Hypoxic conditioned medium from mesenchymal stem cells promotes lymphangiogenesis by regulation of mitochondrial-related proteins

  • Chang Youn Lee
  • , Jin Young Kang
  • , Soyeon Lim
  • , Onju Ham
  • , Woochul Chang
  • , Dae Hyun Jang

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Background: Recently, cell-based therapeutic lymphangiogenesis has emerged and provided hope for lymphatic regeneration. Previous studies have demonstrated that secretomes of mesenchymal stem cells (MSCs) facilitate the regeneration of various damaged tissues. This study was conducted to evaluate the lymphangiogenic potential of hypoxic conditioned media (HCM) from MSCs. Methods: To investigate the effects of MSC-secreted factors in starved human lymphatic endothelial cells (hLEC), hLECs were treated with endothelial basal medium (EBM)-2 (control), normoxic conditioned media (NCM), or HCM in vitro and in vivo. Results: MSCs expressed lymphangiogenic factors including EGF, FGF2, HGF, IGF-1, and VEGF-A and -C. hLECs were treated with each medium. hLEC proliferation, migration, and tube formation were improved under HCM compared with NCM. Moreover, expression of mitochondrial-related factors, MFN1and 2, were improved in HCM-treated hLECs. Lymphedema mice injected with HCM showed markedly decreased lymphedema via increased lymphatic vessel formation when compared with EBM-2- or NCM-treated mice. Conclusions: This study suggested that HCM from MSCs contain high levels of secreted lymphangiogenic factors and promote lymphangiogenesis by regulating mitochondrial-related factors. Thus, treatment with HCM may be a therapeutic strategy for lymphedema.

Original languageEnglish
Article number38
JournalStem Cell Research and Therapy
Volume7
Issue number1
DOIs
StatePublished - 11 Mar 2016

Bibliographical note

Publisher Copyright:
© 2016 Lee et al.

Keywords

  • Hypoxic conditioned media
  • Lymphangiogenesis
  • Lymphatic endothelial cells
  • Mesenchymal stem cells
  • Mitochondrial-related protein

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