Obstetric hemorrhage

Velde, Marc Van de; Varon, Albert J.

doi:10.1097/aco.0000000000000168

Cited by 22 publications

(21 citation statements)

References 28 publications

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“…It has also been used to treat postpartum hemorrhage [42][43][44][45][46][47][48][49][50][51]. Although few prospective data exist, these situations are commonly associated with massive transfusion and the risk for rapid development of coagulopathy.…”

Section: Who Needs Damage Control Resuscitation?mentioning

confidence: 99%

Massive transfusion

Murphy

Hess

2015

Current Opinion in Hematology

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Section: Who Needs Damage Control Resuscitation?mentioning

confidence: 99%

Massive transfusion

Murphy

Hess

2015

Current Opinion in Hematology

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“…Postpartum hemorrhage is one of the most common complications in obstetric practice [1][2][3], resulting in ischemia to the endometrium and necrosis of endometrial cells [1][2][3]. To study the pathophysiology of ischemic death [4,5], the oxygen and glucose deprivation (OGD)re-oxygenation (OGDR) model is a useful approach to investigate ischemic-reperfusion endometrial cell injury [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…To study the pathophysiology of ischemic death [4,5], the oxygen and glucose deprivation (OGD)re-oxygenation (OGDR) model is a useful approach to investigate ischemic-reperfusion endometrial cell injury [6][7][8][9]. Following reperfusion, endometrial ischemia induces oxidative stress to the endometrial cells [1][2][3], leading to the accumulation of reactive oxygen species (ROS) and depletion of antioxidants [10][11][12]. Oxidative injury causes excessive DNA breaks, protein damage and mitochondrial dysfunction [10][11][12], eventually leading to endometrial cell necrosis [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

“…Following reperfusion, endometrial ischemia induces oxidative stress to the endometrial cells [1][2][3], leading to the accumulation of reactive oxygen species (ROS) and depletion of antioxidants [10][11][12]. Oxidative injury causes excessive DNA breaks, protein damage and mitochondrial dysfunction [10][11][12], eventually leading to endometrial cell necrosis [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

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Keap1-targeting microRNA-941 protects endometrial cells from oxygen and glucose deprivation-re-oxygenation via activation of Nrf2 signaling

Cheng

et al. 2020

Cell Commun Signal

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Background: Mimicking ischemia-reperfusion injury, oxygen and glucose deprivation (OGD)-re-oxygenation (OGDR) applied to endometrial cells produces significant oxidative stress and programmed necrosis, which can be inhibited by nuclear-factor-E2-related factor 2 (Nrf2) signaling. MicroRNA (miRNA)-induced repression of Keap1, a Nrf2 suppressor protein that facilitates Nrf2 degradation, is novel strategy to activate Nrf2 cascade. Methods: MicroRNA-941 (miR-941) was exogenously expressed in HESC and primary human endometrial cells, and the Nrf2 pathway examined by Western blotting and real-time quantitative PCR analysis. The endometrial cells were treated with OGDR, cell programmed necrosis and apoptosis were tested. Results: MiR-941 is a novel Keap1-targeting miRNA that regulates Nrf2 activity. In T-HESC cells and primary human endometrial cells, ectopic overexpression of miR-941 suppressed Keap1 3′-UTR (untranslated region) expression and downregulated its mRNA/protein expression, leading to activation of the Nrf2 cascade. Conversely, inhibition of miR-941 elevated Keap1 expression and activity in endometrial cells, resulting in suppression of Nrf2 activation. MiR-941 overexpression in endometrial cells attenuated OGDR-induced oxidative stress and programmed necrosis, whereas miR-941 inhibition enhanced oxidative stress and programmed necrosis. MiR-941 overexpression and inhibition were completely ineffective in Keap1−/Nrf2-KO T-HESC cells (using CRISPR/Cas9 strategy). Restoring Keap1 expression, using an UTR-depleted Keap1 construct, abolished miR-941-induced anti-OGDR activity in T-HESC cells. Thus Keap1-Nrf2 cascade activation is required for miR-941-induced endometrial cell protection. Conclusions: Targeting Keap1 by miR-941 activates Nrf2 cascade to protect human endometrial cells from OGDRinduced oxidative stress and programmed necrosis.

show abstract

“…Postpartum hemorrhage is one of the most common complications in obstetric practice [1][2][3], resulting in ischemia to the endometrium and necrosis of endometrial cells [1][2][3]. To study the pathophysiology of ischemic death [4,5], the oxygen and glucose deprivation (OGD)-re-oxygenation 3 (OGDR) model is a useful approach to investigate ischemic-reperfusion endometrial cell injury [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Keap1-targeting microRNA-941 protects endometrial cells from oxygen and glucose deprivation-re-oxygenation via activation of Nrf2 signaling

Cheng

et al. 2020

Preprint

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Background: Mimicking ischemia-reperfusion injury, oxygen and glucose deprivation (OGD)-re-oxygenation (OGDR) applied to endometrial cells produces significant oxidative stress and programmed necrosis, which can be inhibited by nuclear-factor-E2-related factor 2 (Nrf2) signaling. MicroRNA (miRNA)-induced repression of Keap1, a Nrf2 suppressor protein that facilitates Nrf2 degradation, is novel strategy to activate Nrf2 cascade. Methods: MicroRNA-941 (miR-941) was exogenously expressed in HESC and primary human endometrial cells, and the Nrf2 pathway examined by Western blotting and real-time quantitative PCR analysis. The endometrial cells were treated with OGDR, cell programmed necrosis and apoptosis were tested. Results: MiR-941 is a novel Keap1-targeting miRNA that regulates Nrf2 activity. In T-HESC cells and primary human endometrial cells, ectopic overexpression of miR-941 suppressed Keap1 3’-UTR (untranslated region) expression and downregulated its mRNA/protein expression, leading to activation of the Nrf2 cascade. Conversely, inhibition of miR-941 elevated Keap1 expression and activity in endometrial cells, resulting in suppression of Nrf2 activation. MiR-941 overexpression in endometrial cells attenuated OGDR-induced oxidative stress and programmed necrosis, whereas miR-941 inhibition enhanced oxidative stress and programmed necrosis. MiR-941 overexpression and inhibition were completely ineffective in Keap1-/Nrf2-KO T-HESC cells (using CRISPR/Cas9 strategy). Restoring Keap1 expression, using an UTR-depleted Keap1 construct, abolished miR-941-induced anti-OGDR activity in T-HESC cells. Thus Keap1-Nrf2 cascade activation is required for miR-941-induced endometrial cell protection. Conclusions: Targeting Keap1 by miR-941 activates Nrf2 cascade to protect human endometrial cells from OGDR-induced oxidative stress and programmed necrosis.

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Obstetric hemorrhage

Cited by 22 publications

References 28 publications

Massive transfusion

Massive transfusion

Keap1-targeting microRNA-941 protects endometrial cells from oxygen and glucose deprivation-re-oxygenation via activation of Nrf2 signaling

Keap1-targeting microRNA-941 protects endometrial cells from oxygen and glucose deprivation-re-oxygenation via activation of Nrf2 signaling

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