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Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia

Ischemic diseases represent a challenging worldwide health burden. The current study investigated the therapeutic potential of genetically modified human placenta-derived mesenchymal stem cells (hPDMSCs) with basic fibroblast growth factor (FGF2) and platelet-derived growth factor-BB (PDGF-BB) genes...

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Autores principales: YIN, TAO, HE, SISI, SU, CHAO, CHEN, XIANCHENG, ZHANG, DONGMEI, WAN, YANG, YE, TINGHONG, SHEN, GUOBO, WANG, YONGSHENG, SHI, HUASHAN, YANG, LI, WEI, YUQUAN
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4581748/
https://www.ncbi.nlm.nih.gov/pubmed/26239842
http://dx.doi.org/10.3892/mmr.2015.4089
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author YIN, TAO
HE, SISI
SU, CHAO
CHEN, XIANCHENG
ZHANG, DONGMEI
WAN, YANG
YE, TINGHONG
SHEN, GUOBO
WANG, YONGSHENG
SHI, HUASHAN
YANG, LI
WEI, YUQUAN
author_facet YIN, TAO
HE, SISI
SU, CHAO
CHEN, XIANCHENG
ZHANG, DONGMEI
WAN, YANG
YE, TINGHONG
SHEN, GUOBO
WANG, YONGSHENG
SHI, HUASHAN
YANG, LI
WEI, YUQUAN
author_sort YIN, TAO
collection PubMed
description Ischemic diseases represent a challenging worldwide health burden. The current study investigated the therapeutic potential of genetically modified human placenta-derived mesenchymal stem cells (hPDMSCs) with basic fibroblast growth factor (FGF2) and platelet-derived growth factor-BB (PDGF-BB) genes in hindlimb ischemia. Mesenchymal stem cells obtained from human term placenta were transfected ex vivo with adenoviral bicistronic vectors carrying the FGF2 and PDGF-BB genes (Ad-F-P). Unilateral hindlimb ischemia was surgically induced by excision of the right femoral artery in New Zealand White rabbits. Ad-F-P genetically modified hPDMSCs, Ad-null (control vector)-modified hPDMSCs, unmodified hPDMSCs or media were intramuscularly implanted into the ischemic limbs 7 days subsequent to the induction of ischemia. Four weeks after cell therapy, angiographic analysis revealed significantly increased collateral vessel formation in the Ad-F-P-hPDMSC group compared with the control group. Histological examination revealed markedly increased capillary and arteriole density in the Ad-F-P-hPDMSC group. The xenografted hPDMSCs survived in the ischemic tissue for at least 4 weeks subsequent to cell therapy. The current study demonstrated that the combination of hPDMSC therapy with FGF2 and PDGF-BB gene therapy effectively induced collateral vessel formation and angiogenesis, suggesting a novel strategy for therapeutic angiogenesis.
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spelling pubmed-45817482015-11-30 Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia YIN, TAO HE, SISI SU, CHAO CHEN, XIANCHENG ZHANG, DONGMEI WAN, YANG YE, TINGHONG SHEN, GUOBO WANG, YONGSHENG SHI, HUASHAN YANG, LI WEI, YUQUAN Mol Med Rep Articles Ischemic diseases represent a challenging worldwide health burden. The current study investigated the therapeutic potential of genetically modified human placenta-derived mesenchymal stem cells (hPDMSCs) with basic fibroblast growth factor (FGF2) and platelet-derived growth factor-BB (PDGF-BB) genes in hindlimb ischemia. Mesenchymal stem cells obtained from human term placenta were transfected ex vivo with adenoviral bicistronic vectors carrying the FGF2 and PDGF-BB genes (Ad-F-P). Unilateral hindlimb ischemia was surgically induced by excision of the right femoral artery in New Zealand White rabbits. Ad-F-P genetically modified hPDMSCs, Ad-null (control vector)-modified hPDMSCs, unmodified hPDMSCs or media were intramuscularly implanted into the ischemic limbs 7 days subsequent to the induction of ischemia. Four weeks after cell therapy, angiographic analysis revealed significantly increased collateral vessel formation in the Ad-F-P-hPDMSC group compared with the control group. Histological examination revealed markedly increased capillary and arteriole density in the Ad-F-P-hPDMSC group. The xenografted hPDMSCs survived in the ischemic tissue for at least 4 weeks subsequent to cell therapy. The current study demonstrated that the combination of hPDMSC therapy with FGF2 and PDGF-BB gene therapy effectively induced collateral vessel formation and angiogenesis, suggesting a novel strategy for therapeutic angiogenesis. D.A. Spandidos 2015-10 2015-07-20 /pmc/articles/PMC4581748/ /pubmed/26239842 http://dx.doi.org/10.3892/mmr.2015.4089 Text en Copyright: © Yin. https://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the terms of a Creative Commons Attribution License
spellingShingle Articles
YIN, TAO
HE, SISI
SU, CHAO
CHEN, XIANCHENG
ZHANG, DONGMEI
WAN, YANG
YE, TINGHONG
SHEN, GUOBO
WANG, YONGSHENG
SHI, HUASHAN
YANG, LI
WEI, YUQUAN
Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia
title Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia
title_full Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia
title_fullStr Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia
title_full_unstemmed Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia
title_short Genetically modified human placenta-derived mesenchymal stem cells with FGF-2 and PDGF-BB enhance neovascularization in a model of hindlimb ischemia
title_sort genetically modified human placenta-derived mesenchymal stem cells with fgf-2 and pdgf-bb enhance neovascularization in a model of hindlimb ischemia
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4581748/
https://www.ncbi.nlm.nih.gov/pubmed/26239842
http://dx.doi.org/10.3892/mmr.2015.4089
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