Inhibition of PDGF-Mediated Proliferation of Vascular Smooth Muscle Cells by Calcium Antagonists

Kataoka, Satoshi; Alam, Rita; Dash, Pramod K.; Yatsu, Frank M.

doi:10.1161/01.str.28.2.364

Cited by 20 publications

(10 citation statements)

References 32 publications

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“…The observed reduction in SMC layers in the intimal thickening of animals treated with BW 9798 for 28 days is in agreement with findings by other groups [24]. Although we could see only a tendency towards reduced cellular proliferation it is conceivable that an antimitogenic affect of BW 9798 is accountable for the observed decreased SMC layer since calcium channel antagonists inhibit growth factor mediated proliferation of SMC [44][45][46]. Findings in another study [24] suggested that nifedipine inhibits SMC proliferation by attenuating the MEK-ERK phosphorylation.…”

Section: Discussionsupporting

confidence: 92%

Effect of a Dihydropyridine-Type Calcium Channel Blocker on Vascular Remodelling after Experimental Balloon Angioplasty

Kranzhöfer

Weingärtner²,

Oberhoff³

et al. 2011

CHAMC

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BW 9798 leads to significant changes in vessel wall geometry although the influence on vascular remodeling of this compound is unclear. It can be speculated that the compound affects the homeostasis of extracellular matrix, invasion of inflammatory cells into the vessel wall and the expression of cytokines. However, further investigation needs to clarify the role of BW 9798 on remodelling after BA.

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Section: Discussionsupporting

confidence: 92%

Effect of a Dihydropyridine-Type Calcium Channel Blocker on Vascular Remodelling after Experimental Balloon Angioplasty

Kranzhöfer

Weingärtner²,

Oberhoff³

et al. 2011

CHAMC

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“…On the other hand, the knockout of the mouse c-fos [33]and c-jun [34, 35]genes demonstrated that both genes are not essential for proliferation and differentiation of most cell types, including renal cells. Along the same line, Kataoka et al [36]have recently reported that PDGF-mediated proliferation of vascular smooth muscle cells correlates with activation on protein kinase C but not with induction of AP-1 complexes. Interestingly, dietary sodium restriction reduced AP-1 activation in remaining nephrons at any time of the study.…”

Section: Discussionmentioning

confidence: 87%

Sodium Restriction Decreases AP-1 Activation after Nephron Reduction in the Rat: Role in the Progression of Renal Lesions

Terzi

Burtin

Hekmati

et al. 2000

Nephron Exp Nephrol

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Renal hyperplasia and hypertrophy are early events after nephron reduction which precede progressive destruction of the remnant kidney. Restriction of dietary sodium content was shown to reduce renal lesions following nephron reduction. AP-1 is a transcription factor, resulting from heterodimerization of fos and jun proteins, which mediates the effects of mitogenic growth factors. To elucidate the role of AP-1 in growth processes involved in renal deterioration, we evaluated whether restriction of dietary sodium content (0.25 vs. 0.50% sodium w/w) affected AP-1-DNA binding and hyperplasia in the remnant kidney after nephron reduction (70% nephrectomy). Cell proliferation, evaluated by PCNA immunostaining, increased progressively from day 7 to day 60 in glomeruli, proximal and distal tubules and loops of Henle of nephrectomized (Nx) rats compared to control sham-operated (C) animals. AP-1-DNA binding activity increased 7 and 14 days after surgery, but it was reduced below C values at day 60. c-fos and c-jun expression were also reduced in Nx rats at day 60. Sodium restriction significantly reduced the number of PCNA-stained cells in glomeruli and tubules at days 14 and 60, but not at day 7, whereas it decreased AP-1 activation at all times of the study. This effect was associated to a marked reduction of renal lesions in Nx rats. In conclusion, we showed that, after nephron reduction, the beneficial effect of sodium restriction was associated with a reduction of hyperplasia and AP-1 activation, but that the latter did not parallel delayed cell proliferation rate in remaining nephrons. Thus, we propose that different transduction pathways are involved in cell proliferation after nephron reduction, according to the time of evolution of renal lesions.

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“…Cell cycle arrest in late G1 by cobalt and dihydropyridine-type calcium channel blockers is a well established phenomenon, though pharmacological approaches have failed to identify the mechanisms involved [13,16,[23][24][25][26]. This growth inhibition is at the heart of several therapies proposed to counteract undesirable cell proliferation in sensitive cell types [49].…”

Section: Discussionmentioning

confidence: 99%

“…Although the importance of Ca 2+ in mitogenic signaling is well established, pharmacological approaches using calcium channel blockers have failed to identify the molecular mechanisms that are responsible [13,16,[23][24][25][26]. Using retrovirus-based cDNA libraries [18], we performed genetic screens to identify the mechanism of calcium-based regulation of proliferation.…”

Section: The Human Cystine Transporter Xct Enables Cells To Overcommentioning

confidence: 99%

xCT expression reduces the early cell cycle requirement for calcium signaling

Lastro

Kourtidis

Farley

et al. 2008

Cellular Signalling

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Calcium has long been recognized as an important regulator of cell cycle transitions although the mechanisms are largely unknown. A functional genomic screen has identified genes involved in the regulation of early cell cycle progression by calcium. These genes when overexpressed confer the ability to bypass the G1/S arrest induced by Ca 2+ -channel antagonists in mouse fibroblasts. Overexpression of the cystine-glutamate exchanger, xCT, had the greatest ability to evade calcium antagonist-induced cell cycle arrest. xCT carries out the rate limiting step of glutathione synthesis in many cell types and is responsible for the uptake of cystine in most human cancer cell lines. Functional analysis indicates that the cystine uptake activity of xCT overcomes the G1/S arrest induced by Ca 2+ -channel antagonists by bypassing the requirement for calcium signaling. Since cells overexpressing xCT were found to have increased levels and activity of the AP-1 transcription factor in G1, redox stimulation of AP-1 activity accounts for the observed growth of these cells in the presence of calcium channel antagonists. These results suggest that reduced calcium signaling impairs AP-1 activation and that xCT expression may directly affect cell proliferation.

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Inhibition of PDGF-Mediated Proliferation of Vascular Smooth Muscle Cells by Calcium Antagonists

Abstract: PDGF-mediated proliferation of VSMCs correlates with activation of PKC but not with induction of the AP-1 complexes. In addition, our results suggest that CAs block proliferation of VSMCs by inhibiting DNA synthesis, possibly via PKC.

Cited by 20 publications

References 32 publications

Effect of a Dihydropyridine-Type Calcium Channel Blocker on Vascular Remodelling after Experimental Balloon Angioplasty

Effect of a Dihydropyridine-Type Calcium Channel Blocker on Vascular Remodelling after Experimental Balloon Angioplasty

Sodium Restriction Decreases AP-1 Activation after Nephron Reduction in the Rat: Role in the Progression of Renal Lesions

xCT expression reduces the early cell cycle requirement for calcium signaling

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