Document Detail


Bioactive lipids and cationic antimicrobial peptides as new potential regulators for trafficking of bone marrow-derived stem cells in patients with acute myocardial infarction.
MedLine Citation:
PMID:  23282236     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute myocardial infarction (AMI) triggers mobilization of stem cells from bone marrow (BM) into peripheral blood (PB). Based on our observation that the bioactive sphingophospholipids, sphingosine-1 phosphate (S1P), and ceramide-1 phosphate (C1P) regulate trafficking of hematopoietic stem cells (HSCs), we explored whether they also direct trafficking of non-hematopoietic stem cells (non-HSCs). We detected a 3-6-fold increase in circulating CD34+, CD133+, and CXCR4+ lineage-negative (Lin-)/CD45- cells that are enriched in non-HSCs [including endothelial progenitors (EPCs) and very small embryonic-like stem cells (VSELs)] in PB from AMI patients (P<0.05 vs. controls). Concurrently, we measured a ∼3-fold increase in S1P and C1P levels in plasma from AMI patients. At the same time, plasma obtained at hospital admission and 6 h after AMI strongly chemoattracted human BM-derived CD34+/Lin- and CXCR4+/Lin- cells in Transwell chemotaxis assays. This effect of plasma was blunted after depletion of S1P level by charcoal stripping and was further inhibited by the specific S1P1 receptor antagonist such as W146 and VPC23019. We also noted that the expression of S1P receptor 1 (S1P1), which is dominant in naïve BM, is reduced after the exposure to S1P at concentrations similar to the plasma S1P levels in patients with AMI, thus influencing the role of S1P in homing to the injured myocardium. Therefore, we examined mechanisms, other than bioactive lipids, that may contribute to the homing of BM non-HSCs to the infarcted myocardium. Hypoxic cardiac tissue increases the expression of cathelicidin and β-2 defensin, which could explain why PB cells isolated from patients with AMI migrated more efficiently to a low, yet physiological, gradient of stromal-derived factor-1 in Transwell migration assays. Together, these observations suggest that while elevated S1P and C1P levels early in the course of AMI may trigger mobilization of non-HSCs into PB, cathelicidin and β-2 defensin could play an important role in their homing to damaged myocardium.
Authors:
Anush V Karapetyan; Yuri M Klyachkin; Samy Selim; Manjula Sunkara; Khaled M Ziada; Donald A Cohen; Ewa K Zuba-Surma; Janina Ratajczak; Susan S Smyth; Mariusz Z Ratajczak; Andrew J Morris; Ahmed Abdel-Latif
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-02-19
Journal Detail:
Title:  Stem cells and development     Volume:  22     ISSN:  1557-8534     ISO Abbreviation:  Stem Cells Dev.     Publication Date:  2013 Jun 
Date Detail:
Created Date:  2013-05-20     Completed Date:  2013-12-11     Revised Date:  2014-06-03    
Medline Journal Info:
Nlm Unique ID:  101197107     Medline TA:  Stem Cells Dev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1645-56     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD / blood
Antigens, CD34 / blood
Antimicrobial Cationic Peptides / biosynthesis,  metabolism*
Bone Marrow Cells / metabolism
Cell Hypoxia
Cell Movement
Ceramides / metabolism*
Chemokine CXCL12 / metabolism
Glycoproteins / blood
Hematopoietic Stem Cell Mobilization
Hematopoietic Stem Cell Transplantation*
Hematopoietic Stem Cells / metabolism
Humans
Lysophospholipids / metabolism*
Mice
Mice, Inbred C57BL
Myocardial Infarction / therapy*
Myocardium / cytology,  metabolism
Peptides / blood
Receptors, CXCR4 / blood
Receptors, Lysosphingolipid / blood
Sphingosine / analogs & derivatives*,  metabolism
beta-Defensins / biosynthesis
Grant Support
ID/Acronym/Agency:
1P20RR021954/RR/NCRR NIH HHS; 2R01 DK074720/DK/NIDDK NIH HHS; GM050388/GM/NIGMS NIH HHS; HL078663/HL/NHLBI NIH HHS; P20 GM103527/GM/NIGMS NIH HHS; P20 RR021954/RR/NCRR NIH HHS; R01 DK074720/DK/NIDDK NIH HHS; R01 GM050388/GM/NIGMS NIH HHS; R01 HL078663/HL/NHLBI NIH HHS; R01 HL112788/HL/NHLBI NIH HHS; R01HL078663/HL/NHLBI NIH HHS; UL1 TR000117/TR/NCATS NIH HHS; UL1TR000117/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
0/AC133 antigen; 0/Antigens, CD; 0/Antigens, CD34; 0/Antimicrobial Cationic Peptides; 0/CXCL12 protein, human; 0/CXCR4 protein, human; 0/Ceramides; 0/Chemokine CXCL12; 0/Glycoproteins; 0/Lysophospholipids; 0/Peptides; 0/Receptors, CXCR4; 0/Receptors, Lysosphingolipid; 0/beta-Defensins; 0/ceramide 1-phosphate; 143108-26-3/CAP18 lipopolysaccharide-binding protein; 26993-30-6/sphingosine 1-phosphate; NGZ37HRE42/Sphingosine
Comments/Corrections

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