MicroRNA-376c Impairs Transforming Growth Factor-β and Nodal Signaling to Promote Trophoblast Cell Proliferation and Invasion
Preeclampsia is a major disorder of pregnancy and a leading cause of maternal and perinatal morbidity and mortality. MicroRNAs are small noncoding RNAs that regulate gene expression posttranscriptionally. In this study, we examined the expression of miR-376c and found that miR-376c levels were downr...
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| Published in | Hypertension (Dallas, Tex. 1979) Vol. 61; no. 4; pp. 864 - 872 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
American Heart Association, Inc
01.04.2013
Lippincott Williams & Wilkins |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Preeclampsia is a major disorder of pregnancy and a leading cause of maternal and perinatal morbidity and mortality. MicroRNAs are small noncoding RNAs that regulate gene expression posttranscriptionally. In this study, we examined the expression of miR-376c and found that miR-376c levels were downregulated in both placental and plasma samples collected from preeclamptic patients, when compared with the normal pregnant women at the same gestational stage. Overexpression of miR-376c induced trophoblast cell proliferation, migration, and invasion in HTR8/SVneo cells and promoted placental explant outgrowth. In contrast, inhibition of endogenous miR-376c resulted in a decrease in trophoblast cell invasion and placental explant outgrowth. We identified activin receptor-like kinase 5 (ALK5), a type I receptor for transforming growth factor-β, and ALK7, a type I receptor for Nodal, as targets of miR-376c. Overexpression of miR-376c repressed transforming growth factor-β and Nodal functions, whereas overexpression of ALK5 and ALK7 reversed the effects of miR-376c. These results demonstrate that miR-376c inhibits both ALK5 and ALK7 expression to impair transforming growth factor-β/Nodal signaling, leading to increases in cell proliferation and invasion. An unbalanced Nodal/transforming growth factor-β and miR-376c expression may lead to the development of preeclampsia. |
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| AbstractList | Preeclampsia is a major disorder of pregnancy and a leading cause of maternal and perinatal morbidity and mortality. MicroRNAs are small noncoding RNAs that regulate gene expression posttranscriptionally. In this study, we examined the expression of miR-376c and found that miR-376c levels were downregulated in both placental and plasma samples collected from preeclamptic patients, when compared with the normal pregnant women at the same gestational stage. Overexpression of miR-376c induced trophoblast cell proliferation, migration, and invasion in HTR8/SVneo cells and promoted placental explant outgrowth. In contrast, inhibition of endogenous miR-376c resulted in a decrease in trophoblast cell invasion and placental explant outgrowth. We identified activin receptor-like kinase 5 (ALK5), a type I receptor for transforming growth factor-β, and ALK7, a type I receptor for Nodal, as targets of miR-376c. Overexpression of miR-376c repressed transforming growth factor-β and Nodal functions, whereas overexpression of ALK5 and ALK7 reversed the effects of miR-376c. These results demonstrate that miR-376c inhibits both ALK5 and ALK7 expression to impair transforming growth factor-β/Nodal signaling, leading to increases in cell proliferation and invasion. An unbalanced Nodal/transforming growth factor-β and miR-376c expression may lead to the development of preeclampsia. Preeclampsia is a major disorder of pregnancy and a leading cause of maternal and perinatal morbidity and mortality. MicroRNAs are small noncoding RNAs that regulate gene expression posttranscriptionally. In this study, we examined the expression of miR-376c and found that miR-376c levels were downregulated in both placental and plasma samples collected from preeclamptic patients, when compared with the normal pregnant women at the same gestational stage. Overexpression of miR-376c induced trophoblast cell proliferation, migration, and invasion in HTR8/SVneo cells and promoted placental explant outgrowth. In contrast, inhibition of endogenous miR-376c resulted in a decrease in trophoblast cell invasion and placental explant outgrowth. We identified activin receptor-like kinase 5 (ALK5), a type I receptor for transforming growth factor-β, and ALK7, a type I receptor for Nodal, as targets of miR-376c. Overexpression of miR-376c repressed transforming growth factor-β and Nodal functions, whereas overexpression of ALK5 and ALK7 reversed the effects of miR-376c. These results demonstrate that miR-376c inhibits both ALK5 and ALK7 expression to impair transforming growth factor-β/Nodal signaling, leading to increases in cell proliferation and invasion. An unbalanced Nodal/transforming growth factor-β and miR-376c expression may lead to the development of preeclampsia.Preeclampsia is a major disorder of pregnancy and a leading cause of maternal and perinatal morbidity and mortality. MicroRNAs are small noncoding RNAs that regulate gene expression posttranscriptionally. In this study, we examined the expression of miR-376c and found that miR-376c levels were downregulated in both placental and plasma samples collected from preeclamptic patients, when compared with the normal pregnant women at the same gestational stage. Overexpression of miR-376c induced trophoblast cell proliferation, migration, and invasion in HTR8/SVneo cells and promoted placental explant outgrowth. In contrast, inhibition of endogenous miR-376c resulted in a decrease in trophoblast cell invasion and placental explant outgrowth. We identified activin receptor-like kinase 5 (ALK5), a type I receptor for transforming growth factor-β, and ALK7, a type I receptor for Nodal, as targets of miR-376c. Overexpression of miR-376c repressed transforming growth factor-β and Nodal functions, whereas overexpression of ALK5 and ALK7 reversed the effects of miR-376c. These results demonstrate that miR-376c inhibits both ALK5 and ALK7 expression to impair transforming growth factor-β/Nodal signaling, leading to increases in cell proliferation and invasion. An unbalanced Nodal/transforming growth factor-β and miR-376c expression may lead to the development of preeclampsia. |
| Author | Nadeem, Lubna Manchanda, Tanita Ye, Gang Wang, Yan-Ling Ji, Lei Qiao, Jie Wang, Yongqing Lye, Stephen Yang, Burton B. Zhao, Yangyu Fu, Guodong Peng, Chun |
| AuthorAffiliation | From the Department of Biology, York University, Toronto, Ontario, Canada (G.F., G.Y., L.N., T.M., C.P.); State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China (L.J., Y-L.W.); Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China (Y.W., Y.Z., J.Q.); Research Center for Women’s and Infants Health, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada (S.L.); and Sunnybrook Research Institute, Sunnybrook Health Sciences Center, Toronto, Ontario, Canada (B.B.Y.) |
| AuthorAffiliation_xml | – name: From the Department of Biology, York University, Toronto, Ontario, Canada (G.F., G.Y., L.N., T.M., C.P.); State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China (L.J., Y-L.W.); Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China (Y.W., Y.Z., J.Q.); Research Center for Women’s and Infants Health, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada (S.L.); and Sunnybrook Research Institute, Sunnybrook Health Sciences Center, Toronto, Ontario, Canada (B.B.Y.) |
| Author_xml | – sequence: 1 givenname: Guodong surname: Fu fullname: Fu, Guodong organization: From the Department of Biology, York University, Toronto, Ontario, Canada (G.F., G.Y., L.N., T.M., C.P.); State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China (L.J., Y-L.W.); Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing, China (Y.W., Y.Z., J.Q.); Research Center for Women’s and Infants Health, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada (S.L.); and Sunnybrook Research Institute, Sunnybrook Health Sciences Center, Toronto, Ontario, Canada (B.B.Y.) – sequence: 2 givenname: Gang surname: Ye fullname: Ye, Gang – sequence: 3 givenname: Lubna surname: Nadeem fullname: Nadeem, Lubna – sequence: 4 givenname: Lei surname: Ji fullname: Ji, Lei – sequence: 5 givenname: Tanita surname: Manchanda fullname: Manchanda, Tanita – sequence: 6 givenname: Yongqing surname: Wang fullname: Wang, Yongqing – sequence: 7 givenname: Yangyu surname: Zhao fullname: Zhao, Yangyu – sequence: 8 givenname: Jie surname: Qiao fullname: Qiao, Jie – sequence: 9 givenname: Yan-Ling surname: Wang fullname: Wang, Yan-Ling – sequence: 10 givenname: Stephen surname: Lye fullname: Lye, Stephen – sequence: 11 givenname: Burton surname: Yang middlename: B. fullname: Yang, Burton B. – sequence: 12 givenname: Chun surname: Peng fullname: Peng, Chun |
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| Keywords | Hypertension Cell proliferation Pregnancy disorders Lymph node Fetal membrane Transforming growth factor β miR-376c Cardiovascular disease ALK7 Tumorous infiltration Malignant tumor Metastasis ALK5 Pregnancy toxemia Invasion Pregnancy Nodal Placenta Preeclampsia TGF-β Circulatory system Cancer |
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| PublicationTitle | Hypertension (Dallas, Tex. 1979) |
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| SubjectTerms | Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Cell Proliferation Diseases of mother, fetus and pregnancy Female Gene Expression Regulation Gynecology. Andrology. Obstetrics Humans Medical sciences MicroRNAs - genetics MicroRNAs - metabolism Nodal Protein - biosynthesis Nodal Protein - genetics Placenta - cytology Placenta - metabolism Pre-Eclampsia - genetics Pre-Eclampsia - metabolism Pregnancy Pregnancy. Fetus. Placenta RNA - genetics Signal Transduction - genetics Transforming Growth Factor beta - biosynthesis Transforming Growth Factor beta - genetics Trophoblasts - cytology Trophoblasts - metabolism |
| Title | MicroRNA-376c Impairs Transforming Growth Factor-β and Nodal Signaling to Promote Trophoblast Cell Proliferation and Invasion |
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