Stromal Cell-Derived Factor-1 Enhances Wound Healing through Recruiting Bone Marrow-Derived Mesenchymal Stem Cells to the Wound Area and Promoting Neovascularization

Xu, Xiang; Zhu, Fangqiang; Zhang, Meng; Deng-fen, Zeng; Luo, Dong-Hua; Liu, Guodong; Cui, Wenhui; Wang, Shali; Guo, Wei; Xing, Wei; Liang, Huaping; Li, Lei; Fu, Xiaobing; Jiang, Jianxin; Huang, Hong

doi:10.1159/000342921

Cited by 112 publications

(104 citation statements)

References 57 publications

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“…In the following sections as well as in Supplemental Table S1, we highlight several inflammatory factors that influence chronic fibrosis and tumor progression because of their effects on cellular plasticity related to the WHFC triad. Please note that many of these factors have also been reviewed elsewhere for their effects in regulating the plasticity of mesenchymal stem cells (343,397,406).…”

Section: Chronic Inflammation Is a Driver Of The Whfc Triadmentioning

confidence: 99%

The wound healing, chronic fibrosis, and cancer progression triad

Rybinski

Franco‐Barraza

Cukierman

2014

Physiological Genomics

198

169

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For decades tumors have been recognized as “wounds that do not heal.” Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct signaling pathways, also fuel chronic fibrosis and tumor progression. Hence, here we review the relationship between fibrosis and cancer through the lens of wound healing.

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Section: Chronic Inflammation Is a Driver Of The Whfc Triadmentioning

confidence: 99%

The wound healing, chronic fibrosis, and cancer progression triad

Rybinski

Franco‐Barraza

Cukierman

2014

Physiological Genomics

198

169

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“…Almost all of these studies have shown upregulation of CXCL12, in some form, in and around the site of injury. Some examples of injury include skin burns Xu et al, 2013;Yang et al, 2013), brain lesions (Wang et al, 2008b) and skeletal fracture injury (Kitaori et al, 2009). In one of these studies, CXCL12 production reached peak levels at day 7 post injury (Hu et al), whilst in another, the chemokine displayed bimodal upregulation, with levels peaking at day 1 and then again at day 5 post wounding .…”

Section: Mechanisms Of Msc and Pericyte Recruitment To Sites Of Injurymentioning

confidence: 99%

“…In one of these studies, CXCL12 production reached peak levels at day 7 post injury (Hu et al), whilst in another, the chemokine displayed bimodal upregulation, with levels peaking at day 1 and then again at day 5 post wounding . Despite differences in the kinetics involved, blocking of CXCR4 on MSCs inhibits their recruitment and impaired wound healing Xu et al, 2013). However, in vitro expansion of BM MSCs may result in the downregulation of CXCR4 expression (Karp and Leng Teo, 2009).…”

Section: Mechanisms Of Msc and Pericyte Recruitment To Sites Of Injurymentioning

confidence: 99%

Pericytes, mesenchymal stem cells and their contributions to tissue repair

Wong

Rowley

Redpath

et al. 2015

Pharmacology & Therapeutics

143

102

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Regenerative medicine using mesenchymal stem cells for the purposes of tissue repair has garnered considerable public attention due to the potential of returning tissues and organs to a normal, healthy state after injury or damage has occurred. To achieve this, progenitor cells such as pericytes and bone marrow-derived mesenchymal stem cells can be delivered exogenously, mobilised and recruited from within the body or transplanted in the form organs and tissues grown in the laboratory from stem cells. In this review, we summarise the recent evidence supporting the use of endogenously mobilised stem cell populations to enhance tissue repair along with the use of mesenchymal stem cells and pericytes in the development of engineered tissues. Finally, we conclude with an overview of currently available therapeutic options to manipulate endogenous stem cells to promote tissue repair.

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“…8 Alternatively, a decrease in Cxcl12-dependent recruitment and survival of progenitor cells at the injured site could cause a reduced secretion of such mobilization factors from the recruited cells, as observed after skin wounding. 52 In addition, a different inflammatory context in the neointima could contribute to the observed reduction in progenitor cell mobilization in Cxcr4 …”

Section: Apoementioning

confidence: 99%

Deficiency of Endothelial Cxcr4 Reduces Reendothelialization and Enhances Neointimal Hyperplasia After Vascular Injury in Atherosclerosis-Prone Mice

Noels

Zhou

Tilstam

et al. 2014

ATVB

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Objective— The Cxcl12/Cxcr4 chemokine ligand/receptor axis mediates the mobilization of smooth muscle cell progenitors, driving injury-induced neointimal hyperplasia. This study aimed to investigate the role of endothelial Cxcr4 in neointima formation. Approach and Results— β-Galactosidase staining using bone marrow x kinase ( Bmx ) -CreER T2 reporter mice and double immunofluorescence revealed an efficient and endothelial-specific deletion of Cxcr4 in Bmx-CreER T2+ compared with Bmx-CreER T2− Cxcr4-floxed apolipoprotein E–deficient ( Apoe −/− ) mice (referred to as Cxcr4 EC-KO ApoE −/− and Cxcr4 EC-WT ApoE −/− , respectively). Endothelial Cxcr4 deficiency significantly increased wire injury–induced neointima formation in carotid arteries from Cxcr4 EC-KO ApoE −/− mice. The lesions displayed a higher number of macrophages, whereas the smooth muscle cell and collagen content were reduced. This was associated with a significant reduction in reendothelialization and endothelial cell proliferation in injured Cxcr4 EC-KO ApoE −/− carotids compared with Cxcr4 EC-WT ApoE −/− controls. Furthermore, stimulation of human aortic endothelial cells with chemokine (C-X-C motif) ligand 12 (CXCL12) significantly enhanced their wound-healing capacity in an in vitro scratch assay, an effect that could be reversed with the CXCR4 antagonist AMD3100. Also, flow cytometric analysis showed a reduced mobilization of Sca1 + Flk1 + Cd31 + and of Lin − Sca1 + progenitors in Cxcr4 EC-KO ApoE −/− mice after vascular injury, although Cxcr4 surface expression was unaltered. No differences could be detected in plasma concentrations of Cxcl12, vascular endothelial growth factor, sphingosine 1-phosphate, or Flt3 (fms-related tyrosine kinase 3) ligand, all cytokines with an established role in progenitor cell mobilization. Nonetheless, double immunofluorescence revealed a significant reduction in local endothelial Cxcl12 staining in injured carotids from Cxcr4 EC-KO ApoE −/− mice. Conclusions— Endothelial Cxcr4 is crucial for efficient reendothelialization after vascular injury through endothelial wound healing and proliferation, and through the mobilization of Sca1 + Flk1 + Cd31 + cells, often referred to as circulating endothelial progenitor cells.

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Stromal Cell-Derived Factor-1 Enhances Wound Healing through Recruiting Bone Marrow-Derived Mesenchymal Stem Cells to the Wound Area and Promoting Neovascularization

Cited by 112 publications

References 57 publications

The wound healing, chronic fibrosis, and cancer progression triad

The wound healing, chronic fibrosis, and cancer progression triad

Pericytes, mesenchymal stem cells and their contributions to tissue repair

Deficiency of Endothelial Cxcr4 Reduces Reendothelialization and Enhances Neointimal Hyperplasia After Vascular Injury in Atherosclerosis-Prone Mice

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