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Cited by 31Preterm Birth and ChorioamnionitisAutophagy in Disease and TherapyPregnancy and preeclampsia studies

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Autophagic Degradation of Collagen 1A1 by Cortisol in Human Amnion Fibroblasts

Mi, Yabing, Wang, Wangsheng, Zhang, Chuyue, Liu, Chao, Lu, Jiangwen, Li, Wenjiao, Zuo, Rujuan, Myatt, Leslie, Sun, Kang·2017·Endocrinology
DOI 10.1210/en.2016-1829
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Abstract

Rupture of fetal membranes can initiate parturition at both term and preterm. Collagen is the crucial factor determining the tensile strength of the membranes. Toward the end of gestation, a feed-forward regeneration of cortisol via 11β-hydroxysteroid dehydrogenase 1 exists in fetal membranes. It remains undetermined whether cortisol contributes to collagen reduction in fetal membranes. In this study, we have examined whether cortisol accumulation is a causative factor for collagen reduction in human amnion fibroblasts, the major source of collagens in the membranes. Cortisol had no effect on collagen 1A1 (COL1A1) and 1A2 (COL1A2) messenger RNA (mRNA) abundance but decreased their protein abundance. The latter effect was affected by neither mRNA transcription inhibitor nor protein translation inhibitor. Mechanistic studies revealed that the reduction in COL1A1 but not COL1A2 protein by cortisol was blocked by lysosome inhibitor chloroquine or small interfering RNA (siRNA)-mediated knockdown of autophagy-related protein 7, an essential protein for autophagy, whereas the proteasome inhibitors MG132 and bortezomib were ineffective. Further analysis showed that cortisol dose dependently increased the ratio of LC3II/LC3I, a marker of lysosome activation, an effect blocked by the glucocorticoid receptor (GR) antagonist RU486 and siRNA-mediated knockdown of GR. Consistently, cortisol decreased COL1A1 and COL1A2 protein abundance in amnion tissue explants, and decreased COL1A1 and COL1A2 protein abundance was observed at parturition in the amnion tissue. Conclusively, cortisol regeneration in fetal membranes may contribute to rupture of fetal membranes at parturition by reducing collagen protein abundance. Lysosome-mediated autophagy accounts for the reduction in COL1A1 by cortisol, but the mechanism underlying the reduction in COL1A2 awaits further investigation.

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  • Cortisol decreased abundance of collagen proteins and lysyl oxidase in amnion cells through lysosome-mediated autophagy.

    “Cortisol also decreased the abundance of collagen proteins and lysyl oxidase, a collagen cross-linking enzyme, in amnion cells through lysosome-mediated autophagy [81].”

    From Stress and the HPA Axis: Balancing Homeostasis and Fertility. (2017) · cites this paper as [81]

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Metadata

Authors
Mi, Y., Wang, W., Zhang, C., Liu, C., Lu, J., Li, W., Zuo, R., Myatt, L., & Sun, K.
Affiliations
  • Shanghai Jiao Tong University (CN)
  • Center for Reproductive Medicine, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200135, P.R. China
  • Oregon Health & Science University (US)
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2017-01-17
Volume
158
Issue
4
Pages
1005-1014
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2016-1829
OpenAlex
W2604828749
Cited by
31
References
1
Citations by year
2026: 1 · 2025: 2 · 2024: 4 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 5 · 2019: 7 · 2018: 3 · 2017: 4
FWCI
4.09
Type
journal article
Language
en
Open access
closed
Locations
  • Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Preterm Birth and Chorioamnionitis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
Keywords
cortisol, type I collagen, COL1A1, COL1A2, autophagy, lysosomes, glucocorticoid receptor, fetal membrane rupture, childbirth, 11β-hydroxysteroid dehydrogenase type 1, LC3-II/LC3-I ratio, protein degradation
MeSH terms
Bortezomib, Collagen Type I, alpha 1 Chain, Amnion, Autophagy, Cells, Cultured, Dose-Response Relationship, Drug, Fibroblasts, Humans, Hydrocortisone, Leupeptins, Lysosomes, Receptors, Glucocorticoid, Cysteine Proteinase Inhibitors, Collagen Type I, RNA, Small Interfering

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