Hyperproliferation of Aortic Smooth Muscle Cells and Fibroblasts From Young SHR Rats Is Not Shared by Endothelial Cells

Battle, Thierry; Arnal, Jean‐François; Michel, Jean‐Baptiste

doi:10.1111/j.1440-1681.1994.tb02660.x

Cited by 13 publications

(8 citation statements)

References 34 publications

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“…These studies indicate that the cellular component of rat vein-to-artery grafts is derived almost entirely from the host rat. Any increased propensity for SMC proliferation in SHR (Grunwald et al 1987;Agrotis et al 1993;Battle et al 1994) did not have a measurable effect in the detection of donor cells from SHR grafts.…”

Section: Discussionmentioning

confidence: 71%

“…SHR were used to confirm the results obtained with WKy rat grafts and to determine whether the increased SMC proliferation seen in SHR (Grunwald et al 1987;Agrotis et al 1993;Battle et al 1994) would make detection of donor cells easier in these grafts. The extent of donor cell survival was assessed 2 weeks later by PCR analysis of the DNA extracted from grafts.…”

Section: Resultsmentioning

confidence: 96%

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Cellular survival in rat vein-to-artery grafts

Redwood

Tennant

2001

Cell and Tissue Research

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Microsurgical models of vein-to-artery graft surgery have been developed in rats as a means of assessing vein graft adaptation and neo-intimal hyperplasia. Neo-intimal hyperplasia in these grafts is often attributed, at least in part, to an adaptive response by venous smooth muscle cells to the increased intraluminal pressure of the arterial pressure. However, considerable evidence suggests complete or near-complete cellular replacement in these grafts. A series of experiments were undertaken in which male vein or artery grafts were placed into either allogeneic female nude rat hosts or into syngeneic WKy female hosts as a means of determining donor cell survival. Grafts were removed at postsurgery week 2 or week 6 and the fate of the donor male cells assessed by PCR amplification of the testis-determining gene Sry. The Sry gene was undetectable in 2-week male to female vein grafts. When left for 6 weeks, donor cells were detectable in vein grafts only after multiple 50-cycle PCR analyses. Minimal donor cell survival was not due to an allograft response, as donor male cells were readily detectable in WKy male to female nude rat artery-to-artery grafts. These data were not nude rat specific, as poor donor cell survival was also evidenced in syngeneic male to female vein-to-artery grafts. In conclusion, we demonstrate only marginal survival of donor cells in rat vein-to-artery grafts. Neo-intimal hyperplasia in these grafts was not a consequence of donor venous smooth muscle cell proliferation.

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Section: Discussionmentioning

confidence: 71%

Section: Resultsmentioning

confidence: 96%

Cellular survival in rat vein-to-artery grafts

Redwood

Tennant

2001

Cell and Tissue Research

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“…Previous studies have reported vascular smooth muscle hyper-responsiveness in hypertension both under basal conditions as well as after treatment with a range of growth factors (Hamet et al, 1988;Battle et al, 1994;Begum et al, 1998;Tanner et al, 2003). However, these differences in growth rates have been shown to be specific for individual growth factors.…”

Section: Tablementioning

confidence: 89%

The Impact of Blunted β-Adrenergic Responsiveness on Growth Regulatory Pathways in Hypertension

Gros

Ding²,

Chorazyczewski³

et al. 2005

Mol Pharmacol

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The effects of vasodilator hormones acting through receptors linked to adenylyl cyclase are impaired in the hypertensive state. This has been ascribed to impaired receptor-G protein coupling. However, these receptors also act via effectors not linked to adenylyl cyclase activation. These "alternate" mechanisms may be especially important in growth regulation and might be unaffected (or enhanced) with G protein-coupled receptor-G protein uncoupling. Therefore, we assessed the effects of ␤-adrenergic activation on 1) regulation of phosphatidylinositol 3-kinase (PI3 kinase) and extracellular signalregulated kinase (ERK) activation-two tyrosine kinasedependent enzymes linked to cell growth-and 2) microarray analysis in vascular smooth muscle cells from spontaneously hypertensive rats (SHR). Isoproterenol-stimulated phosphorylation of ERK1/2 was impaired in SHR. The effect of forskolin was unaltered. In contrast, both vasopressin and angiotensin 2-mediated stimulation of ERK activation was enhanced in SHR. In addition, ␤-adrenergic-mediated inhibition of PI3 kinase activity was attenuated in SHR (whereas the effect of forskolin remained intact). In microarray studies, the effect of isoproterenol to regulate transcription was significantly impaired in SHR (as was the effect of forskolin). Together, these data support the hypothesis that the blunted vasodilator effects of hormones linked to adenylyl cyclase activation are an index of a more generalized impairment in modulating growth regulatory pathways. Furthermore, this study supports the hypothesis that the blunting of ␤-adrenergic responses relating to increased G protein-coupled receptor kinase 2 expression reflects a "generalized uncoupling" of ␤-adrenergic-mediated responses and do not support the concept of "enhanced coupling" of "alternate" pathways of ␤-adrenergic growth regulatory pathways in the hypertensive state.

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“…29 All cells were routinely cultured in smooth muscle cell (SMC) medium (Promocell) containing 5% foetal calf serum (FCS), gentamicin-sulfate (50 mg/mL), amphotericin B (50 µg/mL), insulin (5 mg/mL), and growth factors (human epidermal and fibroblast growth factors, respectively 0.5 and 2 µg/mL). Passages 3–6 were used for experiments.…”

Section: Methodsmentioning

confidence: 99%

Epigenetic control of vascular smooth muscle cells in Marfan and non-Marfan thoracic aortic aneurysms

Gomez¹,

Coyet²,

Ollivier³

et al. 2010

Cardiovascular Research

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AimsHuman thoracic aortic aneurysms (TAAs) are characterized by extracellular matrix breakdown associated with progressive smooth muscle cell (SMC) rarefaction. These features are present in all types of TAA: monogenic forms [mainly Marfan syndrome (MFS)], forms associated with bicuspid aortic valve (BAV), and degenerative forms. Initially described in a mouse model of MFS, the transforming growth factor-β1 (TGF-β1)/Smad2 signalling pathway is now assumed to play a role in TAA of various aetiologies. However, the relation between the aetiological diversity and the common cell phenotype with respect to TGF-β signalling remains unexplained.Methods and resultsThis study was performed on human aortic samples, including TAA [MFS, n = 14; BAV, n = 15; and degenerative, n = 19] and normal aortas (n = 10) from which tissue extracts and human SMCs and fibroblasts were obtained. We show that all types of TAA share a complex dysregulation of Smad2 signalling, independent of TGF-β1 in TAA-derived SMCs (pharmacological study, qPCR). The Smad2 dysregulation is characterized by an SMC-specific, heritable activation and overexpression of Smad2, compared with normal aortas. The cell specificity and heritability of this overexpression strongly suggest the implication of epigenetic control of Smad2 expression. By chromatin immunoprecipitation, we demonstrate that the increases in H3K9/14 acetylation and H3K4 methylation are involved in Smad2 overexpression in TAA, in a cell-specific and transcription start site-specific manner.ConclusionOur results demonstrate the heritability, the cell specificity, and the independence with regard to TGF-β1 and genetic backgrounds of the Smad2 dysregulation in human thoracic aneurysms and the involvement of epigenetic mechanisms regulating histone marks in this process.

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Hyperproliferation of Aortic Smooth Muscle Cells and Fibroblasts From Young SHR Rats Is Not Shared by Endothelial Cells

Cited by 13 publications

References 34 publications

Cellular survival in rat vein-to-artery grafts

Cellular survival in rat vein-to-artery grafts

The Impact of Blunted β-Adrenergic Responsiveness on Growth Regulatory Pathways in Hypertension

Epigenetic control of vascular smooth muscle cells in Marfan and non-Marfan thoracic aortic aneurysms

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