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|a (NLM)22336354
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a chi
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|a Li, Gang
|e verfasserin
|4 aut
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|a Integrin β3 pathway mediated connective tissue growth factor-induced proliferation, migration and extracellular matrix deposition of pulmonary arterial smooth muscle cells
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|c 2011
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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|a Band
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|2 rdacarrier
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|a Date Completed 08.04.2013
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|a Date Revised 07.06.2016
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|a published: Print
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|a Citation Status MEDLINE
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|a OBJECTIVE: To explore the effects of integrin β3 pathway on the proliferation, migration and extracellular matrix deposition of pulmonary arterial smooth muscle cells (PASMCs) induced by connective tissue growth factor (CTGF)
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|a METHODS: PASMCs of SD Rats were cultured in M199 culture system in vitro and the 3rd-7th passages of PASMCs were used in the experiments. The cells were randomly divided into three groups: (1) CONTROL GROUP: culture system contained no any stimulation factor; (2) CTGF group: culture system was added into 50 ng/ml CTGF; (3) CTGF+ anti-integrin β3 antibody group:culture system was added with 50 ng/ml CTGF and 10 mg/L anti-integrin β3 antibody. The PASMCs were cultured with 50 ng/ml CTGF and anti-integrin β3 antibody (0, 5, 10, 15, 20 mg/L) for 24, 48, 72 and 96 h, the proliferation of PASMCs was detected by WST-1 Cell Proliferation Assay Kit. The migration of PASMCs was observed by Transwell cell test under the phase contrast microscope. RT-PCR assay was applied to detect the mRNA expression of collagenI-α1, collagen III-α1 and fibronectin-1 gene of PASMCs. The expression of fibronectin protein was examined by Western blotting and immunohistochemistry
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|a RESULTS: The results of WST-1 test showed that the anti-integrin β3 antibody inhibited significantly the proliferation of PASMCs induced by CTGF (P < 0.05), among which the inhibition rate of anti-integrin β3 antibody (10 mg/L) was the most significant. Transwell test results showed that CTGF group of PASMCs migration numbers (25 ± 1.57) were higher than that of the control group (11 ± 2.08, P < 0.01); PASMCs migration numbers of CTGF+ integrin β3 antibody group (17 ± 4.16) were less than that of the CTGF group (P < 0.05). Compared with the control group, the mRNA expression of collagen typeI-α1 (4.28 ± 0.33), collagen typeIII-α1 (4.41 ± 0.35), fibronectin-1 (4.05 ± 0.33) of PASMCs was increased in CTGF group, with a time-dependence (P < 0.01); Compared with the CTGF group, the mRNA expression of collagen typeI-α1 (3.38 ± 0.30), collagen typeIII-α1 (3.40 ± 0.30), fibronectin-1 (3.12 ± 0.29) of PASMCs was reduced in CTGF+ anti-integrin β3 antibody group (P < 0.05), which was higher than that of the control group (P < 0.05); Western blot and immunohistochemical tests showed that compared with the control group, CTGF group could stimulate the expression of fibronectin protein of PASMCs (P < 0.01); the anti-integrin β3 antibody could inhibit the expression of fibronectin protein induced by CTGF(P < 0.01), which was more remarkable than that in the control group (P < 0.01)
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|a CONCLUSION: Integrin β3 pathway can mediate CTGF-induced proliferation, migration and extracellular matrix deposition of PASMCs, CTGF-integrin β3 signaling pathway may play an important role in pulmonary vascular remodeling
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|a English Abstract
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|a Journal Article
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|a Research Support, U.S. Gov't, Non-P.H.S.
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|a Integrin beta3
|2 NLM
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|a Connective Tissue Growth Factor
|2 NLM
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|a 139568-91-5
|2 NLM
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1 |
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|a Hu, Yu
|e verfasserin
|4 aut
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|a Jia, Peng
|e verfasserin
|4 aut
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|a Fu, Jie
|e verfasserin
|4 aut
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|a Lu, Cui-xia
|e verfasserin
|4 aut
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|a Sun, Yu-qin
|e verfasserin
|4 aut
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|a Liu, Bin
|e verfasserin
|4 aut
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773 |
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|i Enthalten in
|t Zhonghua er ke za zhi = Chinese journal of pediatrics
|d 1960
|g 49(2011), 12 vom: 15. Dez., Seite 895-900
|w (DE-627)NLM136249191
|x 0578-1310
|7 nnns
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|g volume:49
|g year:2011
|g number:12
|g day:15
|g month:12
|g pages:895-900
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|d 49
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