| First Author | Lengfeld J | Year | 2012 |
| Journal | Mol Biol Cell | Volume | 23 |
| Issue | 10 | Pages | 1955-63 |
| PubMed ID | 22456512 | Mgi Jnum | J:197798 |
| Mgi Id | MGI:5494544 | Doi | 10.1091/mbc.E11-06-0531 |
| Citation | Lengfeld J, et al. (2012) Protein kinase C delta regulates the release of collagen type I from vascular smooth muscle cells via regulation of Cdc42. Mol Biol Cell 23(10):1955-63 |
| abstractText | Collagen type I is the most abundant component of extracellular matrix in the arterial wall. Mice knocked out for the protein kinase C delta gene (PKCdelta KO) show a marked reduction of collagen I in the arterial wall. The lack of PKCdelta 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, PKCdelta KO SMCs exhibit a significant reduction in levels of cell division cycle 42 (Cdc42) protein and mRNA. Restoring PKCdelta expression partially rescues Cdc42 expression and collagen I secretion in PKCdelta KO SMCs. Inhibition of Cdc42 expression or activity with small interfering RNA or secramine A in PKCdelta WT SMCs eliminates collagen I secretion. Conversely, restoring Cdc42 expression in PKCdelta KO SMCs enables collagen I secretion. Taken together, our data demonstrate that PKCdelta mediates collagen I secretion from SMCs, likely through a Cdc42-dependent mechanism. |
