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[Effect of lipid factor CTRP9 on myocardial remodeling induced by isoproterenol in mice]

C Liang¹, Y Liu, L Gao

¹Department of Cardiology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.

Zhonghua Yi Xue Za Zhi

|November 6, 2018

Abstract:

Objective: To investigate the effect of lipid factor CTRP9 on myocardial remodeling induced by isoproterenol in mice. Methods: Male C57BL/6J mice were randomly assigned to four groups (n=10 per group), then mice were administered 5 mg/kg ISO q12h for 12 days by daily subcutaneous injection to induce myocardial remodeling model. Mice also received subcutaneous injection of CTRP9 (200 μg·kg(-1)·d(-1)) for 12days. Echocardiography was performed to compare the ventricular wall thickness and cardiac function. Heart weight/body weight (HW/BW), lung weight/body weight (LW/BW), heart weight/tibia length (HW/TL) and cross-sectional area of cardiomyocytes were compared between groups. The cardiac hypertrophic markers and fibrotic markers were also compared by RT-PCR between the two groups. Molecular protein changes were evaluated by Western blot. Results: CTRP9 was down-regulated in model group. The LVEDd (4.00 mm vs 4.67 mm), LVEDs (2.60 mm vs 3.12 mm) in mode group were both higher than control group while the LVEF (73% vs 55%) and FS (39% vs 21%) were reduced in mode group. Compared with the control group, the HW/BW, LW/BW, HW/TL and cross-sectional area of cardiomyocytes were much higher in mode group (P<0.05). The transcription level of hypertrophic markers (ANP, BNP, β-MHC) were elevated. Left ventricular collagen volume was increased as well as the transcription level of fibrosis markers collagen Ⅰ, collagen Ⅲ and a-SMA. Western blot results indicated that CTRP9 increased nNOS and eNOS derived NO production but not iNOS expression. Conclusion: CTRP9 could protect against ISO induced myocardial remodeling by increasing nNOS and eNOS derived NO production.

Insights

Cardiotrophin-like cytokine 9 (CTRP9) protects against isoproterenol-induced myocardial remodeling in mice. This lipid factor increases nitric oxide production, mitigating cardiac hypertrophy and fibrosis.

Area of Science:

Cardiovascular Biology
Molecular Cardiology
Biochemistry

Background:

Myocardial remodeling is a pathological process leading to heart failure.
Isoproterenol (ISO) is commonly used to induce experimental myocardial remodeling.
The role of lipid factor CTRP9 in ISO-induced cardiac changes requires investigation.

Purpose of the Study:

To investigate the protective effects of CTRP9 against isoproterenol-induced myocardial remodeling in mice.
To elucidate the molecular mechanisms underlying CTRP9's action in cardiac remodeling.

Main Methods:

Male C57BL/6J mice were subjected to isoproterenol administration to induce myocardial remodeling.
Mice received concurrent treatment with CTRP9.
Cardiac function was assessed via echocardiography.
Cardiac hypertrophy, fibrosis, and molecular markers were evaluated using RT-PCR and Western blot.

Main Results:

CTRP9 levels were decreased in the ISO-induced myocardial remodeling model.
CTRP9 treatment improved cardiac function and reduced cardiac hypertrophy and fibrosis.
CTRP9 upregulated endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) expression, increasing nitric oxide (NO) production.

Conclusions:

CTRP9 exhibits protective effects against isoproterenol-induced myocardial remodeling.
CTRP9 ameliorates cardiac dysfunction and structural changes by enhancing nNOS and eNOS-derived NO production.

Read full analysis

Keywords:

Adipose factor Cardiac remodeling Isoproterenol Nitric oxide synthase

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