The transfection of caldesmon DNA into primary cultured rat aortic vascular smooth muscle.
- Author:
Woong CHOI
1
;
Hee Yul AHN
Author Information
1. Department of Pharmacology, College of Medicine, Chungbuk National University, Cheongju, Chungbuk, Korea.
- Publication Type:Original Article
- Keywords:
Caldesmon;
Overexpression;
Vascular smooth muscle cell;
Growth inhibition;
Cell volume decrease
- MeSH:
Actin Cytoskeleton;
Animals;
Calmodulin-Binding Proteins*;
Cell Count;
Cell Size;
Cytomegalovirus;
Cytoskeleton;
Detergents;
DNA*;
DNA, Complementary;
Genetic Therapy;
Humans;
Hyperplasia;
Hypertrophy;
Intercellular Signaling Peptides and Proteins;
Mitosis;
Molecular Weight;
Muscle, Smooth, Vascular*;
Physiology;
Plasmids;
Rats*;
Transfection*
- From:The Korean Journal of Physiology and Pharmacology
1999;3(6):597-603
- CountryRepublic of Korea
- Language:English
-
Abstract:
Caldesmon (CaD), one of microfilament-associated proteins, plays a key role in microfilament assembly in mitosis. We have investigated the effects of overexpression of the high molecular weight isoform of CaD (h-CaD) on the physiology of vascular smooth muscle cells (VSMCs). Rat aortic VSMCs were stably transfected with plasmids carrying a full length human h-CaD cDNA under control of cytomegalovirus promoter. The majority of the overexpressed h-CaD appears to be localized predominantly on cytoskeleton structures as determined by detergent lysis. The overexpression of h-CaD, however, does not decrease the level of endogenous low molecular weight isoform of CaD. h-CaD overexpressing VSMCs (h-CaD/VSMCs) show a decreased growth rate than that of vector-only transfected cells when determined by (3H)thymidine uptake and cell counting after fetal bovine serum (FBS) stimulation. h-CaD/VSMCs were smaller than vector-transfected cells by 18% in cell diameter. These data suggest that overexpression of h-CaD can inhibit the poliferation and the cell volume of VSMCs stimulated by growth factors and that the gene therapy with h-CaD may be helpful to prevent the conditions associated with hypertrophy and/or hyperplasia of VSMCs after arterial injuries.
