Adv Pharm Bull. 2015;5(2): 141-149.
doi: 10.15171/apb.2015.021
PMID: 26236651
PMCID: PMC4517092
Scopus ID: 84930402997
  Abstract View: 2482
  PDF Download: 2327

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The Effect of Hypoxia on Mesenchymal Stem Cell Biology

Mostafa Ejtehadifar 1, Karim Shamsasenjan 1,2*, Aliakbar Movassaghpour 1, Parvin Akbarzadehlaleh 3, Nima Dehdilani 1, Parvaneh Abbasi 1, Zahra Molaeipour 1, Mahshid Saleh 1

1 Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Iran Blood Transfusion Research Center, High Institute for Research and Education in Transfusion Medicine, Tabriz, Iran.
3 Drug Applied Research Center and Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran.


Although physiological and pathological role of hypoxia have been appreciated in mammalians for decades however the cellular biology of hypoxia more clarified in the past 20 years. Discovery of the transcription factor hypoxia-inducible factor (HIF)-1, in the 1990s opened a new window to investigate the mechanisms behind hypoxia. In different cellular contexts HIF-1 activation show variable results by impacting various aspects of cell biology such as cell cycle, apoptosis, differentiation and etc. Mesenchymal stem cells (MSC) are unique cells which take important role in tissue regeneration. They are characterized by self-renewal capacity, multilineage potential, and immunosuppressive property. Like so many kind of cells, hypoxia induces different responses in MSCs by HIF-1 activation. The activation of this molecule changes the growth, multiplication, differentiation and gene expression profile of MSCs in their niche by a complex of signals. This article briefly discusses the most important effects of hypoxia in growth kinetics, signalling pathways, cytokine secretion profile and expression of chemokine receptors in different conditions.
Keywords: Hypoxia, Mesenchymal stem cells, Hypoxia-inducible factor, Niche
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Submitted: 08 Jun 2014
Revision: 12 Sep 2014
ePublished: 01 Jun 2015
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