scholarly journals The level of markers of apoptosis and cell proliferation in the area of restenosis after lower extremity arterial reconstruction

2021 ◽  
Vol 102 (4) ◽  
pp. 453-458
Author(s):  
R E Kalinin ◽  
I A Suchkov ◽  
E A Klimentova ◽  
A V Shchulkin ◽  
A A Gerasimov ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
P53 Protein ◽  
Lower Extremities ◽  
Platelet Derived Growth Factor ◽  
Femoropopliteal Bypass ◽  
Arterial Reconstruction ◽  
Arteriosclerosis Obliterans ◽  
Spearman Test ◽  
Control Samples

Aim. To assess the number of markers of apoptosis and cell proliferation, as well as their relationships in the area of restenosis of arterial reconstructions. Methods. The study included 14 patients with a diagnosis of arteriosclerosis obliterans of the lower extremities. Post-thrombotic occlusion of femoropopliteal bypass. All patients were males with stage III disease according to the Fontaine classification modified by A.V. Pokrovsky. The average age of the patients was 653.4 years. The mean disease duration was 92.5 months after the initial intervention. Intraoperative material distal anastomosis of femoropopliteal bypass was taken from patients during arterial reconstructions. As a control, we used arterial wall samples obtained at organ procurement from postmortem donors without arteriosclerosis obliterans of the lower extremities. The number of samples is 8. The site of their collection is the popliteal artery. After sampling, they were crushed, and a homogenate was prepared, followed by the determination of the amount of p53, PDGF BB, Bcl2, and Bax proteins using the enzyme immunoassay. Statistical analysis was performed using the Statistica 10.0 software. Group differences were assessed by using the MannWhitney test. Correlation coefficients were determined using the Spearman test. Data are presented as medians and interquartile ranges. Results. In tissue samples of restenosis, the amount of p53 protein was 0.07 units/mg and was significantly reduced compared with the control samples 0.14 units/mg (р=0,015). The amount of platelet-derived growth factor PDGF BB was 0.17 ng/mg (р=0.05), Bcl2 1.61 ng/mg (р=0.008), Bax 6.0 ng/mg (р=0.25) in the restenosis area and was increased in comparison with the control samples (0.04 ng/mg, 0.9 ng/mg, 4.4 ng/mg, respectively). A relationship between p53 and platelet-derived growth factor BB (r=0.724, p=0.002), platelet-derived growth factor BB and Bcl2 (r=0.672, p=0.003) was revealed in samples from restenosis tissue obtained during arterial reconstructions. Conclusion. The decreased apoptosis, expressed in a low level of p53 protein, with an increased Bax/Bcl-2 ratio is associated with an increase in the proliferative response of vascular wall cells in the area of restenosis of arterial reconstruction.

Suppression of Mesangial-Cell Proliferation by Trapidil in Glomerulonephritis Induced by Anti-Thymocyte Serum in Rats

1995 ◽  
Vol 23 (6) ◽  
pp. 458-466 ◽  
Author(s):  
M S Razzaque ◽  
M Cheng ◽  
T Taguchi
Keyword(s):  
Cell Proliferation ◽  
Body Weight ◽  
Single Dose ◽  
Growth Factor ◽  
Mesangial Cell ◽  
Platelet Derived Growth Factor ◽  
Group Iii ◽  
Group I ◽  
Mesangial Cell Proliferation ◽  
Group Ii

Trapadil (Mochida Pharmaceuticals, Japan), an antiplatelet drug, suppresses the growth of several cell types and is thought to antagonize platelet-derived growth factor. The effects of trapidil on mesangial-cell proliferation in glomerulonephritis induced by anti-thymocyte serum in Wistar rats were investigated. Control rats were treated with phosphate-buffered saline (group I); group II rats were injected with a single dose of anti-thymocyte serum (8 ml/kg body weight), and group III rats were treated with both a single dose of anti-thymocyte serum (8 ml/kg body weight) and with trapidil (5 mg/kg body weight/day). Three rats in each group were killed on day 3, and the other three on day 10. Control rats showed no significant histological changes on day 3 or day 10. In group II, on day 3, there was a marked decrease in glomerular cell numbers, with mesangiolysis. Histologically severe mesangial-cell proliferation with expansion of mesangial areas was noted on day 10. None of the rats in group III showed mesangial alterations, histologically, indicating that mesangial-cell proliferation was suppressed by trapidil. This suppression may result from antagonism of the binding of platelet derived growth factor to the specific surface receptors in the mesangial cells. Trapidil may have clinical value in the treatment of mesangial-cell proliferative glomerular diseases.

scholarly journals EXPRESS: Ubiquitin‑specific protease 7 mediates platelet derived growth factor-induced pulmonary arterial smooth muscle cells proliferation

2021 ◽  
pp. 204589402110461
Author(s):  
Yanting Zhu ◽  
Qianqian Zhang ◽  
Xin Yan ◽  
Lu Liu ◽  
Cui Zhai ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Platelet Derived Growth Factor ◽  
Specific Protease ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells ◽  
Pulmonary Arterial Smooth Muscle

Pulmonary arterial hypertension (PAH) is a devastating pulmonary vascular disease, in which the pathogenesis is complicated and unclear. Pulmonary arterial smooth muscle cells (PASMCs) proliferation is a key pathological feature of PAH. It has been shown that ubiquitin-specific protease 7 (USP7) is involved in cancer cell proliferation via deubiquitinating and stabilizing E3 ubiquitin ligase mouse double minute 2 (MDM2). However, the effect of USP7 and MDM2 on platelet derived growth factor (PDGF) -induced PASMCs proliferation is uncertain. This study aims to explore this issue. Our results indicated that PDGF up-regulated USP7 protein expression and stimulated PASMCs proliferation; this was accompanied with the increase of MDM2, forkhead box O4 (FoxO4) reduction and elevation of CyclinD1. While prior transfection of USP7 siRNA blocked PDGF-induced MDM2 up-regulation, FoxO4 down-regulation, increase of CyclinD1 and cell proliferation. Pre-depletion of MDM2 by siRNA transfection reversed PDGF-induced reduction of FoxO4, up-regulation of CyclinD1 and PASMCs proliferation. Furthermore, pre-treatment of cells with proteasome inhibitor MG-132 also abolished PDGF-induced FoxO4 reduction, CyclinD1 elevation and cell proliferation. Our study suggests that USP7 up-regulates MDM2, which facilitates FoxO4 ubiquitinated degradation, and subsequently increases the expression of CyclinD1 to mediate PDGF-induced PASMCs proliferation.

scholarly journals Cbl-mediated Negative Regulation of Platelet-derived Growth Factor Receptor-dependent Cell Proliferation

1999 ◽  
Vol 274 (23) ◽  
pp. 16619-16628 ◽  
Author(s):  
Sachiko Miyake ◽  
Karen P. Mullane-Robinson ◽  
Nancy L. Lill ◽  
Patrice Douillard ◽  
Hamid Band
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Negative Regulation ◽  
Platelet Derived Growth Factor ◽  
Dependent Cell

scholarly journals Evidence for glutathione involvement in platelet-derived growth-factor-mediated signal transduction

1997 ◽  
Vol 324 (3) ◽  
pp. 791-796 ◽  
Author(s):  
Stefania RIGACCI ◽  
Teresa IANTOMASI ◽  
Patrizia MARRACCINI ◽  
Andrea BERTI ◽  
Maria Teresa VINCENZINI ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Growth Factor Receptor ◽  
Receptor Activation ◽  
Platelet Derived Growth Factor ◽  
Glutathione Depletion ◽  
Physiological Processes ◽  
Buthionine Sulphoximine ◽  
Precise Relationship

Recent studies show that glutathione, while being involved in the well-known physiological processes of amino acid transport and detoxification, can also play a part in cell proliferation events. Cell treatment with l-buthionine sulphoximine, which causes glutathione depletion, is accompanied by a decrease in cell proliferation. At present no precise relationship between this thiol and any critical intermediate of the mitogenic cascade has been proved. In this study, conducted on NIH/3T3 murine fibroblasts, we demonstrate a strict correlation between glutathione levels and platelet-derived growth-factor-receptor activation in response to stimulation and cell proliferation. The receptor autophosphorylation is severely impaired at low glutathione cellular levels. The interaction of glutathione with this growth-factor receptor in vivo, while being rather specific, is complex and may involve both cytosolic and extracellular receptor domains.

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