Arterial Smooth Muscle Cell Heterogeneity

Hao, Hiroyuki; Gabbiani, Giulio; Bochaton‐Piallat, Marie‐Luce

doi:10.1161/01.atv.0000090130.85752.ed

Cited by 339 publications

(156 citation statements)

References 146 publications

(176 reference statements)

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“…The heterogeneity of vascular SMCs has been well established in many species, including humans (reviewed in [20]). This concept suggests that the blood vessel wall contains multiple SMC phenotypes, which may play distinct roles in the development of atherosclerosis and restenosis after angioplasty.…”

Section: Introductionmentioning

confidence: 99%

“…Two phenotypes are present in cultured vascular SMCs [21]: spindle-shaped and epithelioid. Epithelioid SMCs have higher proliferation and migration activities [20]. Because these activities are critical in atherogenesis and cells derived from neointima lesions demonstrate an epithelioid phenotype, epithelioid SMCs have been considered to be candidates for 'atheroma-prone' cells.…”

Section: Introductionmentioning

confidence: 99%

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Phenotype-specific inhibition of the vascular smooth muscle cell cycle by high glucose treatment

2007

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Aims/hypothesis Diabetes accelerates the development of atherosclerosis, which critically involves the proliferation of vascular smooth muscle cells (SMCs). However, how high glucose treatment regulates SMC proliferation is controversial. Considering the established SMC heterogeneity, we hypothesised that glucose treatment may have distinct effects on proliferation of the various phenotypic SMCs. Materials and methods We tested this possibility using cloned spindle-shaped and epithelioid SMCs and laser scanning cytometry. Results Our results showed that glucose treatment significantly inhibited the serum-independent proliferation of epithelioid SMCs, but had no effect on the proliferation of spindle-shaped cells either with or without serum stimulation. Furthermore, glucose treatment inhibited DNA synthesis, as detected by bromodeoxyuridine (BrdU) incorporation, and increased the production of reactive oxygen species in epithelioid SMCs. The inhibition of BrdU incorporation by glucose treatment was mimicked by glucosamine and phorbol 2,13-dibutyrate, a protein kinase C (PKC) activator, and reversed by azaserine, an inhibitor of the hexosamine pathway. In addition, the inhibitory effects of glucose treatment were blocked by GF 109203X (a PKC inhibitor) and PD98058 (a MAPK/ERK kinase, MEK inhibitor), and by knockdown of MEK1 by small interfering RNA (siRNA). The addition of either GF 109203X or PD98058 also reduced the phosphorylation of MAP kinase induced by glucose treatment. Conclusions/interpretation Glucose treatment inhibits the proliferation of epithelioid, but not spindle-shaped, vascular SMCs through the activation of PKC and the MAP kinase pathway, suggesting that the effects of hyperglycaemia on vascular disease depend on the phenotype of SMCs involved.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Phenotype-specific inhibition of the vascular smooth muscle cell cycle by high glucose treatment

2007

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“…These differences are observed between SMCs of different vessels as well as amongst SMCs within the same vessel. Part of the variation in SMC populations can be explained by the diverse embryological origins of SMCs, reviewed by Gittenberger-de Groot et al 2 However, the remarkable capability of SMCs to shuttle between different phenotypes, referred to as phenotypic modulation, 3 may be more important, as it is superimposed on the origin-related phenotype.…”

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confidence: 99%

Regulation and characteristics of vascular smooth muscle cell phenotypic diversity

Rensen¹,

Doevendans²,

Eys³

2007

NHJL

760

706

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Vascular smooth muscle cells can perform both contractile and synthetic functions, which are associated with and characterised by changes in morphology, proliferation and migration rates, and the expression of different marker proteins. The resulting phenotypic diversity of smooth muscle cells appears to be a function of innate genetic programmes and environmental cues, which include biochemical factors, extracellular matrix components, and physical factors such as stretch and shear stress. Because of the diversity among smooth muscle cells, blood vessels attain the flexibility that is necessary to perform efficiently under different physiological and pathological conditions. In this review, we discuss recent literature demonstrating the extent and nature of smooth muscle cell diversity in the vascular wall and address the factors that affect smooth muscle cell phenotype. (Neth Heart J 2007;15:100-8.)

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“…25,26 In this study, no distinct morphological features were noted in the cells from the three different groups, which is different from the findings in vascular SM cells. 18,27 Herein, we suppose that cultured CCSM cells from diabetic ED rats have different functional characteristics with respect to cell contractility. Compared with other groups, CCSM cells from diabetic ED rats exhibited significantly less contractility in response to 10% serum and growth factor.…”

Section: Discussionmentioning

confidence: 99%

Characterization of corpus cavernosum smooth muscle cell phenotype in diabetic rats with erectile dysfunction

et al. 2012

Int J Impot Res

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Phenotypic modulation from a contractile to a proliferative state within vascular smooth muscle cells has a critical role in the pathogenesis of a variety of cardiovascular diseases. To investigate the characterization of corpus cavernosum smooth muscle cell phenotype in diabetic rats with erectile dysfunction, a group of Sprague--Dawley rats (n ¼ 30) were induced by intraperitoneal injection of streptozotocin (60 mg kg À1 ) and screened by subcutaneous injection of apomorphine (100 mg kg À1 ) for the measurement and comparison of the penile erections, and then three different groups were defined. Primary corpus cavernosum smooth muscle cells were cultured and passaged. The cavernous tissue segments were subjected to quantitative real-time polymerase chain reaction to determine the expressions of smooth muscle a-actin (SMA), SM myosin heavy chain (SMMHC), smoothelin, calponin and myocardin. Cell contractility in vitro and western blot analysis of SMA and SMMHC in the cavernous tissues and cells were determined. Compared with the control group (n ¼ 8) and the diabetes mellitus group (n ¼ 5), the expressions of SMA, calponin, SMMHC, smoothelin and myocardin mRNA were decreased in the cavernous tissues in rats of the diabetic erectile dysfunction group (n ¼ 15; P ¼ 0.001 and 0.02, P ¼ 0.014 and 0.012, both Po0.001, P ¼ 0.005 and o0.001, P ¼ 0.003 and 0.035, respectively). The levels of SMA and SMMHC proteins showed a significant decrease in cavernous tissues and cultured cells in rats of the diabetic erectile dysfunction group. Cells of the diabetic erectile dysfunction group exhibited significantly less contractility compared with those of other groups (Po0.001). Corpus cavernosum SM cell possesses the ability to modulate the phenotype under hyperglycemic conditions, which could have a key role in the pathogenesis of diabetic erectile dysfunction. Keywords: diabetes mellitus; erectile dysfunction; smooth muscle INTRODUCTION Erectile dysfunction (ED), a distressing complication of diabetes mellitus (DM), 1 is three times more common in diabetic male rats than in non-diabetic male rats. It has been reported that about 35--90% of diabetic male rats suffer from ED. 2,3 The pathogenesis of DM-related ED may be involved in many aspects; however, it was well known that vascular causative factors contribute significantly. 4 Corpus cavernosum smooth muscle (CCSM), the structural basis of cavernous space relaxing and penile erection, has a key role in the change of hemodynamics during penile erection. CCSM cell relaxation mediated by parasympathetic neurotransmission, nitric oxide, electrophysiological events and possibly other regulatory factors is necessary for normal penile erection. 5 It has been observed that the CCSM cell mass was lost in diabetic rats with ED, and the remaining SM cells were unable to achieve sufficient relaxation to attain the high intracorporeal pressures that are necessary for the passive occlusion of the veins that egress the corporal bodies as they traverse underneath and through the tunica albu...

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Arterial Smooth Muscle Cell Heterogeneity

Cited by 339 publications

References 146 publications

Phenotype-specific inhibition of the vascular smooth muscle cell cycle by high glucose treatment

Phenotype-specific inhibition of the vascular smooth muscle cell cycle by high glucose treatment

Regulation and characteristics of vascular smooth muscle cell phenotypic diversity

Characterization of corpus cavernosum smooth muscle cell phenotype in diabetic rats with erectile dysfunction

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