Key result
Intermedin 1-53 reduces post-infarction cardiac fibrosis by down-regulating TGF-β expression in rats.
Why the study?
Myocardial fibrosis contributes to heart failure and adverse cardiac remodeling, but the role and mechanism of intermedin 1-53 in cardiac fibrosis are not fully clear.
p-value: p=<0.05
Intermedin 1-53 attenuates post-MI fibrosis in rats; extends preclinical data but leaves open human translation.
BACKGROUND Myocardial fibrosis is the result of persistent anoxia and ischemic myocardial fibers caused by coronary atherosclerotic stenosis, which lead to heart failure, threatening the patient's life. This study aimed to explore the regulatory role of intermedin 1-53 (IMD1-53) in cardiac fibrosis using neonatal rat cardiac fibroblasts and a myocardial infarction (MI) rat model both in vitro and in vivo. MATERIAL AND METHODS The Western blot method was used to detect the protein expression of collagen I and collagen III in myocardial fibroblasts. The SYBR Green I real-time quantitative polymerase chain reaction (PCR) assay was used to detect the mRNA expression of collagen type I and III, IMD1-53 calcitonin receptor-like receptor (CRLR), transforming growth factor-β (TGF-β), and matrix metalloproteinase-2 (MMP-2). Masson staining was used to detect the area changes of myocardial fibrosis in MI rats. RESULTS Results in vivo showed that IMD1-53 reduced the scar area on the heart of MI rats and inhibited the expression of collagen type I and III both in mRNA and protein. Results of an in vitro study showed that IMD1-53 inhibited the transformation of cardiomyocytes into myofibroblasts caused by angiotensin II (Ang II). The further mechanism study showed that IMD1-53 inhibited the expression of TGF-β and the phosphorylation of smad3, which further up-regulated the expression of MMP-2. CONCLUSIONS IMD1-53 is an effective anti-fibrosis hormone that inhibits cardiac fibrosis formation after MI by down-regulating the expression of TGF-β and the phosphorylation of smad3, blocking fibrous signal pathways, and up-regulating the expression of MMP-2, thereby demonstrating its role in regression of myocardial fibrosis.
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Fang et al. (2017) studied Myocardial infarction and cardiac fibrosis (n=20). Intermedin 1-53 (IMD1-53) vs. Ischemia control (vehicle) was evaluated on Myocardial fibrosis scar area and expression of collagen type I and III (p=<0.05). Intermedin 1-53 significantly reduced the area of cardiac fibrosis and inhibited collagen synthesis in rats after myocardial infarction by down-regulating TGF-β expression.
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