title: Profilin-1 promotes the development of hypertension-induced cardiac hypertrophy.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Geriatric Cardiology, Qilu Hospital of Shandong University, Jinan, PR China.
authors.forename: Shao-hua
authors.initials: SH
authors.lastname: Zhao
authors.forename: Jie
authors.initials: J
authors.lastname: Qiu
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Xiang
authors.initials: X
authors.lastname: Ji
authors.forename: Xiang-ju
authors.initials: XJ
authors.lastname: Liu
authors.forename: Bei-an
authors.initials: BA
authors.lastname: You
authors.forename: Yu-ping
authors.initials: YP
authors.lastname: Sheng
authors.forename: Xiao
authors.initials: X
authors.lastname: Li
authors.forename: Hai-qing
authors.initials: HQ
authors.lastname: Gao
mesh_terms: D000818:Animals; D001483:Base Sequence; D006332:Cardiomegaly / Q000503:physiopathology*; D017931:DNA Primers; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D051304:Profilins / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D060888:Real-Time Polymerase Chain Reaction
chemical_list: D017931:DNA Primers; C495740:Pfn1 protein, rat; D051304:Profilins