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Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
Published on: September 25, 2017
Effect of miR-29a inhibition on ventricular hypertrophy induced by pressure overload
Wei Han1, Yancong Han, Xiaokun Liu
1Department of Internal Medicine, Hebei Medical University, No. 361 Zhongshan East Road, Shijiazhuang, 050017, Hebei, People's Republic of China.
Insights
Inhibition of microRNA-29a (miR-29a) prevents hypertension-induced cardiac hypertrophy and fibrosis. This study found elevated miR-29a in patients and demonstrated its therapeutic potential in a mouse model.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biochemistry
Background:
- Hypertension frequently leads to left ventricular hypertrophy and fibrosis.
- MicroRNAs play a role in cardiac remodeling, but miR-29a's specific function in hypertension-induced changes is unclear.
Purpose of the Study:
- To investigate if inhibiting microRNA-29a (miR-29a) function can prevent hypertension-induced ventricular hypertrophy and fibrosis.
- To assess the correlation between miR-29a levels and cardiac fibrosis markers in patients.
- To evaluate the therapeutic effect of miR-29a inhibition in a mouse model of pressure overload.
Main Methods:
- Serum miR-29a levels were measured in hypertensive patients with and without left ventricular hypertrophy.
- Cardiac fibrosis markers (collagen type I and III) and MMP-9 were quantified.
- A mouse model of transverse aortic constriction (TAC) was used to induce pressure overload.
- Mice received antagomir miR-29a treatment to inhibit miR-29a function.
- Cardiac hypertrophy and fibrosis were assessed histologically and by protein marker expression.
Main Results:
- Hypertensive patients with left ventricular hypertrophy showed significantly higher serum miR-29a levels compared to those with hypertension alone.
- Serum miR-29a levels positively correlated with collagen type I, collagen type III, and MMP-9.
- In TAC mice, antagomir miR-29a treatment significantly suppressed cardiomyocyte hypertrophy and expression of hypertrophy markers (ANP, β-MHC).
- Ventricular fibrosis and associated protein markers were significantly reduced in antagomir miR-29a treated mice.
Conclusions:
- MicroRNA-29a is upregulated in hypertension-associated left ventricular hypertrophy and is positively correlated with cardiac fibrosis markers.
- Inhibition of miR-29a effectively ameliorates cardiac hypertrophy and fibrosis in a pressure overload mouse model.
- Targeting miR-29a represents a potential therapeutic strategy for managing adverse cardiac remodeling in hypertension.
Abstract:
To investigate whether inhibition of miR-29a functioning prevents the hypertension-induced ventricular hypertrophy and fibrosis. Patients diagnosed with hypertension and left ventricular hypertrophy were recruited for the study. Serum levels of miR-29a were determined by RT-PCR. Levels of serum matrix metalloproteinase-9 (MMP-9), collagen type I and III (PINP and PIIINP) were determined by double-antibody enzyme-linked immunosorbent assay. Mouse model of transverse aortic constriction (TAC) was established. 7 days after surgery, TAC mice were injected intraperitoneally with antagomir miR-29a or vehicle once a day for 3 days. After 4 weeks of surgery, animals were sacrificed and cross-sections of the hearts were stained and evaluated for hypertrophy and fibrosis. The expression of the protein markers of hypertrophy and fibrosis was determined by immunoblotting. The serum level of miR-29a in hypertensive patients with left ventricular hypertrophy was significantly higher than those in patients with hypertension alone (p < 0.05). The levels of serum miR-29a were positively correlated with those of PINP, PIIINP, and MMP-9 (r = 0.58, 0.45, 0.66, respectively, p < 0.05). In mouse model of pressure overload, the antagomir miR-29a was found to significantly suppress the hypertrophy of cardiomyocytes and the expression of ANP and β-MHC, the hypertrophy indices. Also, the ventricular fibrosis and expression of the marker proteins were blocked in antagomir treated mice. The inhibition of miR-29a was found to be effective in improving the ventricular remodeling and hypertrophy caused by pressure overload.
