Microparticles from kidney-derived mesenchymal stem cells act as carriers of proangiogenic signals and contribute to recovery from acute kidney injury

PLoS One. 2014 Feb 4;9(2):e87853. doi: 10.1371/journal.pone.0087853. eCollection 2014.

Abstract

We recently demonstrated the use of in vitro expanded kidney-derived mesenchymal stem cells (KMSC) protected peritubular capillary endothelial cells in acute renal ischemia-reperfusion injury. Herein, we isolated and characterized microparticles (MPs) from KMSC. We investigated their in vitro biologic effects on human endothelial cells and in vivo renoprotective effects in acute ischemia-reperfusion renal injury. MPs were isolated from the supernatants of KMSC cultured in anoxic conditions in serum-deprived media for 24 hours. KMSC-derived MPs demonstrated the presence of several adhesion molecules normally expressed on KMSC membranes, such as CD29, CD44, CD73, α4, 5, and 6 integrins. Quantitative real time PCR confirmed the presence of 3 splicing variants of VEGF-A (120, 164, 188), bFGF and IGF-1 in isolated MPs. MPs labeled with PKH26 red fluorescence dye were incorporated by cultured human umbilical vein endothelial cells (HUVEC) via surface molecules such as CD44, CD29, and α4, 5, and 6 integrins. MP dose dependently improved in vitro HUVEC proliferation and promoted endothelial tube formation on growth factor reduced Matrigel. Moreover, apoptosis of human microvascular endothelial cell was inhibited by MPs. Administration of KMSC-derived MPs into mice with acute renal ischemia was followed by selective engraftment in ischemic kidneys and significant improvement in renal function. This was achieved by improving proliferation, of peritubular capillary endothelial cell and amelioration of peritubular microvascular rarefaction. Our results support the hypothesis that KMSC-derived MPs may act as a source of proangiogenic signals and confer renoprotective effects in ischemic kidneys.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / genetics
  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / pathology
  • Animals
  • Apoptosis
  • Biological Transport
  • Cell Proliferation
  • Cell-Derived Microparticles / metabolism*
  • Cell-Derived Microparticles / ultrastructure
  • Disease Models, Animal
  • Endothelial Cells / metabolism*
  • Gene Expression Profiling
  • Gene Transfer, Horizontal
  • Human Umbilical Vein Endothelial Cells
  • Humans
  • Male
  • Mesenchymal Stem Cells / metabolism*
  • Mice
  • Neovascularization, Physiologic
  • Reperfusion Injury / genetics
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Signal Transduction*

Grants and funding

This research was supported by the Basic Science Research Program (NRF-2010-0013373) through the National Research Foundation of Korea funded by the Ministry of Education, Science, and Technology of the Republic of Korea and by the faculty research grant of Yonsei University College of Medicine in 2010 (No. 6-2010-0044). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.