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Background and purpose

HSPA12B is a newly discovered member of the Hsp70 family proteins. This study investigated the effects of HSPA12B on focal cerebral ischemia/reperfusion (I/R) injury in mice.

Methods

Transgenic mice overexpressing human HSPA12B (Tg) and wild-type littermates (WT) were subjected to 60 min of middle cerebral artery occlusion to induce ischemia and followed by reperfusion (I/R). Neurological deficits, infarct volumes and neuronal death were examined at 6 and 24hrs after reperfusion. Blood-brain-barrier (BBB) integrity and activated cellular signaling were examined at 3 hrs after reperfusion.

Results

After cerebral I/R, Tg mice exhibited improvement in neurological deficits and decrease in infarct volumes, when compared with WT I/R mice. BBB integrity was significantly preserved in Tg mice following cerebral I/R. Tg mice also showed significant decreases in cell injury and apoptosis in the ischemic hemispheres. We observed that overexpression of HSPA12B activated PI3K/Akt signaling and suppressed JNK and p38 activation following cerebral I/R. Importantly, pharmacological inhibition of PI3K/Akt signaling abrogated the protection against cerebral I/R injury in Tg mice.

Conclusions

The results demonstrate that HSPA12B protects the brains from focal cerebral I/R injury. The protective effect of HSPA12B is mediated though a PI3K/Akt-dependent mechanism. Our results suggest that HSPA12B may have a therapeutic potential against ischemic stroke."xsd:string
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http://purl.uniprot.org/citations/23046810http://purl.uniprot.org/core/author"Li C."xsd:string
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http://purl.uniprot.org/citations/23046810http://purl.uniprot.org/core/author"Liu L."xsd:string
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http://purl.uniprot.org/citations/23046810http://purl.uniprot.org/core/author"Ding Z."xsd:string
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http://purl.uniprot.org/citations/23046810http://purl.uniprot.org/core/name"Biochim Biophys Acta"xsd:string
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http://purl.uniprot.org/citations/23046810http://purl.uniprot.org/core/title"Overexpression of HSPA12B protects against cerebral ischemia/reperfusion injury via a PI3K/Akt-dependent mechanism."xsd:string
http://purl.uniprot.org/citations/23046810http://purl.uniprot.org/core/volume"1832"xsd:string
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