Notch1 signaling enhances collagen expression and fibrosis in mouse uterus

BioFactors ◽  
2021 ◽  
Author(s):  
Qi‐Xin Xu ◽  
Wang‐Qing Zhang ◽  
Xiao‐Zheng Liu ◽  
Wan‐Kun Yan ◽  
Lei Lu ◽  
...  
Keyword(s):  
Mouse Uterus ◽  
Collagen Expression ◽  
Notch1 Signaling

scholarly journals Overexpression of miRNA-25-3p inhibits Notch1 signaling and TGF-β-induced collagen expression in hepatic stellate cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Berit Genz ◽  
Miranda A. Coleman ◽  
Katharine M. Irvine ◽  
Jamie R. Kutasovic ◽  
Mariska Miranda ◽  
...  
Keyword(s):  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Collagen Expression ◽  
Notch1 Signaling ◽  
Mirna 25

ISOLEMENT ET QUELQUES CARACTERISTIQUES D'UNE GONADOTROPHINE URINAIRE DE MÉNOPAUSE HOMOGÈNE A L'ELECTROPHORÈSE

1960 ◽  
Vol XXXV (II) ◽  
pp. 225-234 ◽  
Author(s):  
R. Bourrillon ◽  
R. Got ◽  
R. Marcy
Keyword(s):  
Sialic Acid ◽  
Histological Study ◽  
Active Material ◽  
Biologically Active ◽  
New Method ◽  
Female Rats ◽  
Mouse Uterus ◽  
Highly Active ◽  
Zone Electrophoresis ◽  
Human Menopausal Gonadotrophin

ABSTRACT A new method for preparation of Human Menopausal Gonadotrophin involves successively alcoholic precipitation, kaolin adsorption and chromatography on ion exchangers. A highly active material is obtained which corresponds to 1 mg per litre of urine and has an activity of 1 mouse uterus unit at a dose of 0.003 mg. This gonadotrophin possesses both follicle stimulating and luteinizing activities in hypophysectomized female rats, by histological study. It contains 13 % hexose, 10% hexosamine and 8.5 % sialic acid. A further purification, by zone electrophoresis on starch, gives a final product, biologically active at 0.001 mg, which behaves as an homogenous substance in free electrophoresis with mobility −4.76 × 10−5 at pH 8.6.

Inhibition of TMEM16A impedes embryo implantation and decidualization in mice

Reproduction ◽  
2018 ◽  
Author(s):  
Qianrong Qi ◽  
Yifan Yang ◽  
Kailin Wu ◽  
Qingzhen Xie
Keyword(s):  
Progesterone Receptor ◽  
Stromal Cells ◽  
Embryo Implantation ◽  
Mouse Uterus ◽  
Endometrial Stromal Cells ◽  
Uterine Endometrium ◽  
Molecule Inhibitor ◽  
Pathway Inhibition ◽  
And Function ◽  
Reproductive Processes

Recent studies revealed that TMEM16A is involved in several reproductive processes, including ovarian estrogen secretion and ovulation, sperm motility and acrosome reaction, fertilization, and myometrium contraction. However, little is known about the expression and function of TMEM16A in embryo implantation and decidualization. In this study, we focused on the expression and regulation of TMEM16A in mouse uterus during early pregnancy. We found that TMEM16A is up-regulated in uterine endometrium in response to embryo implantation and decidualization. Progesterone treatment could induce TMEM16A expression in endometrial stromal cells through progesterone receptor/c-Myc pathway, which is blocked by progesterone receptor antagonist or the inhibitor of c-Myc signaling pathway. Inhibition of TMEM16A by small molecule inhibitor (T16Ainh-A01) resulted in impaired embryo implantation and decidualization in mice. Treatment with either specific siRNA of Tmem16a or T16Ainh-A01 inhibited the decidualization and proliferation of mouse endometrial stromal cells. In conclusion, our results revealed that TMEM16A is involved in embryo implantation and decidualization in mice, compromised function of TMEM16A may lead to impaired embryo implantation and decidualization.

Differential expression and regulation of prostaglandin transporter and metabolic enzymes in mouse uterus during blastocyst implantation

2007 ◽  
Vol 88 (4) ◽  
pp. 1256-1265 ◽  
Author(s):  
Fei Gao ◽  
Wei Lei ◽  
Hong-Lu Diao ◽  
Shi-Jun Hu ◽  
Li-Ming Luan ◽  
...  
Keyword(s):  
Differential Expression ◽  
Metabolic Enzymes ◽  
Mouse Uterus ◽  
Blastocyst Implantation

scholarly journals Jagged1-mediated myeloid Notch1 signaling activates HSF1/Snail and controls NLRP3 inflammasome activation in liver inflammatory injury

2019 ◽  
Vol 17 (12) ◽  
pp. 1245-1256 ◽  
Author(s):  
Yuting Jin ◽  
Changyong Li ◽  
Dongwei Xu ◽  
Jianjun Zhu ◽  
Song Wei ◽  
...  
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Immune Cell ◽  
Ischemia Reperfusion ◽  
Inflammasome Activation ◽  
Inflammatory Injury ◽  
Notch1 Signaling ◽  
Caspase 1 ◽  
Hepatocellular Damage ◽  
Hepatocellular Apoptosis

AbstractNotch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response. Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue. However, it remains unknown whether Jagged1 (JAG1)-mediated myeloid Notch1 signaling regulates NLRP3 function in acute liver injury. Here, we report that myeloid Notch1 signaling regulates the NLRP3-driven inflammatory response in ischemia/reperfusion (IR)-induced liver injury. In a mouse model of liver IR injury, Notch1-proficient (Notch1FL/FL) mice receiving recombinant JAG1 showed a reduction in IR-induced liver injury and increased Notch intracellular domain (NICD) and heat shock transcription factor 1 (HSF1) expression, whereas myeloid-specific Notch1 knockout (Notch1M-KO) aggravated hepatocellular damage even with concomitant JAG1 treatment. Compared to JAG1-treated Notch1FL/FL controls, Notch1M-KO mice showed diminished HSF1 and Snail activity but augmented NLRP3/caspase-1 activity in ischemic liver. The disruption of HSF1 reduced Snail activation and enhanced NLRP3 activation, while the adoptive transfer of HSF1-expressing macrophages to Notch1M-KO mice augmented Snail activation and mitigated IR-triggered liver inflammation. Moreover, the knockdown of Snail in JAG1-treated Notch1FL/FL livers worsened hepatocellular functioning, reduced TRX1 expression and increased TXNIP/NLRP3 expression. Ablation of myeloid Notch1 or Snail increased ASK1 activation and hepatocellular apoptosis, whereas the activation of Snail increased TRX1 expression and reduced TXNIP, NLRP3/caspase-1, and ROS production. Our findings demonstrated that JAG1-mediated myeloid Notch1 signaling promotes HSF1 and Snail activation, which in turn inhibits NLRP3 function and hepatocellular apoptosis leading to the alleviation of IR-induced liver injury. Hence, the Notch1/HSF1/Snail signaling axis represents a novel regulator of and a potential therapeutic target for liver inflammatory injury.

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