Exosomes exert cardioprotection in dystrophin-deficient cardiomyocytes via ERK1/2-p38/MAPK signaling. Sci Rep 2018 Nov 08;8(1):16519
Date
11/10/2018Pubmed ID
30410044Pubmed Central ID
PMC6224575DOI
10.1038/s41598-018-34879-6Scopus ID
2-s2.0-85056282822 (requires institutional sign-in at Scopus site) 36 CitationsAbstract
As mediators of intercellular communication, exosomes containing molecular cargo are secreted by cells and taken up by recipient cells to influence cellular phenotype and function. Here we have investigated the effects of exosomes in dystrophin-deficient (Dys) induced pluripotent stem cell derived cardiomyocytes (iCMs). Our data demonstrate that exosomes secreted from either wild type (WT) or Dys-iCMs protect the Dys-iCM from stress-induced injury by decreasing reactive oxygen species and delaying mitochondrial permeability transition pore opening to maintain the mitochondrial membrane potential and decrease cell death. The protective effects of exosomes were dependent on the presence of exosomal surface proteins and activation of ERK1/2 and p38 MAPK signaling. Based on our findings, the acute effects of exosomes on recipient cells can be initiated from exosome membrane proteins and not necessarily their internal cargo.
Author List
Gartz M, Darlington A, Afzal MZ, Strande JLAuthor
Melanie Gartz PhD Assistant Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
Cell DifferentiationCell Survival
Cells, Cultured
Dystrophin
Exosomes
Humans
Induced Pluripotent Stem Cells
MAP Kinase Signaling System
Membrane Potential, Mitochondrial
Mitochondria
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinases
Myocytes, Cardiac
Sequence Deletion
p38 Mitogen-Activated Protein Kinases
