scholarly journals Effects of angiotensin II and ryanodine on cardiac hypertrophy-related gene expression and calcineurin—NF-AT3 signaling pathway

2000 ◽  
Vol 13 (6) ◽  
pp. S309
Author(s):  
Z Shanjun
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Related Gene

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.

Effects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: reversal of increased β-myosin heavy chain gene expression

2006 ◽  
Vol 84 (8-9) ◽  
pp. 935-941 ◽  
Author(s):  
Baohua Wang ◽  
Jingping Ouyang ◽  
Zhengyuan Xia
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Mrna Expression ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Ang Ii ◽  
Hypertrophic Growth

Thyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an increase in myocardial mass with a compromised contractility accompanied by a shift from α-MHC to the fetal isoform β-MHC (the low ATPase activity isoform), which is considered as a pathological hypertrophy and inevitably leads to the development of heart failure. The present study is designed to assess the effect of thyroid hormone on angiotensin II-induced hypertrophic growth of cardiomyocytes in vitro. Cardiomyocytes were prepared from hearts of neonatal Wistar rats. The effects of Ang II and 3,3′,5-triiodo-thyronine (T3) on incorporations of [3H]-thymine and [3H]-leucine, MHC isoform mRNA expression, PKC activity, and PKC isoform protein expression were studied. Ang II enhanced [3H]-leucine incorporation, β-MHC mRNA expression, PKC activity, and PKCε expression and inhibited α-MHC mRNA expression in cardiomyocytes. T3 treatment prevented Ang II-induced increases in PKC activity, PKCε, and β-MHC mRNA overexpression and favored α-MHC mRNA expression. Thyroid hormone appears to be able to reprogram gene expression in Ang II-induced cardiac hypertrophy, and a PKC signal pathway may be involved in such remodeling process.

4-Nitrophenol exposure alters the AhR signaling pathway and related gene expression in the rat liver

2016 ◽  
Vol 37 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Ruonan Li ◽  
Meiyan Song ◽  
Zhi Li ◽  
Yansen Li ◽  
Gen Watanabe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathway ◽  
Rat Liver ◽  
Related Gene

scholarly journals Endogenously produced adiponectin protects cardiomyocytes from hypertrophy by a PPARγ-dependent autocrine mechanism

2010 ◽  
Vol 299 (3) ◽  
pp. H690-H698 ◽  
Author(s):  
Rajesh H. Amin ◽  
Suresh T. Mathews ◽  
Adebisi Alli ◽  
Todd Leff
Keyword(s):  
Gene Expression ◽  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Receptor Gene ◽  
Peroxisome Proliferator ◽  
Adrenergic Stimulation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Beneficial Effects ◽  
Ppar Γ ◽  
Culture Models

In experimental animal and cell culture models, activation of peroxisome proliferator-activated receptor (PPAR) γ in heart has been shown to have beneficial effects on cardiac function and cardiomyocyte physiology. The goal of this study was to identify the signaling pathway by which PPARγ activation protects cardiomyocytes from the deleterious effects of hypertrophic stimuli. In primary cardiomyocyte cultures, we found that genetic or pharmacological activation of PPARγ protected cells from cardiac hypertrophy induced by α-adrenergic stimulation. Examination of gene expression in these cells revealed a surprising increase in the expression of adiponectin in cardiomyocytes and secretion of the high-molecular-weight form of the hormone into media. Using RNAi to block PPARγ-induced adiponectin production or adiponectin receptor gene expression, we found that the PPARγ-mediated anti-hypertrophic effect required cardiomyocyte-produced adiponectin, as well as an intact adiponectin signaling pathway. Furthermore, mice expressing constitutive-active PPARγ and cardiomyocyte specific adiponectin expression were protected from high-fat diet-induced cardiac hypertrophy and remodeling. These findings demonstrate that functional adiponectin hormone can be produced from the heart and raise the possibility that beneficial effects of PPARγ activation in heart could be due in part to local production of adiponectin that acts on cardiomyocytes in an autocrine manner.

scholarly journals Melatonin Receptor 2 Promotes Lipid Metabolism of Cumulus-oocyte Complexes via the cAMP/PKA Pathway

2021 ◽  
Author(s):  
Jun-Xue Jin ◽  
Hong-Di Cui ◽  
Chao-Qian Jiang ◽  
Zi-Cheng Qi ◽  
Ya Bian ◽  
...  
Keyword(s):  
Gene Expression ◽  
Energy Source ◽  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Oocyte Maturation ◽  
Expression Patterns ◽  
Cumulus Cells ◽  
Related Gene ◽  
Melatonin Receptor ◽  
Significant Difference

Abstract Background: The importance of the processes of lipogenesis and lipolysis in providing an essential energy source during oocyte maturation is increasingly being recognized. Recent our studies have demonstrated that melatonin up-regulated lipid metabolism during oocyte maturation. Nevertheless, there is still limited information regarding the underlying molecular mechanisms of action of melatonin on lipid metabolism in porcine cumulus-oocyte complexes (COCs). Here, our aim was to investigate the effect of melatonin on COCs, and the melatonin receptor-mediated lipid metabolism signaling pathway.Materials/methods: To determine the melatonin-mediated lipolysis pathway in cumulus cells, COCs were treated with melatonin and the correlated metabolic responses were assessed using melatonin receptor-mediated signaling.Results: The results showed that exposure of COCs to melatonin during in vitro maturation significantly increased cumulus expansion index, blastocyst formation rate and total cell numbers/blastocyst, although nuclear maturation was no significant difference. The levels of proteins MT1, MT2, Gsα, PKA, and lipolysis-related factors (AGTL, HSL, PLIN A+B) were significantly increased by melatonin supplementation, and this effect was inhibited by simultaneous treatment with melatonin antagonists (luzindole or 4P-PDOT), although 4P-PDOT treatment did not completely block the effect of melatonin on MT1. Further, the gene expression patterns reflected their relevant protein levels in cumulus cells. Melatonin-mediated lipolysis could significantly reduce lipid droplets (LDs) numbers and increase fatty acid (FA) production and ATP levels by increasing the β-oxidation-related gene expression in cumulus cells. Simultaneously, melatonin significantly increased the amount of LDs, FAs, ATP, and enhanced the lipid metabolism-related gene expression in oocytes. Finally, the oocyte quality was improved by increasing GDF9, BMP15 and GSH and decreasing ROS levels.Conclusion: These findings revealed that the MT2-mediated cAMP/PKA signaling pathway promotes intracellular lipolysis and FA production in cumulus cells, which provided an essential energy source for COCs development.

scholarly journals Bcl-2 Is Involved in Cardiac Hypertrophy through PI3K-Akt Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Xianwei Meng ◽  
Jun Cui ◽  
Guibin He
Keyword(s):  
Gene Expression ◽  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Enrichment Analysis ◽  
B Cell Lymphoma ◽  
Akt Signaling ◽  
Receptor Interaction ◽  
Pathway Enrichment Analysis ◽  
Akt Signaling Pathway ◽  
Upregulated Genes

Cardiac hypertrophy (CH) is a common cause of sudden cardiac death and heart failure, resulting in a significant medical burden. The present study is aimed at exploring potential CH-related pathways and the key downstream effectors. The gene expression profile of GSE129090 was obtained from the Gene Expression Omnibus database (GEO), and 1325 differentially expressed genes (DEGs) were identified, including 785 upregulated genes and 540 downregulated genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway enrichment analysis of DEGs were then performed. Although there were no pathways enriched by downregulated genes, many CH-related pathways were identified by upregulated genes, including PI3K-Akt signaling pathway, extracellular matrix- (ECM-) receptor interaction, regulation of actin cytoskeleton, and hypertrophic cardiomyopathy (HCM). In the deeper analysis of PI3K-Akt signaling pathway, we found all the signaling transduction pointed to B cell lymphoma-2- (Bcl-2-) mediated cell survival. We then demonstrated that PI3K-Akt signaling pathway was indeed activated in cardiac hypertrophy. Furthermore, no matter LY294002, an inhibitor of the PI3K/AKT signaling pathway, or Venetoclax, a selective Bcl-2 inhibitor, protected against cardiac hypertrophy. In conclusion, these data indicate that Bcl-2 is involved in cardiac hypertrophy as a key downstream effector of PI3K-Akt signaling pathway, suggesting a potential therapeutic target for the clinical management of cardiac hypertrophy.

Inhibition of angiotensin II-induced hypertrophy and cardiac dysfunction by North American ginseng (Panax quinquefolius)

2020 ◽  
Author(s):  
Xilan Tang ◽  
Tracey Gan ◽  
Chian Ju Jong ◽  
Venkatesh Rajapurohitam ◽  
Morris Karmazyn
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
North American ◽  
Glucose Oxidation ◽  
American Ginseng ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Expression Levels

We determined whether North American ginseng mitigates the effect of angiotensin II on hypertrophy and heart failure. Angiotensin II (0.3 mg/kg) was administered to rats for 2 or 4 weeks in the presence or absence of ginseng pretreatment. The effect of ginseng (10 μg/mL) on angiotensin II (100 nM) induced hypertrophy was also determined in neonatal rat ventricular myocytes. We also determined effects of ginseng on fatty acid and glucose oxidation by measuring gene and protein expression levels of key factors. Angiotensin II treatment for 2 and 4 weeks induced cardiac hypertrophy as evidenced by increased heart weights as well as the upregulation of the hypertrophy-related fetal gene expression levels with all effects being abolished by ginseng. Ginseng also reduced abnormalities in left ventricular function as well as the angiotensin-induced increased blood pressure. In myocytes, ginseng abolished the hypertrophic response to angiotensin II as assessed by surface area and gene expression of molecular markers of hypertrophy. Ginseng modulated angiotensin II-induced abnormalities in gene expression and protein levels of CD36, CPT1M, Glut4 and PDK4 in vivo and in vitro. In conclusion, ginseng suppresses angiotensin II induced cardiac hypertrophy and dysfunction which is related to normalization of fatty acid and glucose oxidation.

scholarly journals Hyperoside Protects Against Pressure Overload-Induced Cardiac Remodeling via the AKT Signaling Pathway

2018 ◽  
Vol 51 (2) ◽  
pp. 827-841 ◽  
Author(s):  
Xiaofang Wang ◽  
Yuan Liu ◽  
Lili Xiao ◽  
Ling Li ◽  
Xiaoyan Zhao ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Signaling Pathway ◽  
Cardiac Remodeling ◽  
Molecular Mechanisms ◽  
Pressure Overload ◽  
Akt Signaling ◽  
Neonatal Rat ◽  
Control Group ◽  
Akt Signaling Pathway

Background/Aims: Cardiac hypertrophy is a major predisposing factor for heart failure and sudden cardiac death. Hyperoside (Hyp), a flavonoid isolated from Rhododendron ponticum L., is a primary component of Chinese traditional patent medicines. Numerous studies have shown that Hyp exerts marked anti-viral, anti-inflammatory, anti-oxidant, anti-cancer, anti-ischemic, and particularly cardio-protective effects. However, the effects of Hyp on cardiac hypertrophy have not been explored. The aims of this study were to determine whether Hyp could protect against cardiac remodeling and to clarify the potential molecular mechanisms. Methods: Neonatal rat cardiac myocytes were isolated and treated with different concentrations of Hyp, then cultured with angiotensin II for 48 h. Mice were subjected to either aortic banding or sham surgery (control group). One week after surgery, the mice were treated with Hyp (20 mg/kg/day) or vehicle by oral gavage for 7 weeks. Hypertrophy was evaluated by assessing morphological changes, echocardiographic parameters, histology, and biomarkers. Results: Hyp pretreatment suppressed angiotensin II-induced hypertrophy in cardiomyocytes. Hyp exerted no basal effects but attenuated cardiac hypertrophy and dysfunction, fibrosis, inflammation, and oxidative stress induced by pressure overload. Both in vivo and in vitro experiments demonstrated that the effect of Hyp on cardiac hypertrophy was mediated by blocking activation of the AKT signaling pathway. Conclusion: Hyp improves cardiac function and prevents the development of cardiac hypertrophy via AKT signaling. Our results suggest a protective effect of Hyp on pressure overload-induced cardiac remodeling. Taken together, Hyp may have a role in the pharmacological therapy of cardiac hypertrophy.

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