ANG II stimulates phospholipase D through PKCzeta activation in VSMC: implications in adhesion, spreading, and hypertrophy

Parmentier, JH; Pavicevic, Z; Malik, KU

HERO ID

1071213

Reference Type

Journal Article

Year

2006

Language

English

PMID

16113073

HERO ID 1071213
In Press No
Year 2006
Title ANG II stimulates phospholipase D through PKCzeta activation in VSMC: implications in adhesion, spreading, and hypertrophy
Authors Parmentier, JH; Pavicevic, Z; Malik, KU
Journal American Journal of Physiology: Heart and Circulatory Physiology
Volume 290
Issue 1
Page Numbers H46-H54
Abstract ANG II stimulates phospholipase D (PLD) activity and growth of vascular smooth muscle cells (VSMC). The atypical protein kinase C-zeta (PKCzeta) plays a central role in the regulation of cell survival and proliferation. This study was conducted to determine the relationship between ANG II-induced activation of PKCzeta and PLD and their implication in VSMC adhesion, spreading, and hypertrophy. ANG II stimulated PKCzeta activity with maximal activation at 30 s followed by a decline in its activity to 45% above basal at 5 min. Inhibition of PKCzeta activity with a myristoylated pseudosubstrate peptide or overexpression of a kinase-inactive form of PKCzeta decreased ANG II-induced PLD activity. Moreover, depletion of PKCzeta with selective antisense oligonucleotides also decreased ANG II-induced PLD activity. Interaction between PLD2 and PKCzeta in VSMC was detected by coimmunoprecipitation. ANG II-induced PLD activity was inhibited by the primary alcohol n-butanol but not the tertiary alcohol t-butanol. The functional significance of PKCzeta and PLD2 in VSMC adhesion, spreading, and hypertrophy was investigated. Inhibition of PKCzeta and PLD2 activity or expression attenuated VSMC adhesion to collagen I and ANG II-induced cell spreading and hypertrophy. These results demonstrate that ANG II-induced PLD activation is regulated by PKCzeta and suggest a crucial role of PKCzeta-dependent PLD2 in VSMC functions such as adhesion, spreading, and hypertrophy, which are associated with the pathogenesis of atherosclerosis and malignant hypertension.
Doi 10.1152/ajpheart.00769.2005
Pmid 16113073
Wosid WOS:000234148200005
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000234148200005
Is Public Yes
Language Text English
Keyword vascular smooth muscle cells; protein kinase C zeta; angiotensin II
Is Qa No