Growth characteristics of pulmonary artery smooth muscle cells from fawn-hooded rats

1995 ◽  
Vol 268 (3) ◽  
pp. L465-L470 ◽  
Author(s):  
K. Janakidevi ◽  
C. Tiruppathi ◽  
P. J. Del Vecchio ◽  
J. M. Pinheiro ◽  
A. B. Malik
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Specific Binding ◽  
Pulmonary Arteries ◽  
Muscle Cells ◽  
Serum Concentrations ◽  
Egf Receptors ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Epidermal Growth

We compared the proliferative rates of vascular smooth muscle cells (VSMC) from pulmonary arteries of pulmonary hypertensive fawn-hooded rats (FHR) with VSMC from normotensive Sprague-Dawley rats (SDR). VSMC from FHR grew at increased rates and reached higher densities at all serum concentrations studied (5-20%) than the VSMC from SDR. The VSMC from FHR also responded to epidermal growth factor (EGF) at low serum concentrations, as evidenced by significantly greater DNA synthetic rates, than the control VSMC. The increased growth in these cells could be due to increased number and/or affinity of EGF receptors because of the higher specific binding of 125I-EGF to the VSMC from FHR. The VSMC from FHR and SDR were equally sensitive to the antiproliferative effects of heparin, suggesting that the heparin-sensitive pathways are not altered in the VSMC from FHR. These results suggest that the development of pulmonary hypertension in FHR may be related to the higher proliferative capacity of the pulmonary VSMC, which may be coupled to increased activity of the EGF receptors on these cells.

scholarly journals Yixintongmai Inhibits Proliferation, Migration and Promotes Apoptosis of Vascular Smooth Muscle Cells Cultured with High Glucose

2020 ◽  
Author(s):  
JingJing Guo ◽  
Di Zhao ◽  
Pingshuan Dong
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Muscle Cells ◽  
Cell Counting ◽  
Ros Generation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Abstract Background: This study was designed to evaluate the effects of yixintongmai on proliferation, migration, and apoptosis of vascular smooth muscle cells (VSMCs) cultured with high glucose. Methods: VSMCs of the thoracic aorta from 5–8 weeks male Sprague-Dawley rats were cultured with normal (4.5 mM) or high (25 mM) glucose, respectively. The effects of yixintongmai on proliferation, migration, and apoptosis of VSMCs cultured with high glucose were evaluated. The concentration of yixintongmai powder at 360 μg/ml was chosen for this study according to pre-experimental results. Results: Yixintongmai inhibited the proliferation of VSMCs (CCK-8 assay: 0.75 ± 0.04 versus 0.98 ± 0.09 OD, P<0.001; cell counting: 37533 ± 1861 versus 56009 ± 3779 cells/well, P<0.001) and the expression of PCNA (0.74 ± 0.08 folds, P<0.001) as compared with high glucose. Yixintongmai inhibited the migration of VSMCs (transwell assay: 146 ± 16 versus 265 ± 62 cells; P<0.001; scratch wound assay: 2.69 ± 0.22 folds, P<0.001) and the expression of MMP-9 (0.87 ± 0.03 folds, P<0.001) as compared with high glucose. Yixintongmai promoted the apoptosis of VSMCs (0.36 ± 0.12 folds, P<0.001) and inhibited the expression of bcl-2 (0.83 ± 0.07 folds, P<0.01) as compared with high glucose. Yixintongmai inhibited ROS generation (0.58 ± 0.01 folds, P<0.001) and the expression of NF-κB (0.71 ± 0.07 folds, P<0.001) of VSMCs as compared with high glucose. Conclusions: Yixintongmai inhibits the proliferation, migration and promotes the apoptosis of VSMCs cultured with high glucose, which suggests the potential anti-atherosclerotic effects of this traditional Chinese medicine.

scholarly journals Agonist-induced calcium regulation in freshly isolated renal microvascular smooth muscle cells.

1997 ◽  
Vol 8 (4) ◽  
pp. 569-579
Author(s):  
E W Inscho ◽  
M J Mason ◽  
A C Schroeder ◽  
P C Deichmann ◽  
K D Stiegler ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Single Cells ◽  
Control Level ◽  
Muscle Cells ◽  
Detectable Effect ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Transduction Mechanisms ◽  
K Concentration

The studies presented here were performed to determine the effect of agonist stimulation on the cytosolic free Ca2+ concentration ([Ca2+]i) in single smooth muscle cells, freshly isolated from afferent arterioles and interlobular arteries averaging between 10 to 40 microns in diameter. Microvessels were obtained from male Sprague-Dawley rats using an iron oxide collection technique followed by collagenase digestion. Freshly isolated microvascular smooth muscle cells (MVSMC) were loaded with fura 2 and studied using fluorescence photometry techniques. The resting [Ca2+]i averaged 67 +/- 3 nM (N = 82 cells). Increasing the extracellular K+ concentration significantly increased [Ca2+]i dose-dependently (P < 0.05). Involvement of extracellular Ca2+ in the response to KCl-induced depolarization was also evaluated. Resting [Ca2+]i increased approximately 132% from 40 +/- 5 nM to 93 +/- 26 nM in response to 90 mM extracellular KCl. This change was abolished in nominally Ca(2+)-free conditions and markedly attenuated by diltiazem. Inhibition of K+ channels with charybdotoxin or tetraethylammonium chloride produced a modest transient increase in [Ca2+]i during the response to 30 mM K+ and had no detectable effect on responses to 90 mM K+. Studies were also performed to establish whether freshly isolated renal MVSMC exhibit appropriate responses to receptor-dependent physiological agonists. Angiotensin II (100 nM) increased cell Ca2+ from 97 +/- 10 nM to 265 +/- 47 nM (N = 12 cells). Similarly, 100 microM ATP increased MVSMC [Ca2+]i from a control level of 71 +/- 14 nM to 251 +/- 47 nM (N = 11 cells). Norepinephrine administration caused [Ca2+]i to increase from 63 +/- 4 nM to 212 +/- 47 nM (N = six cells), and vasopressin increased [Ca2+]i from 86 +/- 10 nM to 352 +/- 79 nM (N = five cells). These data demonstrate that receptor-dependent and -independent vasoconstrictor agonists increase [Ca2+]i in MVSMC, freshly isolated from rat preglomerular vessels. Furthermore, the ability to measure [Ca2+]i in responses to physiological stimuli in these single cells permits investigation of signal transduction mechanisms involved in regulating renal microvascular resistance.

scholarly journals MicroRNA-137 Inhibited Hypoxia-Induced Proliferation of Pulmonary Artery Smooth Muscle Cells by Targeting Calpain-2

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Xiao-Yue Ge ◽  
Tian-Tian Zhu ◽  
Mao-Zhong Yao ◽  
Hong Liu ◽  
Qian Wu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Vascular Remodeling ◽  
Pulmonary Arteries ◽  
Muscle Cells ◽  
Sprague Dawley ◽  
Pulmonary Vascular Remodeling ◽  
Calpain 2 ◽  
Pulmonary Artery Smooth Muscle

The proliferation of pulmonary artery smooth muscle cells (PASMCs) is an important cause of pulmonary vascular remodeling in pulmonary hypertension (PH). It has been reported that miR-137 inhibits the proliferation of tumor cells. However, whether miR-137 is involved in PH remains unclear. In this study, male Sprague-Dawley rats were subjected to 10% O2 for 3 weeks to establish PH, and rat primary PASMCs were treated with hypoxia (3% O2) for 48 h to induce cell proliferation. The effect of miR-137 on PASMC proliferation and calpain-2 expression was assessed by transfecting miR-137 mimic and inhibitor. The effect of calpain-2 on PASMC proliferation was assessed by transfecting calpain-2 siRNA. The present study found for the first time that miR-137 was downregulated in pulmonary arteries of hypoxic PH rats and in hypoxia-treated PASMCs. miR-137 mimic inhibited hypoxia-induced PASMC proliferation and upregulation of calpain-2 expression in PASMCs. Furthermore, miR-137 inhibitor induced the proliferation of PASMCs under normoxia, and knockdown of calpain-2 mRNA by siRNA significantly inhibited hypoxia-induced proliferation of PASMCs. Our study demonstrated that hypoxia-induced downregulation of miR-137 expression promoted the proliferation of PASMCs by targeting calpain-2, thereby potentially resulting in pulmonary vascular remodeling in hypoxic PH.

Upregulation of profilin, cofilin-2 and LIMK2 in cultured pulmonary artery smooth muscle cells and in pulmonary arteries of monocrotaline-treated rats

2006 ◽  
Vol 44 (5) ◽  
pp. 275-282 ◽  
Author(s):  
Yan-Ping Dai ◽  
Shaner Bongalon ◽  
Honglin Tian ◽  
Samuel D. Parks ◽  
Violeta N. Mutafova-Yambolieva ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Pulmonary Arteries ◽  
Muscle Cells ◽  
Pulmonary Artery Smooth Muscle

Effect of SR-49059, a vasopressin V1a antagonist, on human vascular smooth muscle cells

1995 ◽  
Vol 268 (1) ◽  
pp. H404-H410 ◽  
Author(s):  
C. Serradeil-Le Gal ◽  
J. M. Herbert ◽  
C. Delisee ◽  
P. Schaeffer ◽  
D. Raufaste ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Specific Binding ◽  
Muscle Cells ◽  
Maximal Response ◽  
Receptor Subtypes ◽  
Functional Studies ◽  
Antagonist Binding

The effects of SR-49059, a new nonpeptide and selective arginine vasopressin (AVP) V1a antagonist, were investigated in binding and functional studies on cultured human aortic vascular smooth muscle cells (VSMC). Characterization of human vascular V1a receptors, using a specific V1a radioiodinated ligand, showed that [125I]-linear AVP antagonist binding to human VSMC membranes was time dependent, reversible, and saturable. A single population of high-affinity binding sites (apparent equilibrium dissociation constant = 15 +/- 6 pM; maximum binding density = 36 +/- 5 fmol/mg protein, i.e., approximately 3,000 sites/cell) with the expected V1a profile was identified. Exposure of these cells to AVP dose-dependently produced cytosolic free [Ca2+] increase [AVP concentration required to obtain a half-maximal response (EC50) = 23 +/- 9 nM] and proliferation (EC50 = 3.2 +/- 0.5 nM). SR-49059 strongly and stereospecifically inhibited [125I]-linear AVP antagonist binding to VSMC V1a receptors [inhibition constant (Ki) = 1.4 +/- 0.3 nM], AVP-evoked Ca2+ increase [concentration of inhibitor required to obtain 50% inhibition of specific binding (IC50) = 0.41 +/- 0.06 nM], and the mitogenic effects induced by 100 nM AVP (IC50 = 0.83 +/- 0.04 nM). OPC-21268, another nonpeptide V1a antagonist, was more than two orders of magnitude less potent than SR-49059 in these models. However, the consistent affinity (Ki = 138 +/- 21 nM) and activity found with OPC-21268 on human VSMC in comparison with the inactivity already observed for other human V1a receptors (liver, platelets, adrenals, and uterus) strongly suggested the existence of human AVP V1a-receptor subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)

Trimethylamine But Not Trimethylamine Oxide Increases With Age in Rat Plasma and Affects Smooth Muscle Cells Viability

2019 ◽  
Vol 75 (7) ◽  
pp. 1276-1283 ◽  
Author(s):  
Kinga Jaworska ◽  
Marek Konop ◽  
Tomasz Hutsch ◽  
Karol Perlejewski ◽  
Marek Radkowski ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Cardiovascular Risk ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Biological Effects ◽  
Muscle Cells ◽  
Gut Bacteria ◽  
Sprague Dawley ◽  
Trimethylamine Oxide

Abstract It has been suggested that trimethylamine oxide (TMAO), a liver oxygenation product of gut bacteria-produced trimethylamine (TMA), is a marker of cardiovascular risk. However, mechanisms of the increase and biological effects of TMAO are obscure. Furthermore, the potential role of TMAO precursor, that is TMA, has not been investigated. We evaluated the effect of age, a cardiovascular risk factor, on plasma levels of TMA and TMAO, gut bacteria composition, gut-to-blood penetration of TMA, histological and hemodynamic parameters in 3-month-old and 18-month-old, male, Sprague–Dawley and Wistar–Kyoto rats. Cytotoxicity of TMA and TMAO was studied in human vascular smooth muscle cells. Older rats showed significantly different gut bacteria composition, a significantly higher gut-to-blood TMA penetration, and morphological and hemodynamic alterations in intestines. In vitro, TMA at concentration of 500 µmol/L (2-fold higher than in portal blood) decreased human vascular smooth muscle cells viability. In contrast, TMAO at 1,000-fold higher concentration than physiological one had no effect on human vascular smooth muscle cells viability. In conclusion, older rats show higher plasma level of TMA due to a “leaky gut”. TMA but not TMAO affects human vascular smooth muscle cells viability. We propose that TMA but not TMAO may be a marker and mediator of cardiovascular risk.

Receptors for substance P on isolated intestinal smooth muscle cells of the guinea pig

1987 ◽  
Vol 253 (5) ◽  
pp. G666-G672
Author(s):  
J. C. Souquet ◽  
K. N. Bitar ◽  
J. R. Grider ◽  
G. M. Makhlouf
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Binding Sites ◽  
Specific Binding ◽  
Muscle Cells ◽  
Receptor Subtype ◽  
Longitudinal Muscle Layer ◽  
Substance K

Two radioligands, 125I-labeled substance P (125I-SP) and 125I-labeled substance K (125I-SK), were used to characterize the kinetics and stoichiometry of binding of mammalian tachykinins [substance P (SP), substance K (SK), and neuromedin K (NK)] to smooth muscle cells isolated from the longitudinal muscle layer of guinea pig intestine. Specific binding of 125I-SP and 125I-SK was rapid, saturable, reversible, and temperature dependent. Binding attained 63-70% of steady-state binding within 1 min, coincidentally with the time of optimal contraction. The order of potency with which mammalian tachykinins and the SP antagonist, [D-Pro2, D-Trp7,9]SP, inhibited the binding of both radioligands was identical: SP greater than SK greater than NK greater than [D-Pro2, D-Trp7,9]SP, implying preferential interaction with a site that had highest affinity for SP. SK was 2-3 times, NK 3-4 times, and [D-Pro2, D-Trp7,9]SP 7-23 times less potent than SP (IC50 0.36 nM). Except for NK, the order of potency was similar to that for contraction of isolated muscle cells. The existence of binding sites with even higher affinity was suggested by the ability of muscle cells to contract in response to concentrations as low as 10(-13) M. These binding sites were not detectable at the concentration of radioligands used. It was concluded that a SP receptor is the only tachykinin receptor subtype present on intestinal muscle cells of the guinea pig.

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