Estrogen Receptor Β
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2021 ◽  
pp. 101173
Author(s):  
Masaki Iwamoto ◽  
Takahiro Masuya ◽  
Mari Hosose ◽  
Koki Tagawa ◽  
Tomoka Ishibashi ◽  
...  

2021 ◽  
Vol 206 (Supplement 3) ◽  
Author(s):  
Wei Zhu ◽  
Wenbiao Ren ◽  
Chawnshang Chang ◽  
Edward M. Messing ◽  
Jean V. Joseph ◽  
...  

2021 ◽  
Author(s):  
Wentao Fan ◽  
Chenchen Ding ◽  
Shuihui Liu ◽  
Xiaona Gao ◽  
Xiaofei Shen ◽  
...  

Abstract Estrogen receptor β (ERβ) and NLRP6 are highly expressed in intestinal tissues. Loss of ERβ and NLRP6 exacerbate colitis in mouse models. However, the underlying mechanisms are incompletely understood. Here, we report that ERβ attenuates inflammation by inducing NLRP6-mediated autophagy. Specifically, ERβ directly activates the NLRP6 gene expression via binding to estrogen responsive element (ERE) of Nlrp6 gene promoter. ERβ also physically interacts with the NLRP6 nucleotide-binding domain and promotes NLRP6 inflammasome assembly. The ERβ-NLRP6 axis then interacts with multiple autophagy-related proteins including ULK1, BECN1, ATG16L1, LC3B, p62 to affect the autophagosome biogenesis and control autophagic flux. Finally, NLRP6-mediated autophagy suppresses the inflammatory response by promoting the K48-linked polyubiquitination of ASC, Casp-1 p20, IL-1β, TNF-α, and prohibitin-2. Thus, ERβ-NLRP6 direct an anti-inflammatory response by promoting autophagy. Our work uncovers an ERβ-NLRP6-autophagy pathway as an unrecognized regulatory mechanism that maintains intestinal epithelial cell homeostasis and facilitates tissue repair in colitis.


Stroke ◽  
2021 ◽  
Author(s):  
Kimihiko Yokosuka ◽  
Caleb Rutledge ◽  
Yoshinobu Kamio ◽  
Atsushi Kuwabara ◽  
Hiroki Sato ◽  
...  

Background and Purpose: The incidences of intracranial aneurysm and aneurysmal subarachnoid hemorrhage are high in postmenopausal women. Although population-based studies suggest that hormone replacement therapy is beneficial for postmenopausal women with intracranial aneurysms, estrogen replacement may no longer be recommended for the prevention of chronic diseases given its association with adverse outcomes, such as cancer and ischemic stroke. The isoflavone daidzein and its intestinal metabolite equol are bioactive phytoestrogens and potent agonists of estrogen receptors. Given their estrogenic properties, we investigated whether the isoflavones daidzein and equol are protective against the formation and rupture of intracranial aneurysms in a mouse model of the postmenopausal state. Methods: We induced intracranial aneurysms in ovariectomized adult female mice using a combination of induced systemic hypertension and a single injection of elastase into the cerebrospinal fluid. We fed the mice with an isoflavone-free diet with/without daidzein supplementation, or in a combination of intraperitoneal equol, or oral vancomycin treatment. We also used estrogen receptor beta knockout mice. Results: Both dietary daidzein and supplementation with its metabolite, equol, were protective against aneurysm formation in ovariectomized mice. The protective effects of daidzein and equol required estrogen receptor-β. The disruption of the intestinal microbial conversion of daidzein to equol abolished daidzein’s protective effect against aneurysm formation. Mice treated with equol had lower inflammatory cytokines in the cerebral arteries, suggesting that phytoestrogens modulate inflammatory processes important to intracranial aneurysm pathogenesis. Conclusions: Our study establishes that both dietary daidzein and its metabolite, equol, protect against aneurysm formation in ovariectomized female mice through the activation of estrogen receptor-β and subsequent suppression of inflammation. Dietary daidzein’s protective effect required the intestinal conversion to equol. Our results indicate the potential therapeutic value of dietary daidzein and its metabolite, equol, for the prevention of the formation of intracranial aneurysms and related subarachnoid hemorrhage.


Author(s):  
Liubing Lin ◽  
Mengen Zhou ◽  
Renye Que ◽  
Yirong Chen ◽  
Xiaolin Liu ◽  
...  

Liver fibrosis is the ultimate common pathway in most types of chronic liver damage characterized by imbalance of extracellular matrix degradation and synthesis. Saikosaponin-d (SSd) possesses anti-inflammatory and anti-liver fibrosis effects. However, the underlying mechanism of SSd in repressing hepatic stellate cells (HSCs) activation remains unclear. Here we found that SSd alleviated remarkably carbon tetrachloride (CCl4)-induced liver fibrosis, as evidenced by decreased collagen level and profibrotic markers (COl1a1 and α-smooth muscle actin (SMA)) expression. SSd repressed CCl4-induced NOD-like receptor family pyrin-domain-containng-3 (NLRP3) activation in fibrotic livers, as suggested by decreased level of NLRP3, IL-18, and IL-β. The primary HSCs of CCl4 mice exhibited a significant increase in profibrotic markers expression and NLRP3 activation, but SSd treatment reversed the effect. SSd also repressed TGF-β-induced profibrotic markers expression and NLRP3 activation in vitro. Mechanistically, TGF-β decreased the expression of Estrogen receptor-β (ERβ) in HSCs, whereas SSd treatment reversed the effect. ERβ inhibition enhanced NLRP3 activation in HSCs. More important, ERβ or NLRP3 inhibition destroyed partially the function of SSd on anti-liver fibrosis. In summary, the current data suggest that SSd prevents hepatic fibrosis through regulating ERβ/NLRP3 inflammasome pathway, and suggest SSd as a potential agent for treating liver fibrosis.


2021 ◽  
pp. JN-RM-0164-21
Author(s):  
Teresa A. Milner ◽  
Natalina H. Contoreggi ◽  
Fangmin Yu ◽  
Megan A. Johnson ◽  
Gang Wang ◽  
...  

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