Interleukin-10 deficiency aggravates angiotensin II-induced cardiac remodeling in mice

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Abstract

Aims:

This study examined the role of interleukin (IL)-10 in angiotensin II-induced cardiac remodeling.

Main methods:

Angiotensin II was infused subcutaneously (1.1 mg/kg/day) for one week in IL-10 knockout and wild-type mice, after which cardiac function and hypertrophy were assessed by echocardiogram.

Key findings:

IL-10 gene expression in the heart was increased by angiotensin II infusion. Plasma levels of brain natriuretic peptide (BNP) and gene expression of BNP in the heart were increased by IL-10 deficiency or angiotensin II, and plasma BNP levels were further increased by IL-10 deficiency with angiotensin II. IL-10 deficiency increased the left ventricular dimension, whereas treatment with angiotensin II increased heart weight. Angiotensin II significantly reduced cardiac function in IL-10 knockout mice compared with wild-type mice. Gene expression of tumor necrosis factor-α and interleukin-6 was increased by IL-10 deficiency or angiotensin II infusion, and these increases were further enhanced by IL-10 deficiency with angiotensin II. Gene expression of collagen I/III and collagen III protein levels were increased by angiotensin II but not by IL-10 deficiency. Gene expression of matrix metalloproteinase2/9 was increased by IL-10 deficiency or angiotensin II, and this expression was further increased by IL-10 deficiency with angiotensin II. Akt phosphorylation was increased by IL-10 deficiency or angiotensin II and further increased by IL-10 deficiency with angiotensin II. Phosphorylation of p38 was increased by IL-10 deficiency.

Significance:

These results suggest that IL-10 deficiency causes deterioration in cardiac functions in angiotensin II-infused mice, suggesting that IL-10 plays a protective role against angiotensin II-induced cardiac remodeling.

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