Human Adult CD34<sup>−</sup> Progenitor Cells Functionally Express the Chemokine Receptors CCR1, CCR4, CCR7, CXCR5, and CCR10 but Not CXCR4

Lüttichau, Irene von; Notohamiprodjo, Mike; Wechselberger, Alexandra; Peters, Christina; Henger, Anna; Seliger, Christian; Djafarzadeh, Roghieh; Huss, Ralf; Nelson, Peter J.

doi:10.1089/scd.2005.14.329

Cited by 193 publications

(147 citation statements)

References 32 publications

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“…The involvement of CXCL12 and its cognate receptor CXCR4 in MSC migration to injured tissues is well established (17) in spite of some exceptions (23). In vitro migration assays reported to date have identified growth factors and chemokines that are possibly involved in MSC migration (42,49,60,61). However, the mechanisms of MSC migration are expected to differ with tissue microenvironments induced by diseases.…”

Section: Discussionmentioning

confidence: 99%

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Song

Furuoka

Horiuchi

2011

J Virol

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Bone marrow-derived mesenchymal stem cells (MSCs) have been reported to migrate to brain lesions of neurodegenerative diseases; however, the precise mechanisms by which MSCs migrate remain to be elucidated. In this study, we carried out an in vitro migration assay to investigate the chemoattractive factors for MSCs in the brains of prion-infected mice. The migration of immortalized human MSCs (hMSCs) was reduced by their pretreatment with antibodies against the chemokine receptors, CCR3, CCR5, CXCR3, and CXCR4 and by pretreatment of brain extracts of prion-infected mice with antibodies against the corresponding ligands, suggesting the involvement of these receptors, and their ligands in the migration of hMSCs. In agreement with the results of an in vitro migration assay, hMSCs in the corpus callosum, which are considered to be migrating from the transplanted area toward brain lesions of prion-infected mice, expressed CCR3, CCR5, CXCR3, and CXCR4. The combined in vitro and in vivo analyses suggest that CCR3, CCR5, CXCR3, and CXCR4, and their corresponding ligands are involved in the migration of hMSCs to the brain lesions caused by prion propagation. In addition, hMSCs that had migrated to the right hippocampus of prion-infected mice expressed CCR1, CX3CR1, and CXCR4, implying the involvement of these chemokine receptors in hMSC functions after chemotactic migration. Further elucidation of the mechanisms that underlie the migration of MSCs may provide useful information regarding application of MSCs to the treatment of prion diseases.

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Section: Discussionmentioning

confidence: 99%

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Song

Furuoka

Horiuchi

2011

J Virol

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“…Thus, apparently, G-CSF also induces the mobilization of these cells from the bone marrow in the irradiated salivary glands. Indeed, it is known that next to hematopoietic stem cells, G-CSF also induces the mobilization of a number of mesenchymal progenitor cells (46), which may even home to salivary glands in healthy mice (47). Therefore, one can postulate that mesenchymal cells are involved in the amelioration of radiation-induced damage to the salivary gland.…”

Section: Discussionmentioning

confidence: 99%

Mobilization of Bone Marrow Stem Cells by Granulocyte Colony-Stimulating Factor Ameliorates Radiation-Induced Damage to Salivary Glands

Lombaert¹,

Wierenga²,

Kok³

et al. 2006

Clinical Cancer Research

141

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Purpose: One of the major reasons for failure of radiotherapeutic cancer treatment is the limitation in dose that can be applied to the tumor because of coirradiation of the normal healthy tissue. Late radiation-induced damage reduces the quality of life of the patient and may even be life threatening. Replacement of the radiation-sterilized stem cells with unirradiated autologous stem cells may restore the tissue function. Here, we assessed the potential of granulocyte colony-stimulating factor (G-CSF)–mobilized bone marrow–derived cells (BMC) to regenerate and functionally restore irradiated salivary glands used as a model for normal tissue damage. Experimental Design: Male-eGFP+ bone marrow chimeric female C57BL/6 mice were treated with G-CSF, 10 to 60 days after local salivary gland irradiation. Four months after irradiation, salivary gland morphology and flow rate were assessed. Results: G-CSF treatment induced homing of large number of labeled BMCs to the submandibular glands after irradiation. These animals showed significant increased gland weight, number of acinar cells, and salivary flow rates. Donor cells expressed surface markers specific for hematopoietic or endothelial/mesenchymal cells. However, salivary gland acinar cells neither express the G-CSF receptor nor contained the GFP/Y chromosome donor cell label. Conclusions: The results show that BMCs home to damaged salivary glands after mobilization and induce repair processes, which improve function and morphology. This process does not involve transdifferentiation of BMCs to salivary gland cells. Mobilization of BMCs could become a promising modality to ameliorate radiation-induced complications after radiotherapy.

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“…A greater understanding of the factors that regulate their homing and renoprotective activity may prove equally fruitful in delivering a cell-free approach to renal disease. To this end, Luttichaux et al (65) have begun to define the chemokine receptors that are expressed by MSC in vivo and in culture. Togel et al (64) highlighted a reduction in the production of proinflammatory cytokines and a concomitant increase in anti-inflammatory cytokines such as IL-10, TGF-␣, Bcl2, and basic fibroblast growth factor after infusion of MSC into an ischemia/reperfusion model of acute damage.…”

Section: Nonrenal Adult Stem Cellsmentioning

confidence: 99%

Regrow or Repair

Little

2006

Journal of the American Society of Nephrology

153

121

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Regenerative medicine is being heralded in a similar way as gene therapy was some 15 yr ago. It is an area of intense excitement and potential, as well as myth and disinformation. However, with the increasing rate of end-stage renal failure and limited alternatives for its treatment, we must begin to investigate seriously potential regenerative approaches for the kidney. This review defines which regenerative options there might be for renal disease, summarizes the progress that has been made to date, and investigates some of the unique obstacles to such treatments that the kidney presents. The options discussed include in situ organ repair via bone marrow recruitment or dedifferentiation; ex vivo stem cell therapies, including both autologous and nonautologous options; and bioengineering approaches for the creation of a replacement organ.

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Human Adult CD34⁻ Progenitor Cells Functionally Express the Chemokine Receptors CCR1, CCR4, CCR7, CXCR5, and CCR10 but Not CXCR4

Cited by 193 publications

References 32 publications

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Mobilization of Bone Marrow Stem Cells by Granulocyte Colony-Stimulating Factor Ameliorates Radiation-Induced Damage to Salivary Glands

Regrow or Repair

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Human Adult CD34− Progenitor Cells Functionally Express the Chemokine Receptors CCR1, CCR4, CCR7, CXCR5, and CCR10 but Not CXCR4

Cited by 193 publications

References 32 publications

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Identification of Chemoattractive Factors Involved in the Migration of Bone Marrow-Derived Mesenchymal Stem Cells to Brain Lesions Caused by Prions

Mobilization of Bone Marrow Stem Cells by Granulocyte Colony-Stimulating Factor Ameliorates Radiation-Induced Damage to Salivary Glands

Regrow or Repair

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Human Adult CD34⁻ Progenitor Cells Functionally Express the Chemokine Receptors CCR1, CCR4, CCR7, CXCR5, and CCR10 but Not CXCR4