RGD Reference Report - ANG II stimulates phospholipase D through PKCzeta activation in VSMC: implications in adhesion, spreading, and hypertrophy. - Rat Genome Database

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

Authors: Parmentier, JH  Pavicevic, Z  Malik, KU 
Citation: Parmentier JH, etal., Am J Physiol Heart Circ Physiol. 2006 Jan;290(1):H46-54. Epub 2005 Aug 19.
RGD ID: 1642674
Pubmed: PMID:16113073   (View Abstract at PubMed)
DOI: DOI:10.1152/ajpheart.00769.2005   (Journal Full-text)

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.




Biological Process

  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
PrkczRatactivation of phospholipase D activity  IMP  RGD 
PrkczRatpositive regulation of cell-matrix adhesion  IMP vascular smooth muscle cell adhesion to collagen matrixRGD 

Molecular Function

  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
PrkczRatphospholipase binding  IPIPld2 (Rattus norvegicus) RGD 
Pld2Ratprotein kinase C binding  IPIPrkcz (Rattus norvegicus) RGD 

RGD Manual Annotations


  
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
PrkczRatangiotensin II signaling pathway   IMP  RGD 
Object Symbol
Species
Term
Qualifier
Evidence
With
Notes
Source
Original Reference(s)
Pld2Ratvascular smooth muscle hypertrophy  IDA angiotensin II inducedRGD 
PrkczRatvascular smooth muscle hypertrophy  IDA angiotensin II inducedRGD 

Genes (Rattus norvegicus)
Pld2  (phospholipase D2) Prkcz  (protein kinase C, zeta)