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Cited by 31Preterm Birth and ChorioamnionitisPregnancy and preeclampsia studiesBlood Coagulation and Thrombosis Mechanisms

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Induction of Amnion Epithelial Apoptosis by Cortisol via tPA/Plasmin System

Wang, Wangsheng, Liu, Chao, Sun, Kang·2016·Endocrinology
DOI 10.1210/en.2016-1464
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Abstract

Rupture of fetal membranes (ROM) can initiate parturition at both term and preterm birth. Apoptosis of the amnion epithelium plays a key role in structural remodeling of the membranes preceding ROM. However, the causative factors for apoptosis remain unidentified. Toward the end of gestation, a feed-forward regeneration of cortisol via 11β-hydroxysteroid dehydrogenase 1 exists in the fetal membranes. Here, we have examined whether cortisol accumulation is a causative factor for amnion cells apoptosis. By using primary human amnion epithelial and fibroblast cells, we demonstrated cortisol induced apoptosis specifically in epithelial cells but not in fibroblasts via reciprocal regulation of tissue-type plasminogen activator (tPA)/plasmin system. Cortisol increased PLAT expression, the gene encoding tPA, via glucocorticoid receptor binding to a glucocorticoid response element in PLAT promoter, thereby increasing plasmin activity in epithelial cells. Further study revealed that a Fas-mediated extrinsic apoptotic pathway was involved in the induction of epithelial cells apoptosis by cortisol, which was blocked by inhibiting either tPA or plasmin. Consistently, cortisol increased cleaved-caspase-3 and tPA abundance in amnion tissue explants. Moreover, the abundance of cortisol, cleaved-caspase-3, and tPA was significantly increased in amnion tissue after labor-initiated spontaneous rupture of membranes. In conclusion, local accumulation of cortisol is a causative factor for amnion epithelial apoptosis via activation of tPA/plasmin system toward the end of gestation. This may contribute to the ROM at both term and preterm birth.

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  • Ex vivo culture of human amnion epithelial cells with cortisol induced cell death through the extrinsic apoptotic pathway.

    “Ex vivo culture of human amnion epithelial cells with cortisol-induced cell death through the extrinsic apoptotic pathway [80].”

    From Stress and the HPA Axis: Balancing Homeostasis and Fertility. (2017) · cites this paper as [80]

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Research works printed but not linked: 41

  1. Slattery, 2002, Preterm delivery, Lancet, 360, 1489, 10.1016/S0140-6736(02)11476-0 · DOI · Paper page
  2. Oyen, 2006, Premature rupture of the fetal membranes: is the amnion the major determinant?, Am J Obstet Gynecol, 195, 510, 10.1016/j.ajog.2006.02.010 · DOI
  3. Parry, 1998, Premature rupture of the fetal membranes, N Engl J Med, 338, 663, 10.1056/NEJM199803053381006 · DOI
  4. Menon, 2004, The role of matrix degrading enzymes and apoptosis in rupture of membranes, J Soc Gynecol Investig, 11, 427, 10.1016/j.jsgi.2004.04.001 · DOI
  5. Lei, 1996, A program of cell death and extracellular matrix degradation is activated in the amnion before the onset of labor, J Clin Invest, 98, 1971, 10.1172/JCI119001 · DOI
  6. Kumagai, 2001, Apoptosis in the normal human amnion at term, independent of Bcl-2 regulation and onset of labour, Mol Hum Reprod, 7, 681, 10.1093/molehr/7.7.681 · DOI
  7. Hsu, 2000, Increased apoptosis in human amnion is associated with labor at term, Am J Reprod Immunol, 43, 255, 10.1111/j.8755-8920.2000.430502.x · DOI
  8. Sağol, 2002, Role of apoptosis, bcl-2 and bax protein expression in premature rupture of fetal membranes, J Reprod Med, 47, 809
  9. Runić, 1998, Apoptosis and Fas expression in human fetal membranes, J Clin Endocrinol Metab, 83, 660
  10. Fortunato, 2000, Programmed cell death (apoptosis) as a possible pathway to metalloproteinase activation and fetal membrane degradation in premature rupture of membranes, Am J Obstet Gynecol, 182, 1468, 10.1067/mob.2000.107330 · DOI
  11. Murphy, 1977, Chorionic membrane as an extra-adrenal source of foetal cortisol in human amniotic fluid, Nature, 266, 179, 10.1038/266179a0 · DOI
  12. Sippell, 1981, Unconjugated cortisol and corticosterone levels in amniotic fluid, Am J Obstet Gynecol, 140, 353, 10.1016/0002-9378(81)90302-1 · DOI
  13. Goldkrand, 1976, Maternal and fetal plasma cortisol levels at parturition, Obstet Gynecol, 47, 41
  14. Smith, 2007, Parturition, N Engl J Med, 356, 271, 10.1056/NEJMra061360 · DOI
  15. Wang, 2012, Cortisol induces aromatase expression in human placental syncytiotrophoblasts through the cAMP/Sp1 pathway, Endocrinology, 153, 2012, 10.1210/en.2011-1626 · DOI
  16. Kitterman, 1981, Prepartum maturation of the lung in fetal sheep: relation to cortisol, J Appl Physiol Respir Environ Exerc Physiol, 51, 384
  17. Liggins, 1969, Premature delivery of foetal lambs infused with glucocorticoids, J Endocrinol, 45, 515, 10.1677/joe.0.0450515 · DOI · Paper page
  18. Seckl, 1993, 11 β-hydroxysteroid dehydrogenase isoforms and their implications for blood pressure regulation, Eur J Clin Invest, 23, 589, 10.1111/j.1365-2362.1993.tb00720.x · DOI
  19. Sun, 1997, Differential expression of 11 β-hydroxysteroid dehydrogenase types 1 and 2 in human placenta and fetal membranes, J Clin Endocrinol Metab, 82, 300
  20. Murphy, 1981, Ontogeny of cortisol-cortisone interconversion in human tissues: a role for cortisone in human fetal development, J Steroid Biochem, 14, 811, 10.1016/0022-4731(81)90226-0 · DOI
  21. Sun, 2003, Enhancement of glucocorticoid-induced 11β-hydroxysteroid dehydrogenase type 1 expression by proinflammatory cytokines in cultured human amnion fibroblasts, Endocrinology, 144, 5568, 10.1210/en.2003-0780 · DOI
  22. Yang, 2007, Role of glucocorticoid receptor and CCAAT/enhancer-binding protein α in the feed-forward induction of 11β-hydroxysteroid dehydrogenase type 1 expression by cortisol in human amnion fibroblasts, J Endocrinol, 195, 241, 10.1677/JOE-07-0303 · DOI
  23. Li, 2006, Enhancement of cortisol-induced 11β-hydroxysteroid dehydrogenase type 1 expression by interleukin 1β in cultured human chorionic trophoblast cells, Endocrinology, 147, 2490, 10.1210/en.2005-1626 · DOI
  24. Sun, 2003, Glucocorticoids induce cytosolic phospholipase A2 and prostaglandin H synthase type 2 but not microsomal prostaglandin E synthase (PGES) and cytosolic PGES expression in cultured primary human amnion cells, J Clin Endocrinol Metab, 88, 5564, 10.1210/jc.2003-030875 · DOI
  25. Casey, 1985, Despite a massive increase in cortisol secretion in women during parturition, there is an equally massive increase in prostaglandin synthesis. A paradox?, J Clin Invest, 75, 1852, 10.1172/JCI111899 · DOI
  26. Zakar, 1995, Glucocorticoids stimulate the expression of prostaglandin endoperoxide H synthase-2 in amnion cells, Endocrinology, 136, 1610, 10.1210/endo.136.4.7895671 · DOI
  27. Wang, 2015, Phosphorylation of STAT3 mediates the induction of cyclooxygenase-2 by cortisol in the human amnion at parturition, Sci Signal, 8, ra106, 10.1126/scisignal.aac6151 · DOI
  28. Gruver-Yates, Tissue-specific actions of glucocorticoids on apoptosis: a double-edged sword, Cells, 2, 202, 10.3390/cells2020202 · DOI
  29. Horowitz, 2008, Plasminogen activation induced pericellular fibronectin proteolysis promotes fibroblast apoptosis, Am J Respir Cell Mol Biol, 38, 78, 10.1165/rcmb.2007-0174OC · DOI
  30. Flavin, 2000, Microglial tissue plasminogen activator (tPA) triggers neuronal apoptosis in vitro, Glia, 29, 347, 10.1002/(SICI)1098-1136(20000215)29:4<347::AID-GLIA5>3.0.CO;2-8 · DOI
  31. Kathju, 1994, Synergistic induction of tissue-type plasminogen activator gene expression by glucocorticoids and cyclic nucleotides in rat HTC hepatoma cells, Endocrinology, 135, 1195, 10.1210/endo.135.3.8070363 · DOI
  32. Medcalf, 1988, Glucocorticoid-modulated gene expression of tissue- and urinary-type plasminogen activator and plasminogen activator inhibitor 1 and 2, J Cell Biol, 106, 971, 10.1083/jcb.106.3.971 · DOI
  33. Zhang, 2015, Inhibition of 11β-HSD2 expression by triclosan via induction of apoptosis in human placental syncytiotrophoblasts, J Clin Endocrinol Metab, 100, E542, 10.1210/jc.2014-4376 · DOI
  34. Hengartner, 2000, The biochemistry of apoptosis, Nature, 407, 770, 10.1038/35037710 · DOI
  35. Challis, 2002, Prostaglandins and mechanisms of preterm birth, Reproduction, 124, 1, 10.1530/rep.0.1240001 · DOI
  36. Tanswell, 1977, Human amniotic membrane corticosteroid 11-oxidoreductase activity, J Clin Endocrinol Metab, 45, 721, 10.1210/jcem-45-4-721 · DOI
  37. Alfaidy, 2003, Late gestation increase in 11β-hydroxysteroid dehydrogenase 1 expression in human fetal membranes: a novel intrauterine source of cortisol, J Clin Endocrinol Metab, 88, 5033, 10.1210/jc.2002-021915 · DOI
  38. Guo, 2014, Induction of PGF2α synthesis by cortisol through GR dependent induction of CBR1 in human amnion fibroblasts, Endocrinology, 155, 3017, 10.1210/en.2013-1848 · DOI
  39. Harirah, 2012, Increased apoptosis in chorionic trophoblasts of human fetal membranes with labor at term, Int J Clin Med, 3, 136, 10.4236/ijcm.2012.32027 · DOI
  40. Chan, 2007, Glucocorticoid-induced apoptosis in human decidua: a novel role for 11β-hydroxysteroid dehydrogenase in late gestation, J Endocrinol, 195, 7, 10.1677/JOE-07-0289 · DOI
  41. Bajou, 2008, Plasminogen activator inhibitor-1 protects endothelial cells from FasL-mediated apoptosis, Cancer Cell, 14, 324, 10.1016/j.ccr.2008.08.012 · DOI

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Metadata

Authors
Wang, W., Liu, C., & Sun, K.
Affiliations
Shanghai Jiao Tong University (CN)
Corresponding author
Sun, Kang
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2016-10-03
Volume
157
Issue
11
Pages
4487-4498
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2016-1464
OpenAlex
W2529050989
Cited by
31
References
0
Citations by year
2025: 2 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 1 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 7
FWCI
5.00
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Preterm Birth and Chorioamnionitis
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
Keywords
cortisol, amniotic epithelial cells, apoptosis, tissue plasminogen activator, plasmin system, glucocorticoid receptor, Fas-mediated apoptosis, caspase-3, preterm birth, childbirth, 11β-hydroxysteroid dehydrogenase type 1, glucocorticoid response element
MeSH terms
Amnion, Cells, Cultured, Epithelial Cells, Female, Extraembryonic Membranes, Fibrinolysin, Fibroblasts, Humans, Hydrocortisone, Tissue Plasminogen Activator, Pregnancy, Promoter Regions, Genetic, Protein Binding, Blotting, Western, Apoptosis, In Situ Nick-End Labeling, RNA, Small Interfering, 11-beta-Hydroxysteroid Dehydrogenase Type 1, Chromatin Immunoprecipitation, Caspase 3, In Vitro Techniques

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