scholarly journals Interleukin-10 Deficiency Impairs Bone Marrow–Derived Endothelial Progenitor Cell Survival and Function in Ischemic Myocardium

2011 ◽  
Vol 109 (11) ◽  
pp. 1280-1289 ◽  
Author(s):  
Prasanna Krishnamurthy ◽  
Melissa Thal ◽  
Suresh Verma ◽  
Eneda Hoxha ◽  
Erin Lambers ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Survival ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Interleukin 10 ◽  
Ischemic Myocardium ◽  
Endothelial Progenitor ◽  
And Function

scholarly journals Interleukin-10 Deficiency Impairs Reparative Properties of Bone Marrow-Derived Endothelial Progenitor Cell Exosomes

2017 ◽  
Vol 23 (21-22) ◽  
pp. 1241-1250 ◽  
Author(s):  
Yujia Yue ◽  
Venkata Naga Srikanth Garikipati ◽  
Suresh Kumar Verma ◽  
David A. Goukassian ◽  
Raj Kishore
Keyword(s):  
Bone Marrow ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Interleukin 10 ◽  
Endothelial Progenitor

Abstract 216: Interleukin-10 Deficiency Impairs Reparative Properties of Bone Marrow-Derived Endothelial Progenitor Cell Exosomes

2018 ◽  
Vol 123 (Suppl_1) ◽  
Author(s):  
Yujia Yue ◽  
Venkata N Garikipati ◽  
Yan Tang ◽  
Maria Cimini ◽  
Zhongjian Cheng ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Interleukin 10 ◽  
Endothelial Progenitor

scholarly journals C-Reactive Protein Attenuates Endothelial Progenitor Cell Survival, Differentiation, and Function

Circulation ◽  
2004 ◽  
Vol 109 (17) ◽  
pp. 2058-2067 ◽  
Author(s):  
Subodh Verma ◽  
Michael A. Kuliszewski ◽  
Shu-Hong Li ◽  
Paul E. Szmitko ◽  
Liana Zucco ◽  
...  
Keyword(s):  
Cell Survival ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
C Reactive Protein ◽  
Endothelial Progenitor ◽  
Reactive Protein ◽  
And Function

Endothelial Progenitor Cell Targeting to Ischemic Myocardium Attenuates Hypoxia and Enhances Cardiomyocyte Viability and Function

2006 ◽  
Vol 12 (6) ◽  
pp. S8
Author(s):  
Pavan Atluri ◽  
Kevin J. Morine ◽  
George P. Liao ◽  
Corinna M. Panlilio ◽  
Y. Joseph Woo
Keyword(s):  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Ischemic Myocardium ◽  
Cell Targeting ◽  
Endothelial Progenitor ◽  
And Function

Abstract 40: Interleukin-10 Deficiency Impairs Reparative Properties of Bone Marrow-derived Endothelial Progenitor Cell Exosomes Function in Ischemic Myocardium

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Yujia Yue ◽  
Venkata N Garikipati ◽  
Yan Tang ◽  
Zhongjian Chen ◽  
Jibin Zhou ◽  
...  
Keyword(s):  
Stem Cell ◽  
Systemic Inflammation ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Interleukin 10 ◽  
Ischemic Myocardium ◽  
Common Symptom ◽  
Endothelial Progenitor ◽  
Cell Functions

Endothelial progenitor cell (EPC) based therapy promotes neovascularization in ischemic myocardium. Studies suggest that therapeutic effect of stem cells is largely due to paracrine mechanisms including stem cell-derived exosomes that are emerging as key paracrine mediators of stem cell functions. However, the autologous transplantation of EPCs in patients with systemic inflammation, which is a common symptom in patients with ischemic heart diseases, yield modest results suggesting the compromised cell function and altered exosome performance. We hypothesized that EPCs under inflammatory stress secrete dysfunctional exosomes with altered contents including packaged microRNAs, which eventually compromises exosomes repair ability in ischemic myocardium. Whether modulation of identified targets like specific microRNAs in the cargo of exosomes can rescue and/or enhance their reparative properties of dysfunctional exosomes is not known. We have previously shown in Interleukin-10 (IL-10) KO mice (model mimicking systemic inflammation) that loss of IL-10 impairs EPCs functions via miR-375. After cell expansion, we isolated exosomes from these two groups and compared their functions in terms of cell survival, proliferation, migration and angiogenic capacity in vitro and in vivo . We report that WT-EPC-exosomes (Exo) transplantation in the ischemic myocardium after MI significantly improved post-infarct repair, neovascularization and left ventricle functions. Our in vitro studies revealed that WT-EPC-Exo treatment enhanced endothelial cells proliferation and tube formation and inhibited apoptosis; whereas IL-10 KO-EPC-Exo exhibited opposite effects, suggesting that reparative capacity of WT-EPC-Exo is lost in exosomes derived from IL-10 KO-EPCs. Exosome miRNA profiling revealed a drastically different expression patterns with enrichment of inflammation induced microRNAs including significantly higher expression of miR-375. Interestingly, Knockdown of miR-375 in IL-10-EPCs decreased the expression level of miR-375 in their exosomes and partly rescued their angiogenic dysfunctions. Taken together, our studies suggest that modulation of miR-375 in IL-10 KO-EPC-Exo can rescue its phenotype and promote cardiac repair.

Abstract 119: Potential Role for Bone Marrow Niche and Endothelial Progenitor Cell Dysfunction in Critical Limb Ischemia

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Martin Teraa ◽  
Ralf W Sprengers ◽  
Frans L Moll ◽  
Marianne C Verhaar ◽  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Critical Limb Ischemia ◽  
Progenitor Cell ◽  
Limb Ischemia ◽  
Endothelial Damage ◽  
Inverse Association ◽  
Healthy Controls ◽  
Endothelial Progenitor ◽  
And Function

Background Critical limb ischemia (CLI) is characterized by obstruction of lower extremity arteries and a largely unexplained impaired ischemic neovascularization response. Bone marrow (BM) derived endothelial progenitor cells (EPC) contribute to postnatal neovascularization. We hypothesize that reduced levels and function of circulating progenitor cells and a dysfunctional BM environment contribute to impaired neovascularization in CLI. Methods Levels of primitive (CD34+ and CD133+) progenitors and CD34+KDR+ haemangioblastic EPC were analyzed using flow cytometry in peripheral blood (PB) and BM from 101 CLI patients in the JUVENTAS trial ( NCT00371371 ) and healthy controls (n=37 and n=12 for PB and BM, respectively). Endothelial damage markers (sE-selectin, sICAM-1, sVCAM-1, thrombomodulin) and PB levels of progenitor cell mobilizing (VEGF, SDF-1α, SCF, G-CSF) and inflammatory (IL-6, IL-8, IP-10) factors were assessed by ELISA and multiplex. Levels and activity of the EPC mobilizing protease MMP-9 were assessed in BM plasma by ELISA and zymography. Circulating angiogenic cells (CAC) were cultured from PB, and CAC paracrine function was assessed. Results Endothelial damage markers were higher in CLI ( p< 0.01). PB levels of VEGF, SDF-1α, SCF, G-CSF ( p< 0.05) and of IL-6, IL-8 and IP-10 were higher in CLI ( p< 0.05). Circulating EPC and CD133+ cells and BM CD34+ cells were significantly lower in CLI (all p <0.05), BM levels and activity of MMP-9 were lower in CLI (both p< 0.01). Multivariate regression analysis showed an inverse association between IL-6 levels and BM CD34+ cell levels ( p= 0.007). CAC outgrowth did not differ significantly between CLI patients and healthy controls ( p= 0.137), however CAC from CLI patients had profoundly reduced migration stimulating potential ( p< 0.0001). Conclusion CLI patients have reduced levels of circulating EPC despite profound endothelial injury and an EPC mobilizing response. Moreover, CLI patients have lower BM CD34+ cell levels, which were inversely associated with the inflammatory marker IL-6, and lower BM MMP-9 levels and activity. Our data suggest that reduced levels and function of circulating progenitor cells and BM dysfunction contribute to the defective neovascularization response in CLI.

scholarly journals Insufficient production of IL-10 from M2 macrophages impairs in vitro endothelial progenitor cell differentiation in patients with Moyamoya disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Eiichiro Nagata ◽  
Haruchika Masuda ◽  
Taira Nakayama ◽  
Shizuka Netsu ◽  
Hiroko Yuzawa ◽  
...  
Keyword(s):  
Moyamoya Disease ◽  
Endothelial Progenitor Cell ◽  
Progenitor Cell ◽  
Mononuclear Cells ◽  
Interleukin 10 ◽  
Endothelial Progenitor ◽  
Peripheral Blood Mononuclear ◽  
Cytokine Milieu ◽  
Colony Forming Assay

AbstractMoyamoya disease (MMD) is well known to be caused by insufficient cerebral vascular formation. However, the essential pathogenesis has not yet been identified. Using our recently developed technique of generating vasculogenic and anti-inflammatory cultures, we investigated endothelial progenitor cell (EPC) expansion and differentiation under the cytokine milieu generated by the peripheral blood mononuclear cells (PBMNCs) of the operated and non-operated MMD patients. EPC colony forming assay of the cultured PBMNCs disclosed the decline of the definitive EPC colony numbers in the both MMD patients. The level of interleukin-10 (IL-10) was lower in secretory cytokines from the cultured PBMNCs of MMD patients than that in that of controls using a cytometric bead array. The addition of human recombinant IL-10 to PBMNCs cultured from MMD patients restored the EPC colony forming potential of MMD PBMNCs. Following phorbol myristate acetate stimulation of the cultured PBMNCs, flow cytometry revealed a decrease in intracellular IL-10 storage in the main cell populations of the PBMNCs cultured from MMD patients relative to those cultured from controls. The present data provide the expected mechanism of vascular malformation in MMD pathogenesis originated from the insufficient production of IL-10 secreting cells from PBMNCs fostering EPC expansion and differentiation.

scholarly journals The bone marrow-derived endothelial progenitor cell response is impaired in delayed wound healing from ischemia

2006 ◽  
Vol 43 (1) ◽  
pp. 134-141 ◽  
Author(s):  
Stephen M. Bauer ◽  
Lee J. Goldstein ◽  
Richard J. Bauer ◽  
Haiying Chen ◽  
Mary Putt ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Wound Healing ◽  
Endothelial Progenitor Cell ◽  
Cell Response ◽  
Progenitor Cell ◽  
Endothelial Progenitor ◽  
Delayed Wound Healing
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