scholarly journals The effect of the geometry of the proximal anastomosis, markers of apoptosis and cell proliferation on the long-term patency following reconstructive interventions on the femoropopliteal arterial segment

2021 ◽  
Vol 102 (6) ◽  
pp. 855-861
Author(s):  
R Y Kalinin ◽  
I A Suсhkov ◽  
E A Klimentova ◽  
I N Shanaev
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Femoral Artery ◽  
Neointimal Hyperplasia ◽  
Platelet Derived Growth Factor ◽  
Soluble Form ◽  
Deep Femoral Artery ◽  
Arterial Segment ◽  
Group A ◽  
Group B

Aim. To study changes in the topography of the orifice of the deep femoral artery (DFA), markers of proliferation, and apoptosis in patients after open interventions on the femoropopliteal arterial segment. Methods. The study included 35 patients with atherosclerotic peripheral arterial disease (PAD), femoral-popliteal occlusion, stage IIBIII of the disease according to the classification of A.V. PokrovskyFontaine, who underwent open surgery. The average age of the patients was 694.6 years. These patients included 26 men. Patients were divided into two groups: group A included 18 patients who underwent femoral-popliteal prosthetics (distal End-To-End bypass anastomoses), group B included 17 patients with femoral-popliteal bypass surgery (distal End-To-Side bypass anastomoses). The groups were comparable in terms of age and disease severity (p 0.05). Determination of serum platelet-derived growth factor BB (PDGF BB) and soluble form Fas (sFas) levels was carried out immediately before the intervention, on the 1st, 7th days, and 1 month after the operation. Duplex scanning (DS) was performed on day 7, after 1 and 18 months. Statistica 10.0 software was used for statistical data processing. The significance of differences between unrelated samples was assessed using the Student's t-test. The correlations between variables were analyzed by using Pearson's method. Results. On 1st day, there was a decrease in soluble Fas in patients of group A compared with group B (0.41 ng/ml vs 0.78 ng/ml, p=0.01). On the 7th day, the levels of serum platelet-derived growth factor BB were increased in patients of group A compared with group B (35.2 ng/ml vs 23.2 ng/ml, p=0.00001). After 1 month, the level of serum platelet-derived growth factor BB in patients of group A remained elevated compared with those in patients of group B (22.8 ng/ml vs 14.4 ng/ml, p=0.0003). Conclusion. Femoropopliteal prosthetics leads to a change in branching angle of the deep femoral artery up to 7080%, accompanied by changing dynamics of apoptotic markers and cell proliferation, leading to an increase in the thickness of neointimal hyperplasia and the progression of atherosclerosis.

Inhibitory effect of adenosine on intimal hyperplasia and proliferation of smooth muscle cells in a carotid arterial anastomosis animal model

Vascular ◽  
2014 ◽  
Vol 23 (2) ◽  
pp. 124-131 ◽  
Author(s):  
Gokhan Albayrak ◽  
Erdem Silistreli ◽  
Bekir Ergur ◽  
Sule Kalkan ◽  
Ozalp Karabay ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Neointimal Hyperplasia ◽  
Inhibitory Effect ◽  
Endothelial Cell Proliferation ◽  
Positive Staining ◽  
Significant Difference ◽  
Group A ◽  
Group B

Purpose The effect of adenosine (9-β-0-ribifuranosyladenine) on the endothelial cell proliferation and neointimal hyperplasia is investigated in the rabbit carotid artery anastomosis model. Methods Twenty-eight New Zealand white rabbits were arranged in four groups of seven animals each. The right carotid arteries of each animal were transsected and re-anastomosed. The left sides remained as control. In Group A, no medication was used. In Group B, subcutaneous Adenosine was applied for 3 days. In Group C, the same dose was applied for 7 days, and in Group D for 21 days. After 28 days, the luminal diameters, luminal areas, intima/media ratios were all measured by using histopathological evaluation. Findings The mean luminal diameters and areas of the four groups were smaller than the control ones. Massive thickening of smooth muscle cell proliferation and dense intensifying in the connecting tissues were observed most prominently in Group A, in decreasing degrees within other groups. Intima/media ratio was highest in Group A. Scoring the quantity of e-NOS positive staining also revealed a significant difference between the experimental groups and their control associates. Conclusion The process of endothelial cell proliferation and neointimal hyperplasia can be significantly reduced by the use of adenosine.

scholarly journals Heparin-binding epidermal growth factor inhibits apoptosis in cisplatin-resistant pancreatic cancer cells via upregulation of EGFR and ERCC 1 expressions

2021 ◽  
Vol 18 (6) ◽  
pp. 1167-1171
Author(s):  
Lingyang Zhou ◽  
Yuming Wang ◽  
Shenghong Lan ◽  
Mingfu Hu ◽  
Lipeng Lu
Keyword(s):  
Pancreatic Cancer ◽  
Cell Proliferation ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cancer Cells ◽  
Heparin Binding ◽  
Pancreatic Cancer Cells ◽  
Group A ◽  
Epidermal Growth ◽  
Group B

Purpose: To investigate the influence of heparin-binding epidermal growth factor (HB-EGF) on apoptosis in cisplatin-resistant pancreatic cancer cells, as well as its mechanism of action. Methods: Pancreatic cancer cisplatin-resistant cells (BXPC-3/CDDP) were transfected with HB-EGF small interfering RNA (siRNA). The cells were randomly assigned to four groups, namely, BXPC-3 group (group A), BXPC-3/CDDP group (group B), transfected group A (group Asi) and transfected group B (group Bsi). Cell proliferation was determined using MTT assay, and the levels of expression of HBEGF, epidermal growth factor receptor (EGFR) and excision repair cross-complementation group 1 (ERCC 1) were determined using Western blotting. The extent of apoptosis was determined by flow cytometry. Results: Cell proliferation was increased in group B, relative to group A, but was significantly decreased after transfection with HB-EGF siRNA (p < 0.05). The half-maximal inhibitory concentration (IC50) of group Bsi was reduced, relative to group Asi (p < 0.05). The expression of HB-EGF was significantly upregulated in group B, relative to group A (p < 0.05). In contrast, HB-EGF siRNA transfection of the cells significantly down-regulated HB-EGF expression (p < 0.05). Early apoptosis was significantly higher in group A than in groups B and Bsi. Higher levels of apoptosis were seen in group Bsi, relative to group B after inhibition of HB-EGF expression (p < 0.05). Conclusion: These results indicate that HB-EGF is resistant to cisplatin, and it inhibits apoptosis in pancreatic cancer cells via the upregulation of EGFR and ERCC 1 expressions.

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.

Sign in / Sign up

Export Citation Format

Share Document