Effect of 17β-estradiol on mediators involved in mesenchymal stromal cell trafficking in cell therapy of diabetes

Mirzamohammadi S 1 , Aali E 1 , Najafi R 2 , Kamarul T 3 , Mehrabani M 1 , Aminzadeh A 1 Show all authors , Sharifi AM 4

Affiliations 

  • 1 Razi Drug Research Center and Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran
  • 2 Department of Molecular Medicine, Hamedan University of Medical Sciences, Hamedan, Iran
  • 3 Tissue Engineering Group (TEG) and Research, National Orthopedic Centre of Excellence in Research and Learning (NOCERAL), Department of Orthopedics, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
  • 4 Razi Drug Research Center and Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran; Department of Tissue Engineering and Cell Therapy, School of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: sharifal@Yahoo.com
Cytotherapy, 2015 Jan;17(1):46-57.
PMID: 25457279 DOI: 10.1016/j.jcyt.2014.06.009

Abstract

Mesenchymal stromal cells (MSCs) have shown great promise for cell therapy of a wide range of diseases such as diabetes. However, insufficient viability of transplanted cells reaching to damaged tissues has limited their potential therapeutic effects. Expression of estrogen receptors on stem cells may suggest a role for 17β-estradiol (E2) in regulating some functions in these cells. There is evidence that E2 enhances homing of stem cells. Induction of hypoxia-inducible factor-1α (HIF-1α) by E2 and the profound effect of HIF-1α on migration of cells have previously been demonstrated. We investigated the effect of E2 on major mediators involved in trafficking and subsequent homing of MSCs both in vitro and in vivo in diabetic rats.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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