Characteristics of Coronary Smooth Muscle Cells and Adventitial Fibroblasts

Patel, Sachin; Shi, Yi; Niculescu, Rodica; Chung, Eugene H.; Martin, Jack L.; Zalewski, Andrew

doi:10.1161/01.cir.101.5.524

Cited by 61 publications

(61 citation statements)

References 58 publications

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“…We and others recently reported that cultured porcine coronary artery SMCs maintain a high degree of differentiation in vitro, 9,23 contrary to what has been reported for rodent arterial SMCs. 18,24 In the present study, SMC marker expression was very similar in the populations of neointimal SMCs cultured after either stent or PTCA.…”

Section: Smc Marker Expression In Cultured Cellscontrasting

confidence: 56%

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Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

et al. 2001

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Background-To characterize the cells responsible for neointima formation after porcine coronary artery wall injury, we studied the expression of smooth muscle cell (SMC) differentiation markers in 2 models: (1) self-expanding stent implantation resulting in no or little interruption of internal elastic lamina and (2) percutaneous transluminal coronary angioplasty (PTCA) resulting in complete medial rupture and exposure of adventitia to blood components. Methods and Results-The expression of ␣-smooth muscle (SM) actin, SM myosin heavy chain isoforms 1 and 2, desmin, and smoothelin was investigated by means of immunohistochemistry and Western blots in tissues of the arterial wall collected at different time points and in cell populations cultured from these tissues. The expression of smoothelin, a marker of late SMC differentiation, was used to discriminate between SMCs and myofibroblasts. Both stent-and PTCA-induced neointimal tissues and their cultured cell populations expressed all 4 markers. The adventitial tissue underlying PTCA-induced lesions temporarily expressed ␣-SM actin, desmin, and SM myosin heavy chain isoforms, but not smoothelin. When placed in culture, adventitial cells expressed only ␣-SM actin. Conclusions-Our results suggest that SMCs are the main components of coronary artery neointima after both self-expanding stent implantation and PTCA. The adventitial reaction observed after PTCA evolves with a chronology independent of that of neointima formation and probably corresponds to a myofibroblastic reaction.

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Section: Smc Marker Expression In Cultured Cellscontrasting

confidence: 56%

“…Moreover, it has been reported that porcine coronary SMCs behave differently in vitro from adventitial fibroblasts and from SMCs of elastic arteries. 23 All these data support, albeit indirectly, the SMC origin of intimal lesions.…”

Section: Smc Marker Expression In Cultured Cellsmentioning

confidence: 78%

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

et al. 2001

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“…The responses of porcine coronary SMCs to TGF-␤1 in vitro differ from those of rat arterial SMCs, 23 and coronary SMCs display distinct behavior from noncoronary SMCs in vitro, leading to the suggestion that repair mechanisms may differ between coronary and noncoronary vessels. 24 The stimulatory effect of TGF-␤1 on collagen synthesis by porcine SMCs in vitro is significantly less marked in cells cultured on collagen matrices than on monolayers. 25 This also appears to be true for porcine fibroblasts in vivo, 26 suggesting that the fibrogenic effects of TGF-␤1 on coronary SMCs in vivo, where cells are surrounded by basement membrane within a 3D collagen matrix, may differ from those observed in noncoronary SMC monolayers.…”

Section: Discussionmentioning

confidence: 98%

Adenovirus-Mediated Gene Transfer of a Secreted Transforming Growth Factor-β Type II Receptor Inhibits Luminal Loss and Constrictive Remodeling After Coronary Angioplasty and Enhances Adventitial Collagen Deposition

et al. 2001

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Background-Extracellular matrix (ECM) remodeling is central to the development of restenosis after coronary angioplasty (PTCA). As a regulator of ECM deposition by vascular cells, substantial evidence implicates transforming growth factor-␤1 (TGF-␤1) in the pathogenesis of restenosis. We investigated the effects of intracoronary expression of a transgenic antagonist of TGF-␤1 on luminal loss after PTCA. Methods and Results-Porcine coronary arteries were randomized to receive a recombinant adenovirus expressing a secreted form of TGF-␤ type II receptor (Ad5-RIIs), an adenovirus expressing ␤-galactosidase (Ad5-lacZ), or vehicle only by intramural injection at the site of PTCA. Computerized morphometry 28 days after angioplasty revealed a greater minimum luminal area in Ad5-RIIs-injected arteries (1.71Ϯ0.12 mm 2 ) than in the Ad5-lacZ (1.33Ϯ0.13 mm 2 ) or vehicle-only (1.08Ϯ0.17 mm 2 ; Pϭ0.010 by ANOVA) groups. This was accompanied by greater areas within the internal (Pϭ0.013) and external (Pϭ0.031) elastic laminae in Ad5-RIIs-treated vessels. Adventitial collagen content at the site of injury was increased in the Ad5-RIIs group, in contrast to decreases in the Ad5-lacZ and vehicle-only groups (Pϭ0.004). Conclusions-Adenovirus-mediated

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“…29 SMCs isolated by enzymatic digestion from the NM exhibit a spindle-shaped phenotype and grow in a hill-and-valley configuration, 29,42 similar to SMCs derived from the porcine aortic NM. 43,44 In contrast, SMCs obtained by tissue explantation are either spindle-shaped or rhomboid (flat, but more elongated than epithelioid rat SMCs); the luminal side of the media yields equal proportions of spindle-shaped and rhomboid SMCs, whereas the abluminal side yields a high proportion of rhomboid SMCs (Figure 1). 29 With these same techniques, IT induced 15 days after stent implantation gives rise to a high proportion of rhomboid SMCs.…”

Section: Establishment Of Distinct Smc Populationsmentioning

confidence: 99%

Arterial Smooth Muscle Cell Heterogeneity

Hao

Gabbiani

Bochaton‐Piallat

2003

ATVB

341

139

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Abstract-During atheromatous plaque formation or restenosis after angioplasty, smooth muscle cells (SMCs) migrate from the media toward the intima, where they proliferate and undergo phenotypic changes. The mechanisms that regulate these phenomena and, in particular, the phenotypic modulation of intimal SMCs have been the subject of numerous studies and much debate during recent years. One view is that any SMCs present in the media could undergo phenotypic modulation. Alternatively, the seminal observation of Benditt and Benditt that human atheromatous plaques have the features of a monoclonal or an oligoclonal lesion has led to the hypothesis that a predisposed, medial SMC subpopulation could play a crucial role in the production of intimal thickening. The presence of a distinct SMC population in the arterial wall implies that under normal conditions, SMCs are phenotypically heterogeneous. The concept of SMC heterogeneity is gaining wider acceptance, as shown by the increasing number of publications on this subject. In this review, we discuss the in vitro studies that demonstrate the presence of distinct SMC subpopulations in arteries of various species, including humans. Their specific features and their regulation will be highlighted. Finally, the relevance of an atheroma-prone phenotype to intimal thickening formation will be discussed.

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Characteristics of Coronary Smooth Muscle Cells and Adventitial Fibroblasts

Cited by 61 publications

References 58 publications

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

Mechanisms of Neointima Formation and Remodeling in the Porcine Coronary Artery

Adenovirus-Mediated Gene Transfer of a Secreted Transforming Growth Factor-β Type II Receptor Inhibits Luminal Loss and Constrictive Remodeling After Coronary Angioplasty and Enhances Adventitial Collagen Deposition

Arterial Smooth Muscle Cell Heterogeneity

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