CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.

Previous studies have shown that chemotactic factor stromal-cell derived factor 1α (SDF1α) promotes cell recovery from hypoxic injury via its main receptor C-X-C chemokine receptor type (CXCR) 4. However, the role of its new receptor CXCR7 on cell repair against hypoxia and cell response to SDF1α re...

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Autores principales:	Sufang Liu, Xiaofeng Jia, Changsheng Li, Xuefei Han, Wenhai Yan, Ying Xing
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2252925ba6134f19b3a4f0c4481fe2b2
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spelling	oai:doaj.org-article:2252925ba6134f19b3a4f0c4481fe2b22021-11-18T07:59:11ZCXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.1932-620310.1371/journal.pone.0055290https://doaj.org/article/2252925ba6134f19b3a4f0c4481fe2b22013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23383139/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Previous studies have shown that chemotactic factor stromal-cell derived factor 1α (SDF1α) promotes cell recovery from hypoxic injury via its main receptor C-X-C chemokine receptor type (CXCR) 4. However, the role of its new receptor CXCR7 on cell repair against hypoxia and cell response to SDF1α remains largely unknown. In this study, neurons induced from hippocampal progenitor cells were pre-conditioned in hypoxia for 4 h and subsequently monitored to investigate the function of SDF1α on cell repair after hypoxia. Neurons were assessed for their cell morphology, actin filament polymerization and migration capability. SDF1α protein levels increased significantly 1 h after hypoxia compared to control (P<0.01), and it reached a peak at 24 h after hypoxia. Moreover, addition of SDF1α promoted neurite outgrowth and actin filament polymerization both in normoxic and hypoxic cells compared to untreated cells. Cell migration showed a time-dependent increase with SDF1α stimulation in both groups, and hypoxic cells illustrated a significant augment at 0.5 h, 1 h and 12 h after SDF1α application compared to normoxic cells (P<0.01). CXCR7 expression also increased with time dependence after hypoxia and demonstrated a two-fold upregulation compared to control at 24 h after hypoxia. With CXCR7 silencing, axon elongation and actin filament polymerization induced by SDF1α were inhibited sharply both in normoxic and hypoxic cells. CXCR7 silencing also leads to reduced hypoxic cell migration at 0.5 h, 1 h, 12 h, 24 h and 36 h after SDF1α application (P<0.01), but it failed to reduce normoxic cell migration induced by SDF1α at 0.5 h, 1 h and 12 h (P>0.05). 24 h SDF1α stimulation led to higher ERK1/2 phosphorylation compared to control, and ERK1/2 phosphorylation increased more in hypoxic cells than that in normoxic cells. This study suggested that CXCR7 plays an important role on cell repair processing induced by SDF1α, and CXCR7 silencing attenuates cell adaptive response to acute SDF1α stimulation (≤12 h) after hypoxia.Sufang LiuXiaofeng JiaChangsheng LiXuefei HanWenhai YanYing XingPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 1, p e55290 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sufang Liu Xiaofeng Jia Changsheng Li Xuefei Han Wenhai Yan Ying Xing CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
description	Previous studies have shown that chemotactic factor stromal-cell derived factor 1α (SDF1α) promotes cell recovery from hypoxic injury via its main receptor C-X-C chemokine receptor type (CXCR) 4. However, the role of its new receptor CXCR7 on cell repair against hypoxia and cell response to SDF1α remains largely unknown. In this study, neurons induced from hippocampal progenitor cells were pre-conditioned in hypoxia for 4 h and subsequently monitored to investigate the function of SDF1α on cell repair after hypoxia. Neurons were assessed for their cell morphology, actin filament polymerization and migration capability. SDF1α protein levels increased significantly 1 h after hypoxia compared to control (P<0.01), and it reached a peak at 24 h after hypoxia. Moreover, addition of SDF1α promoted neurite outgrowth and actin filament polymerization both in normoxic and hypoxic cells compared to untreated cells. Cell migration showed a time-dependent increase with SDF1α stimulation in both groups, and hypoxic cells illustrated a significant augment at 0.5 h, 1 h and 12 h after SDF1α application compared to normoxic cells (P<0.01). CXCR7 expression also increased with time dependence after hypoxia and demonstrated a two-fold upregulation compared to control at 24 h after hypoxia. With CXCR7 silencing, axon elongation and actin filament polymerization induced by SDF1α were inhibited sharply both in normoxic and hypoxic cells. CXCR7 silencing also leads to reduced hypoxic cell migration at 0.5 h, 1 h, 12 h, 24 h and 36 h after SDF1α application (P<0.01), but it failed to reduce normoxic cell migration induced by SDF1α at 0.5 h, 1 h and 12 h (P>0.05). 24 h SDF1α stimulation led to higher ERK1/2 phosphorylation compared to control, and ERK1/2 phosphorylation increased more in hypoxic cells than that in normoxic cells. This study suggested that CXCR7 plays an important role on cell repair processing induced by SDF1α, and CXCR7 silencing attenuates cell adaptive response to acute SDF1α stimulation (≤12 h) after hypoxia.
format	article
author	Sufang Liu Xiaofeng Jia Changsheng Li Xuefei Han Wenhai Yan Ying Xing
author_facet	Sufang Liu Xiaofeng Jia Changsheng Li Xuefei Han Wenhai Yan Ying Xing
author_sort	Sufang Liu
title	CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
title_short	CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
title_full	CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
title_fullStr	CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
title_full_unstemmed	CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
title_sort	cxcr7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/2252925ba6134f19b3a4f0c4481fe2b2
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_version_	1718422653204692992

CXCR7 silencing attenuates cell adaptive response to stromal cell derived factor 1α after hypoxia.

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