What is it about?
Glucocorticoids, as a classical anti-inflammatory hormone, have been shown to inhibit matrix metalloproteases in other parts of the body. Unexpectedly, we discovered for the first time that cortisol induced MMP-7, also known as matrilysin, expression by over 1000-fold with consequent degradation of collagen IV in human amnion fibroblasts, the major source of collagens that provide the tensile strength of the fetal membranes. Further mechanistic study revealed that the activated AP-1 mediates the induction of MMP-7 by cortisol. Moreover, we found that labor-initiated spontaneous rupture of membranes which was associated with reciprocal changes in MMP-7 and its substrate, collagen IV. These findings are novel particularly in terms of induction rather than inhibition of MMP-7 by cortisol, which is important in the elucidation of mechanisms underlying the rupture of fetal membranes, the major cause of preterm birth.
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Why is it important?
Our findings indicate that manipulation of the regeneration of glucocorticoids in the fetal membranes is a potential therapeutic strategy for the prevention and treatment of preterm birth induced by preterm premature rupture of membranes.
Perspectives
I think that the obstetricians should pay more attention to the fetal membranes. They are not inert tissue despite lacking innervation and blood supply. The fetal membranes play crucial roles in human parturition. People can find more evidence by searching publications from my laboratory.
Kang Sun
Shanghai Jiao Tong University
Read the Original
This page is a summary of: Drastic induction of MMP-7 by cortisol in the human amnion: implications for membrane rupture at parturition, The FASEB Journal, February 2019, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201801216r.
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