Vascular smooth muscle cells (VSMC) are the main cellular component of vessel wall. The changes of VSMC functions including phenotypic transformation and apoptosis play a critical role in the pathogenesis of intracranial aneurysm (IA). Autophagy can participate in the regulation of vascular function by regulating cell function. In the initial stage of IA, the activation of autophagy can accelerate the phenotypic transformation of VSMC and inhibit VSMC apoptosis. With the progress of IA, the relationship between autophagy and apoptosis changes from antagonism to synergy or promotion, and a large number of apoptotic VSMC lead to the rupture of IA. In this review, we describe the role of autophagy regulating the function of VSMC in the occurrence, development and rupture of IA, for further understanding the pathogenesis of IA and finding molecular targets to prevent the formation and rupture of IA.
Autophagy ; Humans ; Intracranial Aneurysm ; pathology ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology

AIMThe process of vascular calcification involves various genetic alterations which may play a very important role in the vascular calcification. Vascular smooth muscle cells undoubtedly composed the main part of vascular cells, and are involved in vascular calcification. So bovine artery smooth muscle cell (BASMC) was used to investigate the gene changes during BASMC's calcification.

METHODSBovine artery smooth muscle cells cultured in vitro was induced calcified by beta-Glycerophosphate (beta-GP). Using DD-PCR technique to screening differentially expressed genes and those differentially expressed bands were reexamined by reverse Northern blot. All the ESTs were sequenced and BLAST with GenBank.

RESULTSTotal 65 cDNAs were isolated as differentially expressed genes and 40 of them were successfully reamplified. Using reverse-Northern blot, seven of these 40 cDNAs were reproducibly expressed differentially between the two cells. Three of them are new bands and have not been reported before.

CONCLUSIONThis is the first time using DD-PCR to screen differentially expressed genes of BASMC calcification. Seven related ESTs were identified relating to BASMC calcification.

Animals ; Arteriosclerosis ; genetics ; metabolism ; pathology ; Cattle ; Cells, Cultured ; Expressed Sequence Tags ; Genetic Variation ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; metabolism ; pathology ; Vascular Calcification ; genetics ; metabolism ; pathology

AIMAccumulated evidence suggest that the development of vascular calcification is similar to osteogenesis. Here we want to elucidate the effect of the common used osteo-regulatory factor 1,25(OH)2D3 on vascular calcification.

METHODS AND RESULTSAdding 10(-9) mol/L to the culture media 1,25(OH)2D3 time dependently increased the calcium deposition on the in vitro calcification of bovine vascular smooth muscle cells (BVSMCs) induced by beta-GP. It also increased cellular alkaline phosphatase activity by 301.1% during the calcified process. Osteocalcin, one of the osteogenic specific metric proteins, was dramatically elevated by 58.3% during the calcified processes, which indicate the transformation of BVSMCs to osteoblastic cell. 1,25(OH)2D3 had no such effect on non-calcified BVSMCs.

CONCLUSIONThese data suggest that 1,25(OH)2D3 exerts a stimulatory effect on vascular calcification through increasing the synthesis of ALP. This effect shares the same character as osteoblast cells. This effect is limited to the calcified prone vascular cell.

Animals ; Calcitriol ; metabolism ; Cattle ; Cells, Cultured ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; drug effects ; metabolism ; pathology ; Osteocalcin ; metabolism ; Vascular Calcification ; metabolism ; pathology ; Vitamin D ; analogs & derivatives ; pharmacology

Autophagy plays a crucial role in maintaining normal structure and vascular function in vivo. When stress-relevant stimuli are involved, the increases of autophagy can protect vascular smooth muscle cells, promote cell survival, and phenotype transformation, as well as reduce calcification. On the contrary, the decrease of autophagy can accelerate cell senescence, resulting in structural changes and dysfunction of vasomotor and vasodilation. However, excessive activation of autophagy can induce the damage of the healthy protein and essential organelles, and even lead to autophagic cell death, accelerating the progression of vascular disease. Thus, the precise targeting of autophagy opens a novel way for treatment of vascular diseases.
Autophagy ; physiology ; Cell Survival ; Cellular Senescence ; Disease Progression ; Humans ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; physiology ; Vascular Diseases ; pathology ; therapy

Animals ; Cardiovascular Diseases ; genetics ; pathology ; Cell Proliferation ; Genes ; Microfilament Proteins ; genetics ; Muscle Proteins ; genetics ; Muscle, Smooth, Vascular ; pathology ; Rats

Intimal accumulation of smooth muscle cells contributes to the development and progression of atherosclerotic lesions and restenosis following endovascular procedures. Arterial smooth muscle cells display heterogeneous phenotypes in both physiological and pathological conditions. In response to injury, dedifferentiated or synthetic smooth muscle cells proliferate and migrate from the tunica media into the intima. As a consequence, smooth muscle cells in vascular lesions show a prevalent dedifferentiated phenotype compared to the contractile appearance of normal media smooth muscle cells. The discovery of abundant stem antigen-expressing cells in vascular lesions also rarely detected in the tunica media of normal adult vessels stimulated a great scientific debate concerning the possibility that proliferating vascular wall-resident stem cells accumulate into the neointima and contribute to the progression of lesions. Although several experimental studies support this hypothesis, others researchers suggest a positive effect of stem cells on plaque stabilization. So, the real contribute of vascular wall-resident stem cells to pathological vascular remodelling needs further investigation. This review will examine the evidence and the contribution of vascular wall-resident stem cells to arterial pathobiology, in order to address future investigations as potential therapeutic target to prevent the progression of vascular diseases.
Adult ; Endovascular Procedures ; Humans ; Myocytes, Smooth Muscle ; Neointima ; Pathology* ; Phenotype ; Stem Cells* ; Tunica Media ; Vascular Diseases

Vascular calcification is an active and complex pathological process regulated by several factors. Vascular calcification is closely related to the incidence and mortality of the cardiovascular disease, chronic kidney disease and other diseases, which affects multiple organs and systems, thus affecting people's health. Therefore, more and more attention is paid to vascular calcification. At present, the pathogenesis and clinical practice of vascular calcification have been continuously improved, which mainly includes calcium and phosphorus imbalance theory, vascular smooth muscle cell transdifferentiation theory, bone homeostasis imbalance theory, epigenetic regulation theory, inflammation theory, extracellular matrix theory, new cell fate theory and so on. However, there are still many unsolved problems. Since the occurrence and development of vascular calcification affect multiple organs and systems, this expert consensus gathered clinicians and basic research experts engaged in the study of vascular calcification in order to summarize the progress of various disciplines related to vascular calcification in recent years. The purpose of this consensus is to systematically summarize the latest research progress, treatment consensus and controversy of vascular calcification from the aspects of epidemiology, pathogenesis, prevention and treatment, so as to provide theoretical basis and clinical enlightenment for in-depth research in this field.
Humans ; Consensus ; Epigenesis, Genetic ; Vascular Calcification/pathology* ; Cardiovascular Diseases ; Myocytes, Smooth Muscle

The aim of the present study was to investigate the effect of removal of the adventitia on vascular remodeling and vasoconstriction of the carotid artery in New Zealand rabbit. Adventitia of carotid artery was removed mechanically. The histology, morphology and reactivity of the carotid artery was observed by immunohistochemistry and measurement of carotid ring tension immediately, 1 week and 2 weeks after removal of the adventitia. No damage of intima and media was observed after removing the adventitia. Removal of the adventitia caused a remarkable proliferation of the vascular media and formed the neointima. Compared with the control ring, norepinephrine (NE)-induced vasocontraction in adventitia-denuded carotid artery was significantly reduced immediately and 1 week after the operation (P<0.05). Adventitia removal promoted the neointima formation and decreased vasoconstriction of the carotid artery, indicating that the adventitia is involved in the regulation of vascular remodeling and vasoconstriction.
Animals ; Carotid Arteries ; pathology ; physiology ; surgery ; Connective Tissue ; physiology ; surgery ; Muscle, Smooth, Vascular ; pathology ; Rabbits ; Tunica Intima ; pathology ; Vasoconstriction ; physiology

AIM AND METHODSMTT colorimetric assay, in situ hybridization and immunocytochemistry were performed to investigate the effect of endogenous and exogenous CO on the proliferation of PASMCs and the expression of PDGF-B and protooncogene bcl-2, P53 (mutant type) in PASMCs, in order to elucidate the mechanism by which CO suppressed the proliferation of PASMC in hypoxic environment.

RESULTSThe results of in situ hybridization of PDGF-B mRNA and immunocytochemical staining of PDGF-B were negative. Hypoxia could upregulate the expression of Bcl-2, mutant P53 protein in comparison with the control group (P < 0.01). Compared with the hypoxic group, the expression of Bcl-2 and mutant P53 were decreased after treated with hemin or CO, but increased after treated with hemoglobin (P < 0.01).

CONCLUSIONCO could suppress the expression of oncogene bcl-2 and mutant P53. This partially explained how CO suppressed the proliferation of PASMCs in hypoxic environment.

Animals ; Carbon Monoxide ; Cell Hypoxia ; Cell Proliferation ; Cells, Cultured ; Muscle, Smooth, Vascular ; cytology ; metabolism ; pathology ; Myocytes, Smooth Muscle ; cytology ; metabolism ; Pulmonary Artery ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo investigate the novel hyperplasia suppressor gene (HSG) expression in vascular smooth muscle cells derived from normotensive and hypertensive patients underwent bypass surgery.

METHODSCoronary heart disease patients underwent coronary artery bypass graft (CABG) operation in BEIJING ANZHEN hospital from 4 - 9, 2006 were enrolled in this study and divided into hypertensive group (n = 28) and normotensive group (n = 26). The preoperative venous blood samples were taken for serum biochemical and vasoactive peptides measurements. Total RNA was extracted from WBC, explanted-vessels and cultured VSMCs using TRIZOL and HSG expression was determined by Semi-Quantitative RT-PCR.

RESULTSBody mass index (BMI) was significantly higher in hypertensive group compared to normotensive group (P < 0.01) while other biochemic parameters and vasoactive peptides were similar between the groups. BMI and GLU, BMI and SBP, BMI and DBP, GLU and TG, SBP and DBP were positively correlated (all P < 0.05). HSG expression in WBC, VSMCs and vessel tissue were significantly lower in hypertensive group than those in normotensive group (all P < 0.05). HSG expression in tissue was negatively correlated to BMI, SBP and DBP (all P < 0.05).

CONCLUSIONSReduced HSG expression and the negative correlation on vascular tissue HSG expression to BMI, SBP and DBP suggested a possible inhibitory role of HSG on VSMC proliferation and blood pressure.

Aged ; Body Mass Index ; Female ; Gene Expression ; Genes, Suppressor ; Humans ; Hyperplasia ; genetics ; Hypertension ; genetics ; pathology ; Male ; Middle Aged ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; metabolism