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URL Address
<a href="http://doi.org/10.1002/sctm.17-0046" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/sctm.17-0046</a>
Pages
1759–1766
Issue
9
Volume
6
Dublin Core
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Title
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A Novel Role for CAMKK1 in the Regulation of the Mesenchymal Stem Cell Secretome.
Publisher
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Stem cells translational medicine
Date
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2017
2017-09
Subject
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Calcium/calmodulin-dependent protein kinase kinase-1; Cardiac disease; Cardiac regeneration; Mesenchymal stem cells; Secretome
Creator
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Dong Feng; Patnaik Shyam; Duan Zhong-Hui; Kiedrowski Matthew; Penn Marc S; Mayorga Maritza E
Description
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Transplantation of adult stem cells into myocardial tissue after acute myocardial infarction (AMI), has been shown to improve tissue recovery and prevent progression to ischemic cardiomyopathy. Studies suggest that the effects of mesenchymal stem cells (MSC) are due to paracrine factors released by MSC, as the benefits of MSC can be achieved through delivery of conditioned media (CM) alone. We previously demonstrated that downregulation of Dab2 enhances MSC cardiac protein expression and improves cardiac function after AMI following MSC engraftment. In order to define the molecular mechanisms that regulate MSC secretome, we analyzed gene arrays in MSC following downregulation of Dab2 via TGFbeta1 pretreatment or transfection with Dab2:siRNA or miR-145. We identified 23 genes whose expressions were significantly changed in all three conditions. Among these genes, we have initially focused our validation and functional work on calcium/calmodulin-dependent protein kinase kinase-1 (CAMKK1). We quantified the effects of CAMKK1 overexpression in MSC following injection of CM after AMI. Injections of CM from MSC with CAMKK1 over-expression correlated with an increase in vascular density (CAMKK1 CM: 2,794.95 +/- 44.2 versus Control: 1,290.69 +/- 2.8 vessels/mm(2) ) and decreased scar formation (CAMKK1 CM 50% +/- 3.2% versus Control: 28% +/- 1.4%), as well as improved cardiac function. Direct overexpression of CAMKK1 in infarcted tissue using a CAMKK1-encoding plasmid significantly improved ejection fraction (CAMKK1: 83.2% +/- 5.4% versus saline: 51.7% +/- 5.8%. Baseline: 91.3% +/- 4.3%) and decreased infarct size after AMI. Our data identify a novel role for CAMKK1 as regulator of the MSC secretome and demonstrate that direct overexpression of CAMKK1 in infarcted cardiac tissue, results in therapeutic beneficial effects. Stem Cells Translational Medicine 2017;6:1759-1766.
Identifier
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<a href="http://doi.org/10.1002/sctm.17-0046" target="_blank" rel="noreferrer noopener">10.1002/sctm.17-0046</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Calcium/calmodulin-dependent protein kinase kinase-1
Cardiac disease
Cardiac regeneration
Department of Integrative Medical Sciences
Dong Feng
Duan Zhong-Hui
Kiedrowski Matthew
Mayorga Maritza E
Mesenchymal stem cells
NEOMED College of Medicine
Patnaik Shyam
Penn Marc S
Secretome
Stem cells translational medicine