[Targeting of myosin light chain kinase in vascular smooth muscle cells, and its implication for drug discovery].
We constructed a plasmid vector to have a 1.4-kb insert of myosin light chain kinase (MLCK) cDNA in an antisense direction to express antisense mRNA. The construct was then transfected to SM3, a cell line from vascular smooth muscle cells (VSMCs), producing a few stable transformants. We explained the methods in detail. The down-regulation of MLCK expression in the transfectants was confirmed by both Northern and Western blots. The control showed chemotactic motility to the platelet derived growth factor. However, the transfectants did not show chemotactic motility, indicating the essential role of MLCK in the motility. It was discussed that down-regulation of MLCK expression could be utilized to discover the drug for arteriosclerosis which prevents the proliferating VSMCs from forming arterial plaques.
Kohama
K
K
Department of Pharmacology, School of Medicine, Gunma University, Maebashi, Gunma 371-8511, Japan.
Nakamura
A
A
D000595:Amino Acid Sequence; D000818:Animals; D002478:Cells, Cultured; D004247:DNA; D015195:Drug Design; D005822:Genetic Vectors; D006801:Humans; D008969:Molecular Sequence Data; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000201:enzymology*; D009219:Myosin-Light-Chain Kinase / Q000235:genetics / Q000502:physiology; D010957:Plasmids; D016372:RNA, Antisense; D012333:RNA, Messenger; D011817:Rabbits; D014162:Transfection / Q000379:methods*
D016372:RNA, Antisense; D012333:RNA, Messenger; D004247:DNA; D009219:Myosin-Light-Chain Kinase