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J Hypertens. 2013 Mar;31(3):576-86; discussion 586. doi: 10.1097/HJH.0b013e32835d6a56.

Profilin-1 promotes the development of hypertension-induced cardiac hypertrophy.

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1
Department of Geriatric Cardiology, Qilu Hospital of Shandong University, Jinan, PR China.

Abstract

OBJECTIVE:

Cardiac hypertrophy is a major cause of heart failure and sudden cardiac death among hypertensive individuals. The present study examined the effects of profilin-1 on hypertension-induced cardiac hypertrophy.

METHODS:

We used adenovirus injection to knockdown or overexpress profilin-1 in spontaneous hypertensive rats (SHRs). As a control, blank adenovirus was injected into age-matched SHRs and Wistar-Kyoto rats (WKYs). SBP and cardiac mass index were measured. Cardiac tissues were stained with hematoxylin-eosin and sirius red, and cardiac ultrastructure was imaged using transmission electron microscopy. Actin filament was quantified by staining with TRIC-tagged phalloidin. Caveolin-3 abundance and endothelial nitric oxide synthase (eNOS) activity were measured using real-time quantitative PCR, Western blot or immunofluorescence staining.

RESULTS:

Endogenous profilin-1 was highly expressed in hypertrophic myocardium of SHRs compared with WKYs. Lowering profilin-1 expression in SHRs significantly attenuated hypertension-induced cardiac hypertrophy and fibrosis and displayed a significant preservation of myofibrils, sarcolemmal caveolae, abundance of caveolin-3 protein, activity of eNOS and production of nitric oxide (NO). In contrast, transgenic overexpression of profilin-1 in SHRs induced more serious cardiac hypertrophy and fibrosis with significant reduction of sarcolemmal caveolae, caveolin-3 protein, eNOS activity, and production of NO when compared with SHR controls.

CONCLUSION:

Profilin-1 promotes cardiac hypertrophy partly through interfering with the formation of sarcolemmal caveolae and attenuating the eNOS/NO pathway. These results demonstrate a crucial role for profilin-1 in hypertensive cardiac hypertrophy.

PMID:
23615214
DOI:
10.1097/HJH.0b013e32835d6a56
[Indexed for MEDLINE]
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