Oxidative stress induces senescence and sterile inflammation in murine amniotic cavity

Polettini, Jossimara; Richardson, Lauren

doi:10.1016/j.placenta.2018.01.009

Cited by 39 publications

(49 citation statements)

References 28 publications

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“…Similar to our in vitro studies, our laboratory has also reported that OS can cause p38MAPK activation and senescence in the amniotic cavity of CD‐1 mice . OS‐induced p38MAPK activation, senescence, sterile inflammation, and pre‐term labor were inhibited by pharmacologic p38MAPK inhibitor SB203580 and antioxidant N‐acetyl cysteine, supporting the hypothesis that the senescence pathway is functionally active in this model .…”

Section: Introductionsupporting

confidence: 87%

“…OS‐induced p38MAPK activation, senescence, sterile inflammation, and pre‐term labor were inhibited by pharmacologic p38MAPK inhibitor SB203580 and antioxidant N‐acetyl cysteine, supporting the hypothesis that the senescence pathway is functionally active in this model . Senescence‐associated sterile inflammation in these mice contributes to the initiation of labor . We hypothesize that GSK3β and p38MAPK activities are balanced to maintain cellular homeostasis during gestation, but OS at term causes overwhelming p38MAPK activation to suppress GSK3β's function, resulting in senescence.…”

Section: Introductionsupporting

confidence: 60%

“…Activation of p38MAPK coincided with senescence of fetal membranes . This model was further tested by Polettini et al who have shown that OS‐inducing factors can accelerate aging via p38MAPK activation to ultimately cause pre‐term birth. This effect was minimized by p38MAPK inhibitor .…”

Section: Discussionmentioning

confidence: 95%

“…This model was further tested by Polettini et al who have shown that OS‐inducing factors can accelerate aging via p38MAPK activation to ultimately cause pre‐term birth. This effect was minimized by p38MAPK inhibitor . In the present study, we were able to reproduce similar findings where we noted a progressive change in phosphorylation or activation of p38MAPK in fetal membranes of CD‐1 mice as the gestational age increased, replicating the prior reports by Bonney et al This change corresponded to an increase in phosphorylation or inactivation of GSK3β, with maximal inactivation at E18.…”

Section: Discussionmentioning

confidence: 99%

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Changes in mediators of pro‐cell growth, senescence, and inflammation during murine gestation

Lavu

Sheller‐Miller

Kechichian

et al. 2020

American J Rep Immunol

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Problem: Senescence of the fetal membranes and senescence-associated inflammation have been associated with parturition at term and pre-term in both mice and humans. Using a pregnant mouse model, we determined changes in multiple molecular signalers contributing to senescence and inflammation associated with parturition. Method of study:Fetal membranes were collected from timed-pregnant CD-1 mice on gestation days (E) 13, 15, 17, 18, and 19. Immunohistochemistry (IHC) localized pro-cell growth factors glycogen synthase kinase 3β (GSK3β) and β-catenin. Gestational age-associated changes in pro-cell growth vs senescence mediators (p38 mitogen-activated protein kinase [p38MAPK]), prooxidants (heme oxygenase-1 [HO-1], peroxisome proliferator-activated receptor γ [PPARγ]), and pro-and anti-inflammatory cytokines (IL-6, IL-8, IL-10, and IL-1β) were determined by Western blots and Luminex assays. Results: Fetal membrane expressions of phosphorylated forms of GSK3β (inactivation) and p38MAPK (activation) increased, while β-catenin expression decreased, as gestation progressed. Antioxidant HO-1 expression decreased while PPARγ increased toward term gestation. IL-6 and IL-8 concentrations were highest on E19 (day of delivery), while IL-10 and IL-1β concentrations were highest on E15. Conclusion: Mouse fetal membranes showed a progressive senescence marker increase coincided with downregulation of cell growth factors. Development of senescence is associated with inflammation. Senescence-associated changes are natural and physiologic and indicative of fetal membranes' readiness for parturition. K E Y W O R D Sfetal membranes, GSK3β, oxidative stress, p38MAPK, pre-term labor, senescence

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Section: Introductionsupporting

confidence: 87%

Section: Introductionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Changes in mediators of pro‐cell growth, senescence, and inflammation during murine gestation

Lavu

Sheller‐Miller

Kechichian

et al. 2020

American J Rep Immunol

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“…Increased OS at term has been shown to induce laborassociated changes, such as cellular senescence, matrix metallopeptidase 9 up-regulation, and increased proinflammatory cytokine production in fetal membrane cells, including AECs and AMCs (2,23). CSE, a potent and reliable OS inducer (2,17,23,(31)(32)(33)(34)(35), has been shown to recreate the labor phenotype (OS experienced at term labor in amnion membranes) in vitro and to induce a static state of EMT in AECs (17,33). EMT contributes to sustained inflammation that promotes the labor-related cascade of events.…”

Section: Os Induces Changes In Amnion Intermediate Filament Expressiomentioning

confidence: 99%

Amnion membrane organ‐on‐chip: an innovative approach to study cellular interactions

et al. 2019

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The amnion membrane that lines the human intrauterine cavity is composed of amnion epithelial cells (AECs) connected to an extracellular matrix containing amnion mesenchymal cells (AMCs) through a basement membrane. Cellular interactions and transitions are mechanisms that facilitate membrane remodeling to maintain its integrity. Dysregulation of cellular remodeling, primarily mediated by oxidative stress (OS), is often associated with preterm birth. However, the mechanisms that maintain membrane homeostasis remain unclear. To understand these mechanisms, we developed an amnion membrane organ‐on‐chip (AM‐OOC) and tested the interactive and transition properties of primary human AECs and AMCs under normal and OS conditions. AM‐OOC contained 2 chambers connected by type IV collagen—coated microchannels, allowing independent culture conditions that permitted cellular migration and interactions. Cells grown either independently or coculture were exposed to OS inducing cigarette smoke extract, antioxidant N‐acetyl‐l‐cysteine (NAC), or both. When grown independently, AECs transitioned to AMCs and migrated, whereas AMCs migrated without transition. OS caused AECs' transition but prevented migration, whereas AMCs' migration was unhindered. Coculture of cells facilitated transition, migration, and eventual integration in the contiguous population. OS cotreatment in both chambers facilitated AECs' transition, prevented migration, and increased inflammation, a process that was prevented by NAC. AM‐OOC recapitulated cellular mechanisms observed in utero and enabled experimental manipulation of cells to determine their roles during pregnancy and parturition.—Richardson, L., Jeong, S., Kim, S., Han, A., Menon, R. Amnion membrane organ‐on‐chip: an innovative approach to study cellular interactions. FASEB J. 33, 8945–8960 (2019). http://www.fasebj.org

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Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes

et al. 2020

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Oxidative stress induces senescence and sterile inflammation in murine amniotic cavity

Cited by 39 publications

References 28 publications

Changes in mediators of pro‐cell growth, senescence, and inflammation during murine gestation

Changes in mediators of pro‐cell growth, senescence, and inflammation during murine gestation

Amnion membrane organ‐on‐chip: an innovative approach to study cellular interactions

Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes

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