Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (heat shock protein-72) and extracellular-signal-regulated-kinase 1/2

B. Liebelt; P. Papapetrou; A. Ali; M. Guo; X. Ji; C. Peng; R. Rogers; A. Curry; D. Jimenez; Y. Ding

doi:10.1016/j.neuroscience.2009.12.067

Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (heat shock protein-72) and extracellular-signal-regulated-kinase 1/2

B. Liebelt, P. Papapetrou, A. Ali, M. Guo, X. Ji, C. Peng, R. Rogers, A. Curry, D. Jimenez, Y. Ding

Department of Neurosurgery

Research output: Contribution to journal › Article › peer-review

96 Scopus citations

Abstract

Exercise preconditioning induces neuroprotection after stroke. We investigated the beneficial role of heat shock protein-70 (HSP-70) and phosphorylated extracellular-signal-regulated-kinase 1/2 (pERK 1/2), as they pertain to reducing apoptosis and their influence on Bcl-x_L, Bax, and apoptosis-inducing factor (AIF) in rats subjected to ischemia and reperfusion. Adult male Sprague-Dawley rats were subjected to 30 min of exercise on a treadmill for 1, 2, or 3 weeks. Stroke was induced by a 2-h middle cerebral artery (MCA) occlusion using an intraluminal filament. Protein levels of HSP-70, pERK 1/2, Bcl-x_L, Bax, and AIF were analyzed using Western blot. Neuroprotection was based on levels of apoptosis (TUNEL) and infarct volume (Nissl staining). Immunocytochemistry was used for cellular expression of HSP-70 and pERK 1/2. Significant (P<0.05) up-regulation of HSP-70 and pERK 1/2 after 3 weeks of exercise coincided with significant (P<0.05) reduction in neuronal apoptosis and brain infarct volume. Inhibition of either one of these two factors showed a significant (P<0.05) reversal in the neuroprotection. Bax and AIF were down-regulated, while levels of Bcl-x_L were up-regulated in response to stroke after exercise. Inhibiting HSP-70 or pERK 1/2 reversed this resultant increase or decrease. Our results indicate that exercise diminishes neuronal injury in stroke by up-regulating HSP-70 and ERK 1/2.

Original language	English (US)
Pages (from-to)	1091-1100
Number of pages	10
Journal	Neuroscience
Volume	166
Issue number	4
DOIs	https://doi.org/10.1016/j.neuroscience.2009.12.067
State	Published - Apr 14 2010

Keywords

MCA occlusion
anti-apoptotic protein
ischemia/reperfusion injury
neuroprotection
pro-apoptotic protein

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/j.neuroscience.2009.12.067

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Liebelt, B., Papapetrou, P., Ali, A., Guo, M., Ji, X., Peng, C., Rogers, R., Curry, A., Jimenez, D., & Ding, Y. (2010). Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (heat shock protein-72) and extracellular-signal-regulated-kinase 1/2. Neuroscience, 166(4), 1091-1100. https://doi.org/10.1016/j.neuroscience.2009.12.067

Liebelt, B, Papapetrou, P, Ali, A, Guo, M, Ji, X, Peng, C, Rogers, R, Curry, A, Jimenez, D & Ding, Y 2010, 'Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (heat shock protein-72) and extracellular-signal-regulated-kinase 1/2', Neuroscience, vol. 166, no. 4, pp. 1091-1100. https://doi.org/10.1016/j.neuroscience.2009.12.067

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abstract = "Exercise preconditioning induces neuroprotection after stroke. We investigated the beneficial role of heat shock protein-70 (HSP-70) and phosphorylated extracellular-signal-regulated-kinase 1/2 (pERK 1/2), as they pertain to reducing apoptosis and their influence on Bcl-xL, Bax, and apoptosis-inducing factor (AIF) in rats subjected to ischemia and reperfusion. Adult male Sprague-Dawley rats were subjected to 30 min of exercise on a treadmill for 1, 2, or 3 weeks. Stroke was induced by a 2-h middle cerebral artery (MCA) occlusion using an intraluminal filament. Protein levels of HSP-70, pERK 1/2, Bcl-xL, Bax, and AIF were analyzed using Western blot. Neuroprotection was based on levels of apoptosis (TUNEL) and infarct volume (Nissl staining). Immunocytochemistry was used for cellular expression of HSP-70 and pERK 1/2. Significant (P<0.05) up-regulation of HSP-70 and pERK 1/2 after 3 weeks of exercise coincided with significant (P<0.05) reduction in neuronal apoptosis and brain infarct volume. Inhibition of either one of these two factors showed a significant (P<0.05) reversal in the neuroprotection. Bax and AIF were down-regulated, while levels of Bcl-xL were up-regulated in response to stroke after exercise. Inhibiting HSP-70 or pERK 1/2 reversed this resultant increase or decrease. Our results indicate that exercise diminishes neuronal injury in stroke by up-regulating HSP-70 and ERK 1/2.",

keywords = "MCA occlusion, anti-apoptotic protein, ischemia/reperfusion injury, neuroprotection, pro-apoptotic protein",

author = "B. Liebelt and P. Papapetrou and A. Ali and M. Guo and X. Ji and C. Peng and R. Rogers and A. Curry and D. Jimenez and Y. Ding",

note = "Funding Information: We are grateful to Mr. Yandong Zhou and Mr. Shane Sprague for their help in preparation of the manuscript. This work was supported partially by an American Heart Association Grant in Aid (to Yuchuan Ding).",

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AU - Liebelt, B.

AU - Papapetrou, P.

AU - Ali, A.

AU - Guo, M.

AU - Ji, X.

AU - Peng, C.

AU - Rogers, R.

AU - Curry, A.

AU - Jimenez, D.

AU - Ding, Y.

N1 - Funding Information: We are grateful to Mr. Yandong Zhou and Mr. Shane Sprague for their help in preparation of the manuscript. This work was supported partially by an American Heart Association Grant in Aid (to Yuchuan Ding).

PY - 2010/4/14

Y1 - 2010/4/14

N2 - Exercise preconditioning induces neuroprotection after stroke. We investigated the beneficial role of heat shock protein-70 (HSP-70) and phosphorylated extracellular-signal-regulated-kinase 1/2 (pERK 1/2), as they pertain to reducing apoptosis and their influence on Bcl-xL, Bax, and apoptosis-inducing factor (AIF) in rats subjected to ischemia and reperfusion. Adult male Sprague-Dawley rats were subjected to 30 min of exercise on a treadmill for 1, 2, or 3 weeks. Stroke was induced by a 2-h middle cerebral artery (MCA) occlusion using an intraluminal filament. Protein levels of HSP-70, pERK 1/2, Bcl-xL, Bax, and AIF were analyzed using Western blot. Neuroprotection was based on levels of apoptosis (TUNEL) and infarct volume (Nissl staining). Immunocytochemistry was used for cellular expression of HSP-70 and pERK 1/2. Significant (P<0.05) up-regulation of HSP-70 and pERK 1/2 after 3 weeks of exercise coincided with significant (P<0.05) reduction in neuronal apoptosis and brain infarct volume. Inhibition of either one of these two factors showed a significant (P<0.05) reversal in the neuroprotection. Bax and AIF were down-regulated, while levels of Bcl-xL were up-regulated in response to stroke after exercise. Inhibiting HSP-70 or pERK 1/2 reversed this resultant increase or decrease. Our results indicate that exercise diminishes neuronal injury in stroke by up-regulating HSP-70 and ERK 1/2.

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KW - pro-apoptotic protein

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Exercise preconditioning reduces neuronal apoptosis in stroke by up-regulating heat shock protein-70 (heat shock protein-72) and extracellular-signal-regulated-kinase 1/2

Abstract

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