scholarly journals Cholera toxin treatment of vascular smooth muscle cells decreases smooth muscle α-actin content and abolishes the platelet-derived growth factor-BB-stimulated DNA synthesis

2000 ◽  
Vol 130 (7) ◽  
pp. 1561-1570 ◽  
Author(s):  
Agapios Sachinidis ◽  
Claudia Seul ◽  
Ioanna Gouni-Berthold ◽  
Stefan Seewald ◽  
Yon Ko ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Cholera Toxin ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor

Platelet-derived growth factor stimulates Na+ influx in vascular smooth muscle cells

1984 ◽  
Vol 247 (5) ◽  
pp. C501-C505 ◽  
Author(s):  
N. E. Owen
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor ◽  
Ionophore A23187 ◽  
Dependent Manner

Platelet-derived growth factor (PDGF) is known to be a potent mitogenic agent for vascular smooth muscle cells. The effect of PDGF on amiloride-sensitive Na+ influx was investigated in A-10 vascular smooth muscle cells. At a dose which maximally stimulates DNA synthesis, PDGF stimulates net Na+ influx in vascular smooth muscle cells. The PDGF-stimulated Na+ influx is linear over a 5-min time course. PDGF stimulates Na+ influx in a concentration-dependent manner, with a concentration of 0.5 U/ml causing half-maximal inhibition. The effects of PDGF on Na+ influx can be mimicked by 10% fetal bovine serum or by the divalent cation ionophore A23187 (5 microM). Net Na+ influx in response to each of these agents was inhibited by amiloride and by benzamil. PDGF-stimulated net Na+ influx was blocked by the intracellular Ca2+ antagonist 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate as well as by the calmodulin antagonists trifluoperazine, chlorpromazine, and imipramine. These data suggest that PDGF may stimulate an amiloride-sensitive Na+ influx pathway via an elevation in intracellular Ca2+ and formation of a Ca-calmodulin complex. This Na+ influx pathway may be a trigger for PDGF-stimulated DNA synthesis.

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