Cell cycle dependent gene expression in quiescent stimulated and asynchronously cycling arterial smooth muscle cells in culture

Campan, Michel; Des̀granges, Claude; Gadeau, Alain‐Pierre; Millet, Dominique; Belloc, Françis

doi:10.1002/jcp.1041500309

Cited by 25 publications

(18 citation statements)

References 48 publications

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“…Expression of c-myc in particular is analogous to AIF-1, in that it is not limited to the early growth factor response but continues throughout the first and following cell cycles, suggesting that it is important not only in the initiation but also in the maintenance of VSMC proliferation. 30 Thus, its expression may be part of the VSMC response to injury, resulting in proliferation and intimal hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Allograft Inflammatory Factor-1 Promotes Proliferation of Vascular Smooth Muscle Cells by Cell Cycle Deregulation

Autieri

Carbone

2001

ATVB

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Abstract-Allograft inflammatory factor-1 (AIF-1) is not present in normal arteries, but its expression is induced in vascular smooth muscle cells (VSMCs) in several models of arterial injury. The proliferation of VSMCs is a major component of neointimal hyperplasia in many arteriopathies, and the purpose of this study was to determine the role of AIF-1 in the growth of VSMCs. Transfection and constitutive expression of AIF-1 in a primary and a rat VSMC line results in enhanced growth of those cells as measured by cell number and is proportional to the amount of AIF-1 expressed. Constitutive expression of AIF-1 results in a shorter cell cycle, as measured by flow cytometry, and aberrant expression of cell cycle proteins, as determined by Western blot. AIF-1 overexpression also permits growth of these cells in serum-reduced media. Collectively, these data suggest that AIF-1 may participate in the progression of vascular proliferative disease on the basis of its ability to regulate the growth of VSMCs.

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Section: Discussionmentioning

confidence: 99%

Overexpression of Allograft Inflammatory Factor-1 Promotes Proliferation of Vascular Smooth Muscle Cells by Cell Cycle Deregulation

Autieri

Carbone

2001

ATVB

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“…They include inositol trisphosphate turnover, an increase in intracellular pH and [Ca 2+ ], protein phosphorylation, and a time-dependent induction of the expression of a set of genes (cell cycle-dependent [CCD] genes). 6 " 13 In fibroblastic cell lines these CCD genes have been classified in relation to their delay of induction, time of maximal expression, and need for new protein synthesis. 14 This classification has recently been extended to arterial SMCs in culture.…”

Section: Osteopontin Overexpression Is Associated With Arterial Smootmentioning

confidence: 99%

“…When added to the medium, the cycloheximide (from Sigma) concentration was 1.5 ixglm\. Asynchronously cycling SMCs were obtained as described by Campan et al 13 Cells were seeded at a low density (10 4 cells/cm 2 ) in a 75-cm 2 flask in 10% FCS-DMEM and allowed to grow for 3 days with a daily change of medium. The last change of medium was made exactly 24 hours before cell harvesting.…”

Section: Cell Culturementioning

confidence: 99%

“…Elutriation and flow cytometric analysis were performed as reported by Campan et al 13 The SMC suspension (about 1.5 xlO 8 cells in DMEM, 2 mM ethylene glycol-bis(/3-aminoethyl ether)-Af,Af,iV',/V'-tetraacetic acid, and 1% bovine serum albumin) was injected at a flow rate of 6 ml/min into a Beckman JE-6B elutriator (Sanderson chamber) spinning at 1,500 rpm at 4°C. After stabilization of the cell gradient, elution of cell subpopulations was performed by increasing the flow rate to 7, 8.5, 10.5, 12, and 14 ml/min, respectively, for subpopulations a, b, c, d, and e. Cell cycle analysis of these elutriated subpopulations was monitored by flow cytometry.…”

Section: Elutriation and Flow Cytometric Analysismentioning

confidence: 99%

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Osteopontin overexpression is associated with arterial smooth muscle cell proliferation in vitro.

Gadeau

Campan

Millet

et al. 1993

Arterioscler Thromb

124

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To isolate the genes involved in the cell cycle G1 phase progression of arterial smooth muscle cells (SMCs), a cDNA clone (M11) was previously selected by differential hybridization screening of a mid-G1 serum-stimulated SMC cDNA library. The delay of induction after mitogenic stimulation, time of expression, and need for new protein synthesis for full expression made it possible to classify this gene in the "delayed early" gene group. Determination of the partial M11 cDNA sequence showed full homology with the osteopontin gene (secreted phosphoprotein 1, 2ar), an Arg-Gly-Asp-containing extracellular matrix protein. Osteopontin mRNA was also detected in the aorta at levels as high as in the kidney but lower than in bone, two tissues in which it has been previously detected. In vitro analysis of osteopontin expression in serum-stimulated quiescent SMCs and asynchronously cycling SMCs demonstrated that osteopontin overexpression was associated with SMC proliferation. In view of our results, the high osteopontin expression observed by others in the injured carotid artery could be explained by the involvement of SMCs in the proliferative process. Taken together, these results suggest that osteopontin may play an important role in pathological processes that are associated with arterial SMC proliferation, such as atherosclerosis or restenosis.

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“…Mitogen stimulation of quiescent VSMCs rapidly induces c-myc with a peak ofexpression at 2-4 h ( 15, 16). Subsequently, c-myc expression in VSMCs is maintained at a constant low level throughout the first and subsequent cell cycles ( 17). C-myc thus appears to have a role both in entry into the cell cycle and in the maintenance of cell proliferation.…”

Section: Introductionmentioning

confidence: 97%

Inhibition of vascular smooth muscle cell proliferation in vitro and in vivo by c-myc antisense oligodeoxynucleotides.

Bennett¹,

Anglin²,

McEwan³

et al. 1994

J. Clin. Invest.

229

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Restenosis after angioplasty is due predominantly to accumulation of vascular smooth muscle cells (VSMCs). The resistance of restenosis to pharmacological treatment has prompted investigation of genes involved in VSMC proliferation. We have examined the effect on VSMC proliferation of blocking expression of the c-myc proto-oncogene with antisense oligodeoxynucleotides, both in vitro and in a rat carotid artery injury model of angioplasty restenosis. Antisense c-myc oligodeoxynucleotides reduced average cell levels of c-myc mRNA and protein by 50-55% and inhibited proliferation of VSMCs when mitogenically stimulated from quiescence or when proliferating logarithmically (IC5o = 10 ug/ml). Corresponding sense c-myc, two-basepair mismatch antisense c-myc, antisense a-actin or glyceraldehyde phosphate dehydrogenase oligodeoxynucleotides did not suppress c-myc expression or inhibit VSMC proliferation. Antisense c-myc inhibition was relieved by overexpression of an exogenous c-myc gene. After balloon catheter injury, peak cmyc mRNA expression occurred at 2 h. Antisense c-myc applied in a pluronic gel to the arterial adventitia reduced peak c-myc expression by 75% and significantly reduced neointimal formation at 14 d, compared with sense c-myc and gel application alone. We conclude that c-myc expression is required for VSMC proliferation in vitro and in the vessel wall. C-myc is a therefore a potential target for adjunctive therapy to reduce angioplasty restenosis. (J. Clin. Invest. 1994. 93:820-828.

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Cell cycle dependent gene expression in quiescent stimulated and asynchronously cycling arterial smooth muscle cells in culture

Cited by 25 publications

References 48 publications

Overexpression of Allograft Inflammatory Factor-1 Promotes Proliferation of Vascular Smooth Muscle Cells by Cell Cycle Deregulation

Overexpression of Allograft Inflammatory Factor-1 Promotes Proliferation of Vascular Smooth Muscle Cells by Cell Cycle Deregulation

Osteopontin overexpression is associated with arterial smooth muscle cell proliferation in vitro.

Inhibition of vascular smooth muscle cell proliferation in vitro and in vivo by c-myc antisense oligodeoxynucleotides.

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