Protein Kinase C Delta Is Necessary for the secretion of Collagen Type I from Vascular Smooth Muscle Cells

2008 ◽  
Vol 22 (S2) ◽  
pp. 609-609
Author(s):  
Andrew Zohlman ◽  
Kentaro Kamiya ◽  
Kaori Kato ◽  
Susana B Salvarezza ◽  
Stephen B Doty ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Kinase C

scholarly journals Protein kinase C δ regulates the release of collagen type I from vascular smooth muscle cells via regulation of Cdc42

2012 ◽  
Vol 23 (10) ◽  
pp. 1955-1963 ◽  
Author(s):  
Justin Lengfeld ◽  
Qiwei Wang ◽  
Andrew Zohlman ◽  
Susana Salvarezza ◽  
Stephanie Morgan ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Arterial Wall ◽  
Collagen Type ◽  
Collagen Type I ◽  
Collagen I ◽  
Type I ◽  
Kinase C

Collagen type I is the most abundant component of extracellular matrix in the arterial wall. Mice knocked out for the protein kinase C δ gene (PKCδ KO) show a marked reduction of collagen I in the arterial wall. The lack of PKCδ diminished the ability of arterial smooth muscle cells (SMCs) to secrete collagen I without significantly altering the intracellular collagen content. Moreover, the unsecreted collagen I molecules accumulate in large perinuclear puncta. These perinuclear structures colocalize with the trans-Golgi network (TGN) marker TGN38 and to a lesser degree with cis-Golgi marker (GM130) but not with early endosomal marker (EEA1). Associated with diminished collagen I secretion, PKCδ KO SMCs exhibit a significant reduction in levels of cell division cycle 42 (Cdc42) protein and mRNA. Restoring PKCδ expression partially rescues Cdc42 expression and collagen I secretion in PKCδ KO SMCs. Inhibition of Cdc42 expression or activity with small interfering RNA or secramine A in PKCδ WT SMCs eliminates collagen I secretion. Conversely, restoring Cdc42 expression in PKCδ KO SMCs enables collagen I secretion. Taken together, our data demonstrate that PKCδ mediates collagen I secretion from SMCs, likely through a Cdc42-dependent mechanism.

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