Journal Info

Journal Info

副标题

For Authors

For Authors

副标题

For Reviewers

For Reviewers

副标题

2022, Vol. 26 ›› Issue (31): 5020-5025

Effects of myeloid-derived growth factor on ventricular remodeling in aging mice

Sun Ying1, Xiang Guangda1, 2, Xu Xiaoli2   

  1. 1Graduate School of Wuhan University of Science and Technology, Wuhan 430081, Hubei Province, China; 2Department of Endocrinology, Central Theater Command General Hospital of Chinese People’s Liberation Army, Wuhan 430070, Hubei Province, China

  • Received:2021-03-25 Accepted:2021-05-12 Online:2022-11-08 Published:2022-04-25

  • Contact: Xiang Guangda, MD, Chief physician, Graduate School of Wuhan University of Science and Technology, Wuhan 430081, Hubei Province, China; Department of Endocrinology, Central Theater Command General Hospital of Chinese People’s Liberation Army, Wuhan 430070, Hubei Province, China

  • About author:Sun Ying, Master, Graduate School of Wuhan University of Science and Technology, Wuhan 430081, Hubei Province, China

  • Supported by:

    2018 National Natural Science Foundation of China, No. 81870573 (to XGD); 2015 National Natural Science Foundation of China, No. 81570730 (to XGD)


Abstract: BACKGROUND: Aging is a predominant risk factor for many developing diseases, such as cardiovascular disease, neurodegenerative disease, and osteoporosis. Cardiovascular disease has become one of the main causes of death in the elderly.  
OBJECTIVE: To investigate the effect of myeloid-derived growth factor (MYDGF) on ventricular remodeling in aging mice.
METHODS:   15-month-old C57BL/6 mice (WT mice) and MYDGF-/- mice (KO mice) were randomly divided into four groups as follows: WT group, KO group, adeno-associated virus-green fluorescent protein group, and adeno-associated virus-MYDGF group according to the presence and absence of AAV MYDGF intervention. After the intervention for 12 weeks, the mice were subjected to cardiac ultrasound to evaluate their cardiac structure and function, and to detect various blood biochemical indicators related to cardiac function. The heart weight was weighed and the length of the tibia was measured. Hematoxylin-eosin staining and Masson staining were used to observe the degree of cardiomyocyte hypertrophy and interstitial fibrosis.  
RESULTS AND CONCLUSION: (1) Compared with the WT group, the heart weight, body weight, and heart weight to tibia length of KO group were increased (P < 0.05). (2) Left ventricular end-diastolic diameter and left ventricular end-systolic dimension in the KO group were enlarged compared with the WT group. Importantly, the ejection fractions and fractional shortening were decreased (P < 0.05). (3) Pathological results showed that compared with the WT group, the myocardial cells of the KO group were significantly enlarged, and the degree of myocardial fibrosis was deepened. (4) The sensitivity to insulin of the mice in the KO group decreased, and the rate of blood glucose decline was lower than that in the WT group (P < 0.05). There was a significant increase in brain natriuretic peptide, plasma renin activity, angiotensin II, aldosterone, and norepinephrine levels in the circulation of KO mice compared to WT mice (P < 0.05). (5) After treatment of MYDGF, the above indicators had been improved. (6) There was no significant difference in food intake, fasting blood glucose, total cholesterol, triacylglycerol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and glycosylated hemoglobin levels among the groups (P > 0.05). (7) It is indicated that the lack of MYDGF can lead to pathological structural changes and decreased cardiac function in mouse cardiomyocytes, and finally cause ventricular remodeling; aging ventricular remodeling can be improved after MYDGF replenishment. MYDGF may become a new drug for the treatment of ventricular remodeling in elderly mice.
Key words: myeloid-derived growth factor, gene knockout, heart aging, cardiac hypertrophy, myocardial fibrosis, gene therapy, insulin resistance


分享到:

Publishing Information

Publishing House of Chinese Journal of Tissue Engineering Research


The Official Publication of

Chinese Association of Rehabilitation Medicine

Contact Us

General editorial enquiries:

Email: bwb01@crter.org

Copyright related contact:

Email: crter@crter.org

Commercial Sales contact (Reprints, advertising, etc.):

Email: bwb@crter.org