Roles of Progesterone Receptor Membrane Component 1 in Oxidative Stress—Induced Aging in Chorion Cells

Feng, Liping; Allen, Terrence K.; Marinello, William P.; Murtha, Amy P.

doi:10.1177/1933719118776790

Cited by 31 publications

(29 citation statements)

References 49 publications

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“…Our findings demonstrate that MPA but not P4 inhibit IL1β-induced MMP1 mRNA expression and IL8 mRNA levels and secreted protein levels through GR and not through PGRMC1 in amnion mesenchymal cells. These findings are similar to our previous work in amnion epithelial cells which demonstrated that the inhibition of cytokine-induced MMP9 activity and mRNA levels in amnion epithelial cells was mediated through GR ( Allen et al, 2019 ). Additionally, PGRMC1 localizes to the perinuclear area and the nucleus which is stark contrast to its expression pattern in amnion epithelial cells where it primarily localized to the cytoplasm and perinuclear area ( Allen et al, 2019 ).…”

Section: Discussionsupporting

confidence: 92%

“…We have previously demonstrated that PGRMC1 protein expression is diminished in PPROM patients when compared with term and preterm no labor patients highlighting the fact that PGRMC1 may play a role in molecular mechanisms that lead to fetal membrane rupture ( Feng et al, 2014 ). Functionally we have shown that PGRMC1 partially mediates the inhibition of progestins on cytokine induced MMP9 activity in the HTR8 cytotrophoblast cell line and primary amnion epithelial cells ( Allen et al, 2014 , 2019 ). PGRMC1 may also play a role in oxidative stress induced senescence in fetal membranes ( Feng et al, 2019 ).…”

Section: Introductionmentioning

confidence: 88%

“…Functionally we have shown that PGRMC1 partially mediates the inhibition of progestins on cytokine induced MMP9 activity in the HTR8 cytotrophoblast cell line and primary amnion epithelial cells ( Allen et al, 2014 , 2019 ). PGRMC1 may also play a role in oxidative stress induced senescence in fetal membranes ( Feng et al, 2019 ). These findings demonstrate that PGRMC1 plays a role in maintaining fetal membrane integrity but its role in the amnion mesenchymal cells still remains unknown.…”

Section: Introductionmentioning

confidence: 88%

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Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells

2020

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Preterm premature rupture of membranes is a leading cause of preterm births. Cytokine induced matrix metalloproteinase1 and interleukin 8 production from amnion mesenchymal cells may contribute to fetal membrane weakening and rupture. Progestins inhibit inflammation induced fetal membrane weakening but their effect on the inflammatory response of amnion mesenchymal cells is unknown. This study was designed to determine the role of progesterone receptor membrane component 1 and the glucocorticoid receptor in mediating the effects of progestins on interleukin-1β induced matrix metalloproteinase 1 and interleukin-8 expression in human amnion mesenchymal cells. Primary amnion mesenchymal cells harvested from human fetal membranes were passaged once and treated with vehicle, progesterone or medroxyprogesterone acetate at 10 −6 M for 1 h followed by stimulation with interleukin-1β at 1 ng/ml for 24 h. Medroxyprogesterone acetate but not progesterone inhibited interleukin-1β-induced interlukin-8 and matrix metalloproteinase 1 mRNA expression. In subsequent dose response studies, medroxyprogesterone acetate, but not progesterone, at doses of 10 −6-10 −8 M inhibited interleukin-1β induced interleukin-8 and matrix metalloproteinase 1 mRNA expression. We further demonstrated that inhibition of glucocorticoid receptor expression, but not progesterone receptor membrane component 1 knockdown with small interfering RNA transfection, resulted in a reversal in medroxyprogesterone acetate's (10 −7 M) inhibition of interleukin-1β-induced matrix metalloproteinase 1 mRNA expression and interleukin-8 mRNA expression and protein expression. Our findings demonstrate that medroxyprogesterone acetate exerts its anti-inflammatory effect primarily through the glucocorticoid receptor in human amnion mesenchymal cells. Modulation of glucocorticoid receptor signaling pathways maybe a useful therapeutic strategy for preventing inflammation induced fetal membrane weakening leading to preterm premature rupture of membranes.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 88%

See 1 more Smart Citation

Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells

2020

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“…Two-dimensional (2D) single cell type culture experiments are most easy to run and low cost, and thus broadly utilized (Kendal-Wright, 2007;Menon et al, 2013;Meng et al, 2016;Sato et al, 2016;Feng et al, 2018b;Hadley et al, 2018;Jin et al, 2018). However, regardless of the cell origin (i.e., primary or immortalized) or cell layer (i.e., amnion or chorion), the major drawback is the limitations stemming from studying only a small part of the whole organ.…”

Section: In Vitro Cell Culture Techniquesmentioning

confidence: 99%

Organ-On-Chip Technology: The Future of Feto-Maternal Interface Research?

et al. 2020

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“…These effects are potentially mediated by nPRs functioning in the cytoplasm to directly affect other cell signaling pathways (66,67), by membrane-associated PRs (mPRs) that are coupled to specific intracellular signaling pathways (68)(69)(70)(71)(72)(73)(74), and/or by P4 (or its metabolites) interacting with neurotransmitter and peptide hormone receptors (75). Although the physiology role of putative mPRs as mediators of P4 actions is somewhat controversial (76)(77)(78), several studies suggest that certain forms mediate distinct pro-gestational actions of P4 in the myometrium, cervix and fetal membranes (79)(80)(81)(82)(83)(84)(85)(86).…”

Section: P4/pr Signaling In Human Pregnancy and Parturitionmentioning

confidence: 99%

Progestin therapy to prevent preterm birth: History and effectiveness of current strategies and development of novel approaches

et al. 2019

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In the 1930s the "progestin" hormone produced by the corpus luteum was isolated and found to be a Δ 4-keto-steroid. It was aptly named progesterone (P4) and in the following 30 years the capacity of P4 and derivatives to prevent preterm birth (PTB) was examined. Outcomes of multiple small studies suggested that progestin prophylaxis beginning at mid-gestation decreases the risk for PTB. Subsequent larger trials found that prophylaxis with weekly intramuscular injections of 17αhydroxyprogesterone caproate (17HPC) beginning at midgestation decreased PTB risk in women with a history of PTB. Other trials found that daily vaginal P4 prophylaxis, also beginning at midgestation decreased PTB risk in women with a short cervix. Currently, prophylaxis with 17HPC (in women with a history of PTB) or vaginal P4 (in women with a short cervix) are used to prevent PTB. Recent advances in understanding the molecular biology of P4 signaling in uterine cells is revealing novel progestin-based targets for PTB prevention. One possibility is to use selective P4 receptor (PR) modulators (SPRMs) to boost PR anti-inflammatory activity that blocks labor, while simultaneously preventing PR phosphorylation that causes loss of P4/PR anti-inflammatory activity. This may be achieved by SPRMs that induce a specific PR conformation that prevents site-specific serine phosphorylation that inhibits anti-inflammatory activity. Further advances in understanding how P4 promotes uterine quiescence and how its labor blocking actions are withdrawn to trigger parturition will reveal novel therapeutic targets to more effectively prevent PTB.

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Roles of Progesterone Receptor Membrane Component 1 in Oxidative Stress—Induced Aging in Chorion Cells

Abstract: This study further demonstrated that oxidative stress-induced cell aging is one of the mechanisms of PPROM and PGRMC1 acts as a protective element for maintaining fetal membrane integrity by inhibiting oxidative stress-induced chorion cell aging.

Cited by 31 publications

References 49 publications

Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells

Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells

Organ-On-Chip Technology: The Future of Feto-Maternal Interface Research?

Progestin therapy to prevent preterm birth: History and effectiveness of current strategies and development of novel approaches

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