Correlation between protein 4.1R and the progression of heart failure in vivo.
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 < 0.05), while the left ventricle shortening fraction was remarkably lower than that in the controls (P < 0.05). Electrocardiography showed faster heart rates in the HF group than in the control group (P < 0.05). Both the LVMI and the myocardial tissue pathological score were significantly higher (P < 0.01) in the HF group than in the controls. 4.1R localized mostly to the plasma membrane and was distributed discretely in the cytosol of myocardial cells. The proportion of 4.1R-positive cells was significantly higher in the HF group (P < 0.01) than in the controls, which was confirmed by the positive mRNA expression of 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.
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.|Institute of Clinical Medicine, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
Z
Z
Wei
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
G
G
Yang
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
R
R
Xu
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
C
C
Zhu
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
F
F
He
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
Q
Q
Dou
Department of Geriatrics Cardiology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China.
J
J
Tang
D000818:Animals; D004195:Disease Models, Animal; D018450:Disease Progression; D004452:Echocardiography; D004562:Electrocardiography; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008297:Male; D051379:Mice; D008840:Microfilament Proteins / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology
C514956:Epb41 protein, mouse; D008840:Microfilament Proteins