SIRT1 regulates trophoblast senescence in premature placental aging in preeclampsia

Wang, Yujia; Zhang, Yingye; Wu, Yongqi; He, Yunbiao; Xiang, Jingwen; Huang, Jieqiong; Lash, Gendie E.; Li, Ping

doi:10.1016/j.placenta.2022.04.001

Cited by 24 publications

(14 citation statements)

References 39 publications

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“…Downregulation of ZEB1 or ZEB2 triggers senescence both in vivo and in vitro via p53 or p21 activation 19 , 55 , 56 . Moreover, ZEB1 and ZEB2 expression are associated with SIRT1 overexpression and have been implicated in the suppression of p53 and p38 MAP 49 , 57 . Thus, EMT-competent cells may be capable to negating senescence checkpoint functions through ZEB1 and ZEB2, whereas cellular senescence may prevent SIRT1 from inducing ZEB to activate the EMT program.…”

Section: Discussionmentioning

confidence: 99%

“…Tissues were fixed, embedded in paraffin, sectioned (5 µm thick) and stained with haematoxylin and eosin (H&E) and Masson’s trichrome. The methods was performed as previously described 57 . Antibodies were used against the following targets: β-galactosidase (β-gal) (1:100 dilution, Santa Cruz, USA), p16 (1:100 dilution, CST, USA), p38 (1:50 dilution, Abcam, USA), E-cadherin (1:100 dilution, BD Biosciences, USA), vimentin (1:100 dilution, CST, USA) and SIRT1 (1:200 dilution, Abcam, USA).…”

Section: Methodsmentioning

confidence: 99%

“…RT–qPCR and western blotting were performed as previously described 57 . The specific primers and antibodies are presented in Supplementary Table S2 .…”

Section: Methodsmentioning

confidence: 99%

“…Senescent cells were detected using the Senescence β-Galactosidase Staining Kit (Beyotime, China) and observed under a phase-contrast microscope 57 . The quantification of positive cells was performed by counting the cells in 5 random fields per dish.…”

Section: Methodsmentioning

confidence: 99%

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SIRT1 upregulation promotes epithelial-mesenchymal transition by inducing senescence escape in endometriosis

Wang

et al. 2022

Sci Rep

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Endometrial epithelial cells carry distinct cancer-associated alterations that may be more susceptible to endometriosis. Mouse models have shown that overexpression of SIRT1 associated with oncogene activation contributes to the pathogenesis of endometriosis, but the underlying reason remains elusive. Here, we used integrated systems biology analysis and found that enrichment of endometrial stromal fibroblasts in endometriosis and their cellular abundance correlated negatively with epithelial cells in clinical specimens. Furthermore, endometrial epithelial cells were characterized by significant overexpression of SIRT1, which is involved in triggering the EMT switch by escaping damage or oncogene-induced induced senescence in clinical specimens and in vitro human cell line models. This observation supports that genetic and epigenetic incident favors endometrial epithelia cells escape from senescence and fuel EMT process in endometriosis, what could be overcome by downregulation of SIRT1.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…RT–qPCR and western blotting were performed as previously described 57 . The specific primers and antibodies are presented in Supplementary Table S2 .…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

SIRT1 upregulation promotes epithelial-mesenchymal transition by inducing senescence escape in endometriosis

Wang

et al. 2022

Sci Rep

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“…Studies have shown that oxidative stress can lead to premature placental aging by damaging lipids, proteins, and DNA, and it can also trigger the secretion of placental factors that result in enhanced inflammatory reactions and endothelial dysfunction, ultimately provoking PE symptoms [ 69 , 70 ]. It has been reported that PE patients have increased placental oxidative stress, manifested by increased lipid peroxides and the decreased expression and activity of antioxidants [ 71 ].…”

Section: Discussionmentioning

confidence: 99%

Puerariae lobatae Radix Alleviates Pre-Eclampsia by Remodeling Gut Microbiota and Protecting the Gut and Placental Barriers

Huang

Liu

et al. 2022

Nutrients

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Pre-eclampsia (PE) is a serious pregnancy complication, and gut dysbiosis is an important cause of it. Puerariae lobatae Radix (PLR) is a medicine and food homologous species; however, its effect on PE is unclear. This study aimed to investigate the efficacy of PLR in alleviating PE and its mechanisms. We used an NG-nitro-L-arginine methyl ester (L-NAME)-induced PE mouse model to examine the efficacy of preventive and therapeutic PLR supplementation. The results showed that both PLR interventions alleviated hypertension and proteinuria, increased fetal and placental weights, and elevated the levels of VEGF and PlGF. Moreover, PLR protected the placenta from oxidative stress via activating the Nrf2/HO-1/NQO1 pathway and mitigated placental damage by increasing intestinal barrier markers (ZO-1, Occludin, and Claudin-1) expression and reducing lipopolysaccharide leakage. Notably, preventive PLR administration corrected gut dysbiosis in PE mice, as evidenced by the increased abundance and positive interactions of beneficial bacteria including Bifidobacterium, Blautia, and Turicibacter. Fecal microbiota transplantation confirmed that the gut microbiota partially mediated the beneficial effects of PLR on PE. Our findings revealed that modulating the gut microbiota is an effective strategy for the treatment of PE and highlighted that PLR might be used as an intestinal nutrient supplement in PE patients.

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Impact of Aging and Cellular Senescence in the Pathophysiology of Preeclampsia

Suvakov,

Kattah,

Gojkovic

et al. 2023

Comprehensive Physiology

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The incidence of hypertensive disorders of pregnancy is increasing, which may be due to several factors, including an increased age at pregnancy and more comorbid health conditions during reproductive years. Preeclampsia, the most severe hypertensive disorder of pregnancy, has been associated with an increased risk of future disease, including cardiovascular and kidney diseases. Cellular senescence, the process of cell cycle arrest in response to many physiologic and maladaptive stimuli, may play an important role in the pathogenesis of preeclampsia and provide a mechanistic link to future disease. In this article, we will discuss the pathophysiology of preeclampsia, the many mechanisms of cellular senescence, evidence for the involvement of senescence in the development of preeclampsia, as well as evidence that cellular senescence may link preeclampsia to the risk of future disease. Lastly, we will explore how a better understanding of the role of cellular senescence in preeclampsia may lead to therapeutic trials. © 2023 American Physiological Society. Compr Physiol 13:5077‐5114, 2023.

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SIRT1 regulates trophoblast senescence in premature placental aging in preeclampsia

Cited by 24 publications

References 39 publications

SIRT1 upregulation promotes epithelial-mesenchymal transition by inducing senescence escape in endometriosis

SIRT1 upregulation promotes epithelial-mesenchymal transition by inducing senescence escape in endometriosis

Puerariae lobatae Radix Alleviates Pre-Eclampsia by Remodeling Gut Microbiota and Protecting the Gut and Placental Barriers

Impact of Aging and Cellular Senescence in the Pathophysiology of Preeclampsia

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