2.Role of cytosolic Ca2+ in the proliferation of vascular smooth muscle cells.
Korean Journal of Medicine 1999;57(4):402-407
No abstract available.
Cytosol*
;
Muscle, Smooth, Vascular*
4.The Effect of Midazolam on Outward K+ Channel Currents in Rabbit Cerebral Arterial Smooth Muscle Cells.
Young Chul SHIN ; Jae Hang SHIM ; Woo Jae JEON ; Sang Yoon CHO ; Woo Jong SHIN ; Kyoung Hun KIM ; Jong Hoon YEOM
Korean Journal of Anesthesiology 2007;52(1):67-71
BACKGROUND: Midazolam has a direct relaxing effect on vascular smooth muscle, but the mechanisms that this agent produces muscle relaxation are not fully understood. The current study was performed to identify the effects of the midazolam on K+ channels current in rabbit cerebral arterial smooth muscle cells. METHODS: Whole cell patch-clamp recording technique was used to evaluate the effects of midazolam (0.1 to 100micrometer) on outward K+ channel currents in dispersed rabbit cerebral arterial smooth muscle cells. RESULTS: Outward K+ currents of rabbit cerebral artery smooth muscle cells were voltage-dependent. Midazolam (10, 100micrometer) tested significantly inhibited outward K+ currents in a dose-dependent manner and half-blocking concentration (IC50) was 15.94micrometer at 60 mV. CONCLUSIONS: Midazolam inhibit outward K+ currents of rabbit cerebral arterial smooth muscle cells. Further study will be needed to determine the effect of midazolam on calcium channel current because it is unclear if the inhibitory effect of midazolam on outward K+current induces vasoconstriction.
Calcium Channels
;
Cerebral Arteries
;
Midazolam*
;
Muscle Relaxation
;
Muscle, Smooth*
;
Muscle, Smooth, Vascular
;
Myocytes, Smooth Muscle*
;
Vasoconstriction
5.The Role of MicroRNAs in Vascular Diseases; Smooth Muscle Cell Differentiation and De-Differentiation.
Korean Circulation Journal 2014;44(4):218-219
No abstract available.
MicroRNAs*
;
Myocytes, Smooth Muscle*
;
Vascular Diseases*
6.Effects of Monocyte Chemoattractant Protein-1 on Growth and Migration of Cultured Human Vascular Smooth Muscle Cells.
Ho Chul PARK ; Jung Whan CHOI ; Soo Myung OH ; Jae Kyung PARK
Journal of the Korean Society for Vascular Surgery 1999;15(1):12-21
No abstract available.
Chemokine CCL2*
;
Humans*
;
Monocytes*
;
Muscle, Smooth, Vascular*
7.Effects of Tetrandrine on the Nitric Oxide Production by Vascular Smooth Muscle Cells of the Rat.
Gi Su OH ; Na Young KIM ; Hyun Ock BAE ; Youn Chul KIM ; Jong Hyun HAN ; Young Myung KIM ; Byoung Sun AHN ; Hun Taeg CHUNG
Korean Journal of Immunology 2000;22(4):247-252
No abstract available.
Animals
;
Muscle, Smooth, Vascular*
;
Nitric Oxide*
;
Rats*
8.Effects and mechanism of fibroblast growth factor 21 on rat vascular smooth muscle cells calcification.
Kun FU ; Yi XIN ; Yuchen SHI ; Xuwei ZHENG ; Yuan LYU ; Zhenye XU ; Jinghua LIU ; Email: LIUJINGHUA@VIP.SINA.COM.
Chinese Journal of Cardiology 2015;43(10):879-886
OBJECTIVETo observe the effect and mechanism of fibroblast growth factor 21 (FGF21) on rat vascular smooth muscle cells (VSMCs) calcification in vitro.
METHODSVSMCs was treated with calcification medium containing calcium chloride and β-glycerophosphate to induce rat VSMCs calcification in vitro. VSMCs were divided into 5 groups: the control group (cultured in normal medium), the calcification group (incubated in calcified medium), the FGF21 group (cultured in calcified medium and FGF21), the PD166866 group (cultured in calcified medium and FGF21 and PD166866, inhibitor of fibroblast growth factor receptor-1 (FGFR1)), the GW9662 group (cultured in calcified medium and FGF21 and GW9662, inhibitor of peroxisome proliferators activated receptor-γ (PPAR-γ)). The calcification of VSMCs was detected by calcium content, alkaline phosphatase activity and alizarin red staining. The protein and mRNA expression of FGFR1, β-Klotho, osteocalcin and smooth muscle 22α (SM22α) were determined by western blot analysis and realtime-PCR, respectively.
RESULTS(1) The mRNA (P < 0.01) and protein expressions of β-Klotho and FGFR1 were significantly downregulated in calcification group compared with control group (P < 0.05 or 0.01). (2) The protein levels and mRNA expression of calcium content, alkaline phosphatase activity and osteocalcin were significantly downregulated, while the protein levels and mRNA of SM22α were significantly increased in FGF21 group compared with calcification group (all P < 0.05). Moreover, alizarin red staining verified positive red nodules on calcified VSMCs was significantly reduced in FGF21 group than in calcification group. (3) Calcium content, alkaline phosphatase activity and alizarin red staining were similar between PD166866 group and calcification group (all P > 0.05). (4) Calcium content, alkaline phosphatase activity and alizarin red staining were similar between GW9662 group and calcification group (all P > 0.05).
CONCLUSIONThe inhibition of VSMCs calcification by FGF21 is mediated by further downregulating FGFR1 and β-Klotho while activating PPAR-γ pathways.
Animals ; Calcium ; Fibroblast Growth Factors ; Glycerophosphates ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Rats ; Vascular Calcification
9.New insights into vascular mechanobiology: roles of matrix mechanics in regulating smooth muscle cell function.
Jin WANG ; Juan-Juan ZHU ; Jing ZHOU
Acta Physiologica Sinica 2021;73(2):160-174
Vascular smooth muscle cell (vSMC) is the predominant cell type in the blood vessel wall and is constantly subjected to a complex extracellular microenvironment. Mechanical forces that are conveyed by changes in stiffness/elasticity, geometry and topology of the extracellular matrix have been indicated by experimental studies to affect the phenotype and function of vSMCs. vSMCs perceive the mechanical stimuli from matrix via specialized mechanosensors, translate these stimuli into biochemical signals controlling gene expression and activation, with the consequent modulation in controlling various aspects of SMC behaviors. Changes in vSMC behaviors may further cause disruption of vascular homeostasis and then lead to vascular remodeling. A better understanding of how SMC senses and transduces mechanical forces and how the extracellular mechano-microenvironments regulate SMC phenotype and function may contribute to the development of new therapeutics for vascular diseases.
Biophysics
;
Cells, Cultured
;
Extracellular Matrix
;
Humans
;
Muscle, Smooth, Vascular
;
Myocytes, Smooth Muscle
;
Phenotype
;
Vascular Remodeling
10.Role of non-coding RNAs in vascular smooth muscle cell calcification.
Acta Physiologica Sinica 2022;74(6):885-893
Vascular calcification, the deposition of calcium in the arterial wall, is often linked to increased stiffness of the vascular wall. Vascular calcification is one of the important factors for high morbidity and mortality of cardiovascular and cerebrovascular diseases, as well as an important biomarker in atherosclerotic cardiovascular events, stroke and peripheral vascular diseases. The mechanism of vascular calcification has not been fully elucidated. Recently, non-coding RNAs have been found to play an important role in the process of vascular calcification. In this paper, the main types of non-coding RNAs and their roles involved in vascular smooth muscle cell calcification are reviewed, including the changes of osteoblast-related proteins, calcification signaling pathways and intracellular Ca2+.
Humans
;
Muscle, Smooth, Vascular/metabolism*
;
Vascular Calcification/metabolism*
;
Myocytes, Smooth Muscle/metabolism*