Research Article

Correlation between protein 4.1R and the progression of heart failure in vivo

Published: May 13, 2016
Genet. Mol. Res. 15(2): gmr8648 DOI: 10.4238/gmr.15028648

Abstract

We aimed to assess the protein 4.1R (4.1R) expression of the membrane skeleton in cardiomyocytes and to determine the potential role of 4.1R in the pathogenesis of heart failure (HF). Forty-two male mice were randomly divided into two groups: an HF group (N = 22) and control group (N = 20). The HF model was established by abdominal subcutaneous injection of 5 mg⋅kg-1⋅day-1 isopropyl adrenaline to the mice for 14 days. Electrocardiography was carried out and cardiac function was assessed by ultrasonic cardiogram. The left ventricular weight index (LVMI) was measured after mice were sacrificed, and the pathological changes of the heart were observed by hematoxylin and eosin staining. The expression of 4.1R in cardiomyocytes was analyzed by immunohistochemistry, immunofluorescence, and reverse transcription polymerase chain reaction. The echocardiographs showed that the left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) were significantly higher in the HF group than in the controls (P 4.1R. 4.1R localized mostly to the plasma membrane of myocardial cells and was upregulated with the progression of HF. This suggests that 4.1R may be associated with HF progression and therefore 4.1R represents a promising therapeutic target in HF.

We aimed to assess the protein 4.1R (4.1R) expression of the membrane skeleton in cardiomyocytes and to determine the potential role of 4.1R in the pathogenesis of heart failure (HF). Forty-two male mice were randomly divided into two groups: an HF group (N = 22) and control group (N = 20). The HF model was established by abdominal subcutaneous injection of 5 mg⋅kg-1⋅day-1 isopropyl adrenaline to the mice for 14 days. Electrocardiography was carried out and cardiac function was assessed by ultrasonic cardiogram. The left ventricular weight index (LVMI) was measured after mice were sacrificed, and the pathological changes of the heart were observed by hematoxylin and eosin staining. The expression of 4.1R in cardiomyocytes was analyzed by immunohistochemistry, immunofluorescence, and reverse transcription polymerase chain reaction. The echocardiographs showed that the left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) were significantly higher in the HF group than in the controls (P 4.1R. 4.1R localized mostly to the plasma membrane of myocardial cells and was upregulated with the progression of HF. This suggests that 4.1R may be associated with HF progression and therefore 4.1R represents a promising therapeutic target in HF.