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Novel protective role of HSP72‐mediated exercise preconditioning against spinal cord injury in rats
Author(s) -
Lin MaoTsun,
Chang ChingPing
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.677.13
Subject(s) - spinal cord , spinal cord injury , heat shock protein , medicine , apoptosis , astrocyte , central nervous system , neuroscience , anesthesia , chemistry , biology , biochemistry , gene , psychiatry
The heat shock protein 72 (HSP72) is a universal marker of stress protein whose expression can be induced by physical exercise. Here we report that, in a localized model of spinal cord injury (SCI), exercise rats (given pre‐SCI exercise) had significantly higher levels of neuronal and astroglial HSP72, a lower functional deficit, fewer spinal cord contusions, and fewer apoptotic cells than did non‐exercise rats. pSUPER plasmid expressing hsp72 small interfering RNA ( siRNA‐hsp72 ) was injected into the injured spinal cord. In addition to reducing neuronal and astroglial HSP72, the ( siRNA‐hsp72 ) significantly attenuated the beneficial effects of exercise preconditioning in reducing functional deficits as well as spinal cord contusion and apoptosis. Because exercise preconditioning induces increased neuronal and astroglial levels of HSP72 in the gray matter of normal spinal cord tissue, exercise preconditioning promoted functional recovery in rats after SCI by upregulating neuronal and astroglial HSP72 in the gray matter of the injured spinal cord. We reveal an important function of neuronal and astroglial HSP72 on protecting neuronal and astroglial apoptosis in the injured spinal cord. We conclude that HSP72‐mediated exercise preconditioning is a promising strategy for facilitating functional recovery from SCI.