Role of Protein Kinase C in Abnormal Proliferation of Vascular Endothelial Cell induced by 1,2-Dimethylhydrazine; Analysis of Isoform.
- Author:
Jin LEE
1
;
Yong Chan BAE
;
Suk Young PARK
;
Jae Sul MOON
;
Su Bong NAM
Author Information
1. Lee Jin Aesthetic Clinic, Busan, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Cell Proliferation;
Protein Kinase C;
Endothelial cells
- MeSH:
1,2-Dimethylhydrazine*;
Cell Proliferation;
Dimenhydrinate;
Endothelial Cells*;
Oxidoreductases;
Protein Kinase C*;
Protein Kinases*;
RNA;
Signal Transduction;
Tyrosine;
Umbilical Veins
- From:Journal of the Korean Society of Plastic and Reconstructive Surgeons
2007;34(1):8-12
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Protein tyrosine kinase(PTK), protein kinase C(PKC), oxidase, as a mediator, have been known to take a role in signal transduction pathway of angiogenesis. The authors confirmed that PKC is the most noticeable mediator for abnormal proliferation of vascular endothelial cells through in vitro study model using the inhibitors, targeting the formation of three co-enzymes. In this study, we would investigate which isoform of PKC play an important role in abnormal angiogenesis of vascular endothelial cell. METHODS: In 96 well plates, 10(4) HUVECs(human umbilical vein endothelial cells) were evenly distributed. Two groups were established; the control group without administration of DMH(1,2-dimethylhydrazine) and the DMH group with administration of 7.5x10(-9)M DMH. RNA was extracted from vascular endothelial cell of each group and expression of the PKC isoform was analyzed by RT-PCR(reverse transcriptase-polymerase chain reaction) method. RESULTS: RT-PCR analysis showed that PKCalpha, -betaI, -betaII, -eta, -micron and -zeta were expressed in vascular endothelial cells of each group. DMH incresed the expression of PKCalpha and PKCmicron, and decreased PKCbetaI, PKCbetaII expression dominantly. CONCLUSION: Based on the result of this study, it was suggested that PKCalpha and PKCmicron may have significant role in abnormal proliferation of vascular endothelial cell.
