Prostaglandin E1 attenuates AngII-induced cardiac hypertrophy via EP3 receptor activation and Netrin-1upregulation

Shen, Yejiao; Wang, Xia; Yuan, Ruosen; Pan, Xin; Yang, Xiaoxiao; Cai, Jiali; Li, Yang; Yin, Anwen; Xiao, Qingqing; Ji, Qingqi; Li, Yanjie; He, Ben; Shen, Linghong

doi:10.1016/j.yjmcc.2021.06.009

Cited by 7 publications

(8 citation statements)

References 46 publications

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“…The regulation of relevant signaling pathways is essential for the prevention and treatment of pathological heart hypertrophy. The research have shown that cardiac hypertrophy is regulated by multiple pathways, such as JAK/STAT, MAPK and PI3K (Varghese et al, 2022;Shen et al, 2021). However, PI3K is a critical enzyme in the induction of heart hypertrophy, interstitial brosis and cardiac dysfunction, while AKT1 is the main target of PI3K signaling and plays an important role in improving cardiac hypertrophy (Cheng et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

Qian,

Zhou,

et al. 2023

Preprint

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The role of magnesium isoglycyrrhizinate (MgIG) in myocardial remodeling is being investigated. We evaluated the result of MgIG on isoproterenol (ISO) -enticed myocardial remodeling in mice by activating the PI3K/AKT1 pathway. The heart function of mice was tested by echocardiography, and it was found that MgIG could improve the left ventricular function. Pathological staining analysis showed that MgIG could decrease the degree of myocardial injury caused by ISO. The serum data detected by ELISA showed that MgIG could reduce the content of CK-MB, MDA and LDH, and increase the activity of GSH-Px. Western blotting showed that the protein expressions of Collagen Ⅰ, BNP, Bax, Cleaved caspase-3, p-PI3K and p-AKT1 were decreased, while the protein expressions of Bcl-2, COX2 and SOD1 were increased. Meanwhile activation of the PI3K activator (740Y-P) reverses the cardioprotective effect of MgIG. These findings suggest that the myocardial remodeling induced by ISO could be improved by MgIG, and its mechanism may be associated with inhibite PI3K/AKT1 pathway to regulate apoptosis and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

Qian,

Zhou,

et al. 2023

Preprint

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“…The mice were infused with 1.44 mg/kg/d or 2.5 mg/kg/d Ang II (Sigma-Aldrich, Cat# A9525) for two weeks through subcutaneous osmotic minipumps (Model 2002, ALZA Scientific Products, Mountain View, CA, USA). These two doses of Ang II were chosen based on their well-known effects to induce vascular remodeling or abdominal aortic aneurysm and cardiac hypertrophy [ 17 – 19 ]. Saline-infused mice served as the controls.…”

Section: Methodsmentioning

confidence: 99%

Angiotensin II Promotes White Adipose Tissue Browning and Lipolysis in Mice

Cai

Fang

Jiang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Emerging evidence has revealed that all components of the renin-angiotensin system (RAS) are present in adipose tissue. Angiotensin II (Ang II), the major bioactive component of the RAS, has been recognized as an adipokine involved in regulating energy homeostasis. However, the precise role of Ang II in white adipose tissue (WAT) remodeling remains to be elucidated. In this present study, C57BL/C male mice were continuously infused with different doses of Ang II (1.44 mg/kg/d or 2.5 mg/kg/d) or saline for 2 weeks and treated with or without the Ang II type 1 receptor blocker valsartan. H&E staining and immunohistochemistry were conducted to investigate the white-to-brown fat conversion. The level of serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) was measured. RNA sequencing was employed to explore the differentially expressed genes and their enriched pathways between control and Ang II groups. Our results showed that Ang II substantially resulted in loss of body weight and fat mass. Most importantly, Ang II treatment induced WAT browning in mice, which was partially attenuated by valsartan treatment. Furthermore, Ang II perturbed the serum lipid profiles. Ang II treatment elevated serum levels of TC, TG, LDL-C, and HDL-C in mice. Mechanistically, thermogenesis, cell respiration, and lipid metabolism-associated mRNAs showed significantly increased expression profiling in Ang II-treated WATs compared with control WATs. Moreover, we found that Ang II treatment enhanced AMPK phosphorylation in adipocytes. Therefore, Ang II promotes WAT browning and lipolysis via activating the AMPK signaling pathway.

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“…Cardiac hypertrophy, an early pathological change in heart failure, is a response to increased load-induced ventricular wall pressure to maintain cardiac output and persistent myocardial hypertrophy eventually leads to decompensation 3,4 . There are many reasons for myocardial hypertrophy, such as angiotensin II 5 , stress-induced 6 or mediated by certain chemical substances 7 . Some adipokines are independent risk factors for cardiac hypertrophy 8,9 .…”

Section: Introductionmentioning

confidence: 99%

Resistin Induces Cardiomyocyte Hypertrophy in H9c2 Embryonic Rat Myocardial Cells via Inhibition of MiR-489-3p

Yang,

Hao,

et al. 2023

Trends Med. Res

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Background and Objective:The miRNAs play an important regulatory role in resistin-induced cardiac hypertrophy. The purpose of this experiment was to investigate the effect of resistin-induced myocardial hypertrophy in H9c2 cardiomyocytes by inhibiting the expression of miR-489-3p. Materials and Methods: After treatment with resistin or resistin plus miR-489-3p mimic, Image J was used to measure cell surface area. The BCA method and cell counting were used to measure protein synthesis. RT-qPCR was used to measure the relative expression levels of atrial natriuretic factor (ANF), brain natriuretic factor (BNF) and miR-489-3p. Results: Overexpression of the miR-489-3p reduced resistin-induced increase in cardiomyocyte area. Overexpression of miR-489-3p attenuated protein synthesis induced by resistin. Overexpression of miR-489-3p decreased the relative expression of cardiac hypertrophy marker ANF and BNF increased by resistin. Resistin inhibited the expression of miR-489-3p. Conclusion:Resistin induces cardiomyocyte hypertrophy by inhibiting the expression of miR-489-3p. This study provides a theoretical basis for further research on the role of miRNA in resistin-induced cardiomyocyte hypertrophy.

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Prostaglandin E1 attenuates AngII-induced cardiac hypertrophy via EP3 receptor activation and Netrin-1upregulation

Cited by 7 publications

References 46 publications

Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

Magnesium isoglycyrrhizinate regulates oxidative stress and apoptosis via PI3K/AKT1 pathway to improve myocardial remodeling in mice

Angiotensin II Promotes White Adipose Tissue Browning and Lipolysis in Mice

Resistin Induces Cardiomyocyte Hypertrophy in H9c2 Embryonic Rat Myocardial Cells via Inhibition of MiR-489-3p

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