Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 28, Issue 5, Pages 1009-1016Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.jcbfm.9600600
Keywords
astrocyte; mitochondria; ischemia; oxidative stress; heat shock protein; mortalin
Categories
Funding
- NIGMS NIH HHS [R01 GM049831-13, R01 GM049831, GM49831] Funding Source: Medline
- NINDS NIH HHS [P01 NS037520, P50 NS014543, NS014543, P01 NS037520-080004, P50 NS014543-240018, NS37520, P01 NS014543] Funding Source: Medline
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Mitochondrial heat shock protein 70 (mtHsp70/Hsp75/Grp75/mortalin/TRAP-1/PBP74) is an essential mitochondrial chaperone and a member of the heat shock protein 70 (HSP70) family. Although many studies have shown the protective properties of overexpression of the cytosolic inducible member of the HSP70 family, Hsp72, few studies have investigated the protective potential of Hsp75 against ischemic injury. Mitochondria are one of the primary targets of ischemic injury in astrocytes. In this study, we analyzed the effects of Hsp75 overexpression on cellular levels of reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, and viability during the ischemia-like conditions of oxygen-glucose deprivation (OGD) or glucose deprivation (GD) in primary astrocytic cultures. We show that Hsp75 overexpression decreases ROS production and preserves mitochondrial membrane potential during GD, and preserves ATP levels and cell viability during OGD. These findings indicate that Hsp75 can provide protection against ischemia-like in vitro injury and suggest that it should be further studied as a potential candidate for protection against ischemic injury.
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