2007 ident: 6351_CR19 publication-title: Arthritis Rheum doi: 10.1002/art.22512 – volume: 15 start-page: 274 year: 2003 ident: 6351_CR28 publication-title: Curr Opin Rheumatol doi: 10.1097/00002281-200305000-00015 – volume: 65 start-page: 1725 year: 2013 ident: 6351_CR26 publication-title: Arthritis Rheum doi: 10.1002/art.37986 – volume: 8 start-page: 941 year: 2015 ident: 6351_CR9 publication-title: Dis Model Mech – volume: 19 start-page: 761 year: 2009 ident: 6351_CR13 publication-title: Expert Opin Ther Pat doi: 10.1517/13543770902895727 – volume: 19 start-page: 6367 year: 1999 ident: 6351_CR25 publication-title: Mol Cell Biol doi: 10.1128/mcb.19.9.6367 – volume: 8 start-page: e70939 year: 2013 ident: 6351_CR20 publication-title: PLoS One doi: 10.1371/journal.pone.0070939 – ident: 6351_CR1 doi: 10.1038/nrrheum.2012.237 – ident: 6351_CR2 doi: 10.3389/fgene.2019.00570 – volume: 152A start-page: 472 year: 2010 ident: 6351_CR11 publication-title: Am J Med Genet A doi: 10.1002/ajmg.a.33261 – volume: 10 start-page: 570 year: 2019 ident: 6351_CR17 publication-title: Front Genet doi: 10.3389/fgene.2019.00570 – volume: 40 start-page: BSR20191779 year: 2020 ident: 6351_CR29 publication-title: Biosci Rep doi: 10.1042/BSR20191779 – volume: 11 start-page: 11 year: 2020 ident: 6351_CR21 publication-title: Autoimmun Highlights doi: 10.1186/s13317-020-00135-z – volume: 12 start-page: e0185820 year: 2017 ident: 6351_CR23 publication-title: PLoS One doi: 10.1371/journal.pone.0185820 – volume: 279 start-page: 18091 year: 2004 ident: 6351_CR24 publication-title: J Biol Chem doi: 10.1074/jbc.M311786200 – volume: 31 start-page: 315 year: 1988 ident: 6351_CR16 publication-title: Arthritis Rheum Off J Am Coll Rheumatol doi: 10.1002/art.1780310302 – volume: 8 start-page: 15057 year: 2018 ident: 6351_CR6 publication-title: Sci Rep doi: 10.1038/s41598-018-32888-z – volume: 58 start-page: 2012 year: 2008 ident: 6351_CR14 publication-title: Arthritis Rheum doi: 10.1002/art.23594 – volume: 7 start-page: 1 year: 2016 ident: 6351_CR4 publication-title: Nat Commun doi: 10.1038/ncomms13227 – volume: 20 start-page: 7 year: 2019 ident: 6351_CR8 publication-title: Nat Rev Genet doi: 10.1038/s41576-018-0072-4 – volume: 6 start-page: 1 year: 2015 ident: 6351_CR22 publication-title: Nat Commun doi: 10.1038/ncomms7795 – volume: 372 start-page: 298 year: 2008 ident: 6351_CR10 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2008.05.056 – volume: 444 start-page: 682 year: 2014 ident: 6351_CR15 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2014.01.195 – volume: 496 start-page: 475 year: 2018 ident: 6351_CR27 publication-title: Biochem Biophys Res Commun doi: 10.1016/j.bbrc.2018.01.048 |
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Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications... Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications contribute to... BackgroundRheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications... BACKGROUND: Rheumatoid arthritis (RA) is an autoimmune condition that causes progressive inflammation. It seems that alternations in epigenetic modifications... |
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SubjectTerms | Acetyltransferase Acetyltransferases - genetics Acetyltransferases - metabolism Arthritis, Rheumatoid Autoimmune diseases blood Case-Control Studies chromatids Chromosomal Proteins, Non-Histone - genetics Chromosomal Proteins, Non-Histone - metabolism cohesion Enzymes Epigenetics Erythrocyte sedimentation rate Gene Expression Humans inflammation Leukocytes (mononuclear) Leukocytes, Mononuclear - metabolism Lysine lysine N-acetyltransferase Medicine Medicine & Public Health messenger RNA N-Acetyltransferase 2 Original Article p300-CBP Transcription Factors - genetics p300-CBP Transcription Factors - metabolism Peripheral blood mononuclear cells quantitative polymerase chain reaction Reverse transcription Rheumatoid arthritis Rheumatology Up-Regulation |
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Title | Upregulation of KAT2B and ESCO2 gene expression level in patients with rheumatoid arthritis |
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