Enhanced vascularization of PCL porous scaffolds through VEGF-Fc modification

2018 ◽  
Vol 6 (27) ◽  
pp. 4474-4485 ◽  
Author(s):  
Ke Xu ◽  
Chuanshun Zhu ◽  
Jinghui Xie ◽  
Xiaoning Li ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Porous Scaffolds ◽  
Mapk Pathways ◽  
And Migration ◽  
Huvec Proliferation ◽  
Proliferation And Migration

VEGF-Fc interface improves the vascularization of PCL scaffolds by enhancing HUVEC proliferation and migration through activating VEGFR/Pi3k and VEGFR/MAPK pathways.

scholarly journals High shear stress suppresses proliferation and migration but promotes apoptosis of endothelial cells co-cultured with vascular smooth muscle cells via down-regulating MAPK pathway

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Qiang Ji ◽  
Yu Lin Wang ◽  
Li Min Xia ◽  
Ye Yang ◽  
Chun Sheng Wang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Culture System ◽  
Stress Condition ◽  
Mapk Pathway ◽  
High Shear ◽  
High Shear Stress ◽  
Cellular Processes ◽  
Mapk Pathways ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Early neointimal hyperplasia of vein graft may be ameliorated via enhancing intravenous surface shear stress. Cellular processes including proliferation, apoptosis and migration of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) may play very important roles in the process of neointimal hyperplasia of vein graft; and mitogen-activated protein kinase (MAPK) pathways including extracellular signal-regulated kinase (ERK1/2) and p38 pathways play vital roles in regulating a large variety of cellular processes. This study evaluated the impacts of shear stress and MAPK pathways on cellular processes of ECs in a co-culture system with VSMCs, and aimed to test the hypothesis that high shear stress suppresses proliferation and migration but promotes apoptosis of ECs co-cultured with VSMCs via down-regulating MAPK pathway. Methods Primary ECs and VSMCs derived from porcine great saphenous vein were collected, respectively. 4–7 generation of cells were used as work cells. ECs and VSMCs were co-cultured and synchronized under high and low shear stress using Parallel-Plate Flow Chamber system. And then, ECs co-cultured with VSMCs were incubated with U0126 (ERK1/2 inhibitor) or PD98059 (p38 inhibitor) under different shear stress. Proliferation, apoptosis and migration of ECs in a co-culture system with VSMCs were detected by 4,5-dimethyl-2-thiazolyl (MTT) assay and bromodeoxyuridine (BrdU) assay, fluorescent-activated cell sorting (FACS) technique, and Transwell assay separately. Each test repeated 3 times. Additionally, protein expressions of ERK1/2 and p38 MAPK were detected by using Western blot, respectively. Results Under higher level of shear stress condition, proliferation and migration of ECs co-cultured with VSMCs were suppressed, while cell apoptosis was promoted. And blocking ERK1/2 pathway by U0126 or blocking p38 pathway by PD98059, proliferation and migration of ECs co-cultured with VSMCs were further suppressed, while cell apoptosis was further promoted. Additionally, protein expressions of phosphorylation of ERK1/2 and p38MAPK were decreased under higher level of shear stress condition, and were further reduced by blocking ERK1/2 or p38 pathway under shear stress condition. Conclusions High shear stress may suppress proliferation and apoptosis of ECs in a co-culture system with VSMCs but promote cell migration via down-regulating ERK1/2 and p38 MAPK pathways.

Long non-coding RNA BANCR promotes proliferation and migration of lung carcinoma via MAPK pathways

2015 ◽  
Vol 69 ◽  
pp. 90-95 ◽  
Author(s):  
Wenjun Jiang ◽  
Dandan Zhang ◽  
Baoning Xu ◽  
Zhuo Wu ◽  
Siyang Liu ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Mapk Pathways ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Modulation of Vascular Human Endothelial and Rat Smooth Muscle Cell Growth by a Fucosylated Chondroitin Sulfate from Echinoderm

2000 ◽  
Vol 84 (08) ◽  
pp. 332-337 ◽  
Author(s):  
B. Drouet ◽  
S. Matou ◽  
P. A. S. Mourão ◽  
A. Bros ◽  
D. Letourneur ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Smooth Muscle Cell ◽  
Chondroitin Sulfate ◽  
Glucuronic Acid ◽  
Antithrombotic Agent ◽  
Enhancing Effect ◽  
And Migration ◽  
Huvec Proliferation ◽  
Proliferation And Migration

SummaryFucosylated chondroitin sulfate is a glycosaminoglycan extracted from the sea cucumber Ludwigothurea grisea. This polysaccharide has the same structure as a mammalian chondroitin sulfate but some of the glucuronic acid residues display sulfated fucose branches. Anticoagulant and antithrombotic properties of fucosylated chondroitin sulfate have already been described. In order to further investigate its potential therapeutic use as an antithrombotic agent, we studied its effect on vascular smooth muscle cell (SMC) proliferation and endothelial cell proliferation, migration and Tissue Factor Pathway Inhibitor (TFPI) release. The experiments were performed on SMC from rat thoracic aorta and on human umbilical vein endothelial cell (HUVEC) in culture with or without added fibroblast growth factors (FGF-1 and FGF-2). Our results showed that: (i) fucosylated chondroitin sulfate had a strong inhibitory effect on SMC proliferation (IC50 =10 ± 5 µg/ml) and (ii) no effect on HUVEC proliferation and migration assays, in the absence of exogenous FGF, while heparin had inhibitory effects; (iii) fucosylated chondroitin sulfate (10 µg/ml) enhanced FGF-1 and FGF-2 induced HUVEC proliferation by 45% (145.4 ± 7.2%) and 27% (126.9 ± 4.2%), respectively; (iv) on FGF-induced HUVEC migration, fucosylated chondroitin sulfate (10 µg/ml) had a strong enhancing effect with FGF-1, +122% (222.2 ± 15.8%), three times higher than that of heparin, and a lower enhancing effect with FGF-2, +43% (142.7 ± 4.6%), whereas heparin had no effect; (v) fucosylated chondroitin sulfate stimulated TFPI release, mainly on the free form, +98% (198.2 ± 25.%). In addition, the structural features of the polysaccharide associated with its biological activity were resolved using chemically modified fucosylated chondroitin sulfates. Sulfated fucose branches groups are essential to the potentiating effect of the polysaccharide on HUVEC proliferation and migration. Surprisingly, removal of fucose branches from the fucosylated chondroitin sulfate did not abolish TFPI release. Finally, partial reduction of the glucuronic acid carboxyl groups limited the potentiating effect on HUVEC proliferation and migration but did not affect TFPI release. In conclusion, this fucosylated chondroitin sulfate from invertebrate origin reveals useful properties for an antithrombotic agent: inhibition of SMC proliferation, enhancement of endothelium wound repair and TFPI release. These properties on vascular cells, associated with a low bleeding tendency and an antithrombotic activity, strongly suggest its potential use as a new therapeutic agent in arterial thrombosis and restenosis, with a more favorable effect than heparin.

scholarly journals S100A6 stimulates proliferation and migration of colorectal carcinoma cells through activation of the MAPK pathways

2013 ◽  
Vol 44 (3) ◽  
pp. 781-790 ◽  
Author(s):  
LIANG DUAN ◽  
RUI WU ◽  
ZHENGYU ZOU ◽  
HAIYAN WANG ◽  
LIWEI YE ◽  
...  
Keyword(s):  
Colorectal Carcinoma ◽  
Carcinoma Cells ◽  
Mapk Pathways ◽  
And Migration ◽  
Proliferation And Migration

Role of microenvironment on proliferation and migration of an SDHB silenced murine Pheochromocytoma cell line

2017 ◽  
Author(s):  
Serena Martinelli ◽  
Vanessa D'Antongiovanni ◽  
Susan Richter ◽  
Letizia Canu ◽  
Tonino Ercolino ◽  
...  
Keyword(s):  
Cell Line ◽  
Pheochromocytoma Cell ◽  
And Migration ◽  
Proliferation And Migration

ARFGAP3 an androgen target gene promotes prostate cancer cell proliferation and migration.

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Biology ◽  
Adaptor Protein ◽  
Cancer Cell Proliferation ◽  
Lncap Cells ◽  
Gtpase Activating Protein ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

ADP ribosylation factor GTPase-activating protein 3 (ARFGAP3) is a GTPase-activating protein that associates with the Golgiapparatus and regulates the vesicular trafficking pathway. In the present study, we examined the contribution of ARFGAP3 toprostate cancer cell biology. We showed that ARFGAP3 expression was induced by 100 nM of dihydrotestosterone (DHT) atboth the mRNA and protein levels in androgen-sensitive LNCaP cells. We generated stable transfectants of LNCaP cells withFLAG-tagged ARFGAP3 or a control empty vector and showed that ARFGAP3 overexpression promoted cell proliferation andmigration compared with control cells. We found that ARFGAP3 interacted with paxillin, a focal adhesion adaptor protein thatis important for cell mobility and migration. Small interfering RNA (siRNA)-mediated knockdown of ARFGAP3 showed thatARFGAP3 siRNA markedly reduced LNCaP cell growth. Androgen receptor (AR)-dependent transactivation activity on prostatespecificantigen (PSA) enhancer was synergistically promoted by exogenous ARFGAP3 and paxillin expression, as shown byluciferase assay in LNCaP cells. Thus, our results suggest that ARFGAP3 is a novel androgen-regulated gene that can promoteprostate cancer cell proliferation and migration in collaboration with paxillin.

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