Influence of hypoxia on apoptosis and glucose intake in bone marrow derived mesenchymal stem cells in rats.
- Author:
Wei-Wei ZHANG
1
;
Hong-Liang KONG
;
Zhang-Quan LI
Author Information
1. Department of Angiocardiology, Shengjing Hospital, China Medical University, Shenyang 110003, Liaoning Province, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
physiology;
Bone Marrow Cells;
cytology;
Cell Hypoxia;
Cells, Cultured;
Female;
Glucose;
metabolism;
Male;
Mesenchymal Stromal Cells;
metabolism;
pathology;
Rats;
Rats, Wistar
- From:
Journal of Experimental Hematology
2008;16(3):593-597
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effects of hypoxia on the apoptosis and glucose intake of mesenchymal stem cells (MSCs), MSCs derived from bone marrow of rats were incubated in the atmosphere of 1% O(2) for a series of time points and their glucose-intaking capacity, ultrastructural changes and apoptotic proportions were analyzed by (3)H-labeling assay, electron microscopy and flow cytometry, respectively. The results showed that the cultured cells took the fibroblast-like morphology and could be induced into osteoblasts and adipocytes under appropriate conditions. The proportions of apoptotic cells after hypoxia treatment for 1, 4 and 8 hours were 13.7 +/- 2.26%, 14.1 +/- 2.78% and 14.7 +/- 4.01%, respectively, all of which were significantly higher than that observed in normoxic counterparts (0.09 +/- 2.03%, p < 0.05). Also, cell death occurred after hypoxia treatment and the death rates were 3.11 +/- 2.14%, 4.72 +/- 2.05% and 4.91 +/- 3.72% for 1, 4 and 8 hours incubation respectively. Under hypoxia culture in vitro, cell membrane microvillus began to fall off and the mitochondrias became swelling at 1 hour, and the above changes increasingly aggravated along with hypoxia time prolongation. The (3)H-glucose intaking ratios of MSCs at different hypoxia time points significantly decreased than those in normoxic cells (p < 0.01). It is concluded that the acute hypoxia can induce down-regulation of glucose-intaking capacity, ultrastructural changes and apoptosis of MSCs.
