Up-regulation of the Ang II/AT1 receptor may compensate for the loss of gastric antrum ICC via the PI3k/Akt signaling pathway in STZ-induced diabetic mice

2016 ◽  
Vol 423 ◽  
pp. 77-86 ◽  
Author(s):  
C.M. Zhang ◽  
X. Huang ◽  
H.L. Lu ◽  
X.M. Meng ◽  
D.H. Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
At1 Receptor ◽  
Gastric Antrum ◽  
Ang Ii ◽  
Diabetic Mice ◽  
Akt Signaling Pathway

Capn4 aggravates angiotensin II-induced cardiac hypertrophy by activating the IGF-AKT signaling pathway

2021 ◽  
Author(s):  
Yuanping Cao ◽  
Qun Wang ◽  
Caiyun Liu ◽  
Wenjun Wang ◽  
Songqing Lai ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Expression Patterns ◽  
Akt Signaling ◽  
Calpain Inhibitor ◽  
Ang Ii ◽  
Akt Signaling Pathway ◽  
Calpain Activity

Abstract Capn4 belongs to a family of calpains that participate in a wide variety of biological functions, but little is known about the role of Capn4 in cardiac disease. Here, we show that the expression of Capn4 was significantly increased in Angiotensin II (Ang II)-treated cardiomyocytes and Ang II-induced cardiac hypertrophic mouse hearts. Importantly, in agreement with the Capn4 expression patterns, the maximal calpain activity measured in heart homogenates was elevated in Ang II-treated mice, and oral coadministration of SNJ-1945 (calpain inhibitor) attenuated the total calpain activity measured in vitro. Functional assays indicated that overexpression of Capn4 obviously aggravated Ang II-induced cardiac hypertrophy, whereas Capn4 knockdown resulted in the opposite phenotypes. Further investigation demonstrated that Capn4 maintained the activation of the insulin-like growth factor (IGF)-AKT signaling pathway in cardiomyocytes by increasing c-Jun expression. Mechanistic investigations revealed that Capn4 directly bound and stabilized c-Jun, and knockdown of Capn4 increased the ubiquitination level of c-Jun in cardiomyocytes. Additionally, our results demonstrated that the antihypertrophic effect of Capn4 silencing was partially dependent on the inhibition of c-Jun. Overall, these data suggested that Capn4 contributes to cardiac hypertrophy by enhancing the c-Jun-mediated IGF-AKT signaling pathway and could be a potential therapeutic target for hypertrophic cardiomyopathy.

413-P: SIRT1 Overexpression Restores the Protective Effects of Ischemic Post-conditioning in Diabetic Mice via Modulating Akt Signaling Pathway

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 413-P
Author(s):  
MINGGE DING ◽  
KE ZENG ◽  
MINGZHE YU ◽  
CHAOYANG LIU ◽  
FENG FU
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
Protective Effects ◽  
Diabetic Mice ◽  
Akt Signaling Pathway

scholarly journals Angiotensin II enhances the proliferation of Natural Killer/T-cell lymphoma cells via activating PI3K/Akt signaling pathway

2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Gui-Hua Zhang ◽  
Fa-An Miao ◽  
Jin-Ge Xu ◽  
Yan Zhang
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Signaling Pathway ◽  
Nude Mice ◽  
Cell Lymphoma ◽  
Akt Signaling ◽  
T Cell Lymphoma ◽  
Ang Ii ◽  
Akt Signaling Pathway ◽  
Natural Killer T

Abstract The present study was to determine the roles of Angiotensin (Ang) II in the growth of lymphoma in nude mice and the proliferation and viability of the human Natural Killer/T (NK/T)-cell lymphoma cell line SNK-6, and the activation of downstream signaling pathway. Lymphoma samples and corresponding normal tissues were obtained from lymphoma patients. Proliferation of SNK-6 cells was detected by CCK8 or MTT assay. The levels of Ang II and its receptor Ang II type 1 receptor (AT1R) were higher in lymphoma tissues than those in control tissues. Ang II increased the lymphoma volume and size in nude mice, the proliferation and viability and the proliferating cell nuclear antigen (PCNA) and Ki67 levels of SNK-6 cells. Losartan, an antagonist of AT1R, reduced lymphoma volume and size in nude mice, and the proliferation and viability and the PCNA and Ki67 levels of SNK-6 cells. The levels of phosphorylated phosphatidylinositol 3-kinase (p-PI3K) and phosphorylated protein kinase B (p-Akt) were increased by Ang II and then reduced by losartan in SNK-6 cells. The proliferation and viability of SNK-6 cells were increased by Ang II, but these increases were inhibited by PI3K inhibitor wortmannin and Akt inhibitor MK2206. The increases of PCNA and Ki67 induced by Ang II were inhibited by wortmannin or MK2206 in SNK-6 cells. These results indicate that Ang II/AT1R is activated in lymphoma, and Ang II promotes the progression of lymphoma in nude mice and the proliferation and viability of SNK-6 cells via activating PI3K/Akt signaling pathway.

scholarly journals AT1 receptor knockdown prevents the T3‐induced cardiomyocyte hypertrophy: modulation of the Akt Signaling Pathway

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Gabriela Placoná Diniz ◽  
Marcela Sorelli Carneiro‐Ramos ◽  
Maria Luiza Morais Barreto‐Chaves
Keyword(s):  
Signaling Pathway ◽  
Akt Signaling ◽  
At1 Receptor ◽  
Cardiomyocyte Hypertrophy ◽  
Akt Signaling Pathway
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