Effects of PGF2α-induced luteolysis and progesterone on follicular growth in pregnant mice

Peluso, John J.; Leiper, S.; Steger, Richard W.

doi:10.1016/0090-6980(80)90077-5

Cited by 13 publications

(7 citation statements)

References 18 publications

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“…Progesterone (P4) slows the rate at which granulosa cells and immortalized cells derived from granulosa cells, that is, spontaneously immortalized granulosa cells (SIGCs), undergo mitosis and apoptosis in vitro [1][2][3][4][5][6][7][8][9]. However, the classic nuclear progesterone receptor (PGR) does not mediate P4's actions because granulosa cells of growing follicles and SIGCs do not express PGR [10][11][12][13].…”

Section: Introductionmentioning

confidence: 98%

Expression of Progesterone Receptor Membrane Component-2 Within the Immature Rat Ovary and Its Role in Regulating Mitosis and Apoptosis of Spontaneously Immortalized Granulosa Cells1

Griffin

Liu

Pru

et al. 2014

Biology of Reproduction

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Progesterone receptor membrane component 2 (Pgrmc2) mRNA was detected in the immature rat ovary. By 48 h after eCG, Pgrmc2 mRNA levels decreased by 40% and were maintained at 48 h post-hCG. Immunohistochemical studies detected PGRMC2 in oocytes and ovarian surface epithelial, interstitial, thecal, granulosa, and luteal cells. PGRMC2 was also present in spontaneously immortalized granulosa cells, localizing to the cytoplasm of interphase cells and apparently to the mitotic spindle of cells in metaphase. Interestingly, PGRMC2 levels appeared to decrease during the G1 stage of the cell cycle. Moreover, overexpression of PGRMC2 suppressed entry into the cell cycle, possibly by binding the p58 form of cyclin dependent kinase 11b. Conversely, Pgrmc2 small interfering RNA (siRNA) treatment increased the percentage of cells in G1 and M stage but did not increase the number of cells, which was likely due to an increase in apoptosis. Depleting PGRMC2 did not inhibit cellular (3)H-progesterone binding, but attenuated the ability of progesterone to suppress mitosis and apoptosis. Taken together these studies suggest that PGRMC2 affects granulosa cell mitosis by acting at two specific stages of the cell cycle. First, PGRMC2 regulates the progression from the G0 into the G1 stage of the cell cycle. Second, PGRMC2 appears to localize to the mitotic spindle, where it likely promotes the final stages of mitosis. Finally, siRNA knockdown studies indicate that PGRMC2 is required for progesterone to slow the rate of granulosa cell mitosis and apoptosis. These findings support a role for PGRMC2 in ovarian follicle development.

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Section: Introductionmentioning

confidence: 98%

Expression of Progesterone Receptor Membrane Component-2 Within the Immature Rat Ovary and Its Role in Regulating Mitosis and Apoptosis of Spontaneously Immortalized Granulosa Cells1

Griffin

Liu

Pru

et al. 2014

Biology of Reproduction

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“…This expression pattern is consistent with PGRMC1 being a mediator of progesterone's actions in granulosa cells. Specially, the ability of progesterone (P4) to slow ovarian follicular growth has been demonstrated in hypophysectomized hamsters (Moore and Greenwald, 1974), gonadotropin-primed hamsters (Kim and Greenwald, 1987) rats (Buffler and Roser, 1974), mice (Peluso et al, 1980), and monkeys (Dizerega and Hodgen, 1982). Given these findings, this mini review will focus on the experimental evidence that supports a role for P4-PGRMC1 signaling in regulating the granulosa cell functions of mitosis and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Progesterone receptor membrane component 1 and its role in ovarian follicle growth

Peluso¹

2013

Front. Neurosci.

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Progesterone (P4) is synthesized in the ovary and acts directly on granulosa cells of developing ovarian follicles to suppress their rate of mitosis and apoptosis. Granulosa cells do not express nuclear progesterone receptor (PGR) but rather progesterone receptor membrane component-1 (PGRMC1). PGRMC1 binds P4 and mediates P4's actions, as evidenced by PGRMC1 siRNA studies. PGRMC1 acts by binding plasminogen activator inhibitor 1 RNA-binding protein and regulating gene expression. Specifically, PGRMC1 suppresses some genes that promote cell death (i.e., Bad, Caspase-3, Caspase-4). P4 regulates gene expression in part by inhibiting PGRMC1 binding to Tcf/Lef transcription sites, thereby reducing Tcf/Lef transcriptional activity. Since Tcf/Lef transcription sites are located within the promoters of genes that initiate mitosis and/or apoptosis (i.e., c-jun and c-myc), P4-PGRMC1 mediated suppression of these Tcf/Lef regulated genes could account for P4's actions. PGRMC1 expression is also altered in women with polycystic ovarian syndrome, premature ovarian failure and infertility. Collectively, these observations support a role for PGRMC1 in regulating human ovarian follicle development.

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“…In mice, P4 is secreted by the corpus luteum of the ovary throughout the entire pregnancy where it is canonically regulated by the prostaglandin (PG) F2α (Diaz et al, 2002; Peluso et al, 1980). To evaluate if secreted PGF2α upregulation was associated with reduced P4, PGF2α as well as PGE2, a prostaglandin that has been observed to be upregulated with IAV infection in nonpregnant mice (Coulombe et al, 2014), were measured in the lungs (i.e., the site of IAV replication), systemic circulation, and the ovaries (i.e., the site of P4 secretion) of IAV-infected and mock inoculated dams at 1 and 3 dpi ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, IAV infection during pregnancy is associated with pulmonary tissue damage, impaired epithelial regeneration, reduced progesterone (P4) concentrations, and a shift of alveolar macrophages from a classical to an alternative activation state (Lauzon-Joset et al, 2019; Marcelin et al, 2011; Swieboda et al, 2020; Vermillion et al, 2018). Pregnant dams infected with IAV have reduced adaptive immune responses including reduced IAV-specific antibody titers, numbers of circulating CD4 + and CD8 + T cells, and IAV-specific cytotoxic T cell activity, with these effects associated with changes in circulating P4 and estrogens (Chan et al, 2010; Engels et al, 2017; Peluso et al, 1980; Swieboda et al, 2020). Whether IAV-induced changes in circulating concentrations of sex steroids are a cause or consequence of maternal disease during infection has not been determined.…”

Section: Introductionmentioning

confidence: 99%

Suppression of progesterone by influenza A virus mediates adverse maternal and fetal outcomes in mice

Creisher,

Parish,

Lei

et al. 2023

Preprint

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Influenza A virus infection during pregnancy can cause adverse maternal and fetal outcomes, but the mechanism responsible remains elusive. Infection of outbred mice with 2009 H1N1 at embryonic day (E) 10 resulted in significant maternal morbidity, placental tissue damage and inflammation, fetal growth restriction, and developmental delays that lasted through weaning. Restriction of pulmonary virus replication was not inhibited during pregnancy, but infected dams had suppressed circulating and placental progesterone (P4) concentrations that were caused by H1N1-induced upregulation of pulmonary cyclooxygenase (COX)-1, but not COX-2-, dependent synthesis and secretion of prostaglandin (PG) F2α. Treatment with 17-α-hydroxyprogesterone caproate (17-OHPC), a synthetic progestin that is safe to use in pregnancy, ameliorated the adverse maternal and fetal outcomes from H1N1 infection and prevented placental cell death and inflammation. These findings highlight the therapeutic potential of progestin treatments for influenza during pregnancy.

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Effects of PGF2α-induced luteolysis and progesterone on follicular growth in pregnant mice

Cited by 13 publications

References 18 publications

Expression of Progesterone Receptor Membrane Component-2 Within the Immature Rat Ovary and Its Role in Regulating Mitosis and Apoptosis of Spontaneously Immortalized Granulosa Cells1

Expression of Progesterone Receptor Membrane Component-2 Within the Immature Rat Ovary and Its Role in Regulating Mitosis and Apoptosis of Spontaneously Immortalized Granulosa Cells1

Progesterone receptor membrane component 1 and its role in ovarian follicle growth

Suppression of progesterone by influenza A virus mediates adverse maternal and fetal outcomes in mice

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