Endothelial Progenitor Cells Possess Monocyte-like Antigen-presenting and T-cell-Co-stimulatory Capacity

Raemer, Patrick C.; Haemmerling, Susanne; Giese, Thomas; Canaday, David H.; Katus, Hugo A.; Dengler, Thomas J.; Shankar, Sivanandam G. Vijay

doi:10.1097/tp.0b013e3181957308

Cited by 24 publications

(16 citation statements)

References 31 publications

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“…Bone marrow-derived progenitor cells are also reported to favor the formation of premetastatic niches, which precondition the environment to facilitate the implantation of tumor cells and the consecutive recruitment of other progenitor cells to promote the neovascularization of metastases (6)(7). More recently, EPCs were documented to act as antigen-presenting cells similar to monocytes (9,10), confirming previous reports identifying populations of EPCs with an intermediate phenotype expressing both endothelial and monocytic/macrophagic properties (11,12).…”

Section: Introductionsupporting

confidence: 67%

Preconditioned Endothelial Progenitor Cells Reduce Formation of Melanoma Metastases through SPARC-Driven Cell–Cell Interactions and Endocytosis

et al. 2011

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Tumor progression is associated with the release of signaling substances from the primary tumor into the bloodstream. Tumor-derived cytokines are known to promote the mobilization and the recruitment of cells from the bone marrow, including endothelial progenitor cells (EPC). Here, we examined whether such paracrine influence could also influence the capacity of EPC to interfere with circulating metastatic cells. We therefore consecutively injected EPC prestimulated by tumor-conditioned medium (EPC-CM) and luciferase-expressing B16 melanoma cells to mice. A net decrease in metastases spreading (vs. nonstimulated EPC) led us to carry out a 2-dimensional difference gel electrophoresis (2D-DIGE) proteomic study to identify possible mediators of EPC-driven protection. Among 33 proteins exhibiting significant changes in expression, secreted protein, acidic and rich in cysteine (SPARC) presented the highest induction after EPC exposure to CM. We then showed that contrary to control EPC, SPARC-silenced EPC were not able to reduce the extent of metastases when injected with B16 melanoma cells. Using adhesion tests and the hanging drop assay, we further documented that cell-cell interactions between EPC-CM and melanoma cells were promoted in a SPARC-dependent manner. This interaction led to the engulfment of melanoma cells by EPC-CM, a process prevented by SPARC silencing and mimicked by recombinant SPARC. Finally, we showed that contrary to melanoma cells, the prometastatic human breast cancer cell line MDA-MB231-D3H2 reduced SPARC expression in human EPC and stimulated metastases spreading. Our findings unravel the influence of tumor cells on EPC phenotypes through a SPARC-driven accentuation of macrophagic capacity associated with limitations to metastatic spread. Cancer Res; 71(14); 4748-57. Ó2011 AACR.

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Section: Introductionsupporting

confidence: 67%

Preconditioned Endothelial Progenitor Cells Reduce Formation of Melanoma Metastases through SPARC-Driven Cell–Cell Interactions and Endocytosis

et al. 2011

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“…Migration and adhesion are two important steps in EPC homing. Several reports showed that EPCs expressed the Pselectin glycoprotein ligand-1 (PGSL-1), the ligand of P/E selectin, and adhesion molecules on ischemic ECs would have an important role in recruiting circulating EPCs to the murine vasculature (Raemer et al, 2009). In the present study, we observed that endothelial cells in ischemic tissue …”

Section: Discussionsupporting

confidence: 65%

“…1G, H). Adhesion and migration were very important steps in EPC homing to impaired tissues; the expression of P-selectin glycoprotein ligand-1 (PGSL-1), a ligand of P/E selectin, on EPCs has been previously reported (Urao et al, 2008;Raemer et al, 2009). To investigate the effect of apo (a) on EPC adhesion, we treated EPCs with 0.2, 1, 5, 10, 15 mg/mL apo (a) and adopted an RT-PCR method to detect P/E-selectin expressed in the ECs of ischemic tissues, which could promote adhesion of circular EPCs to the endothelium of injured tissues.…”

Section: Apo (A) Attenuated Epcs Adhesion and Migrationmentioning

confidence: 99%

Apolipoprotein (a) Impairs Endothelial Progenitor Cell-Mediated Angiogenesis

Ren

Zhang

et al. 2013

DNA and Cell Biology

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Improvement of blood flow and promotion of angiogenesis are important therapeutic measures for the treatment of ischemic peripheral vascular diseases. Since apolipoprotein (a) (apo (a)) is a glycoprotein with repetitive kringle domains exhibiting 75% to 98% structural homology with plasminogen (Plg), apo (a) may also have a negative effect on endothelial progenitor cell (EPC)-induced angiogenesis through Plg-like inhibitory effects on EPC proliferation, adhesion, migration, and angiogenesis. To evaluate the effect of apo (a) on EPCs-induced angiogenesis, EPCs were isolated from the bone marrow of apo (a) transgenic mice, wild-type litter mates, and normal mice. These cells were cultured without or with apo (a) before transplantation. Hindlimb ischemia models were surgically induced in mice, which then received an intravenous injection of 3 · 10 5 EPCs. At 3, 7, and 14 days post EPC transplantation, the adhesion, migration abilities, and capillary density in calf muscles were assessed. Results indicate that apo (a) significantly reduced the adhesion and migration abilities of EPCs. Furthermore, the tubule-like formation of EPCs on Matrigel gels was damaged. In vivo experiments showed the homing of EPCs to ischemic peripheral vascular, and the number of capillary vessels decreased significantly in apo(a) transgenic mice. This study demonstrated that apo (a) could attenuate the adhesion, migration, and homing abilities of EPCs and could impair the angiogenesis ability of EPCs.

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“…Thus, the emerging consensus is that EPCs identified with cell surface markers CD34 and VEGFR2 contain very few, if any, genuine EC progenitors, and are more accurately described as angiogenic macrophages. Three recent papers have further strengthened this view (73–75). However, another study has most comprehensively demonstrated that so-called EPCs are predominantly of monocytic lineage (76).…”

Section: Endothelial Progenitor Cells (Epcs)mentioning

confidence: 91%

Endothelial progenitor cells in atherosclerosis

Du¹

2012

Front Biosci

119

104

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Endothelial progenitor cells (EPCs) are involved in the maintenance of endothelial homoeostasis and in the process of new vessel formation. Experimental and clinical studies have shown that atherosclerosis is associated with reduced numbers and dysfunction of EPCs; and that medications alone are able to partially reverse the impairment of EPCs in patients with atherosclerosis. Therefore, novel EPC-based therapies may provide enhancement in restoring EPCs’ population and improvement of vascular function. Here, for a better understanding of the molecular mechanisms underlying EPC impairment in atherosclerosis, we provide a comprehensive overview on EPC characteristics, phenotypes, and the signaling pathways underlying EPC impairment in atherosclerosis.

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Endothelial Progenitor Cells Possess Monocyte-like Antigen-presenting and T-cell-Co-stimulatory Capacity

Cited by 24 publications

References 31 publications

Preconditioned Endothelial Progenitor Cells Reduce Formation of Melanoma Metastases through SPARC-Driven Cell–Cell Interactions and Endocytosis

Preconditioned Endothelial Progenitor Cells Reduce Formation of Melanoma Metastases through SPARC-Driven Cell–Cell Interactions and Endocytosis

Apolipoprotein (a) Impairs Endothelial Progenitor Cell-Mediated Angiogenesis

Endothelial progenitor cells in atherosclerosis

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