Loss of hsp70.1 Decreases Functional Motor Recovery after Spinal Cord Injury in Mice

Hyun Jeong Kim; Ji-In Jung; Youngkyung Kim; Jae-Seon Lee; Young Wook Yoon; Junesun Kim

doi:10.4196/kjpp.2010.14.3.157

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Kim, Jung, Kim, Lee, Yoon, and Kim: Loss of hsp70.1 Decreases Functional Motor Recovery after Spinal Cord Injury in Mice

Original Article

Korean J Physiol Pharmacol 2010;14(3):157-161.

Published online: 18 February 2010

DOI: https://doi.org/10.4196/kjpp.2010.14.3.157

Loss of hsp70.1 Decreases Functional Motor Recovery after Spinal Cord Injury in Mice

Hyun Jeong Kim¹, Ji-In Jung², Youngkyung Kim², Jae-Seon Lee⁴, Young Wook Yoon², Junesun Kim^3,

¹Department of Dental Anesthesiology and Dental Research Institute, Seoul National University School of Dentistry, Seoul 110-744, Korea

²Department of Physiology, Korea University College of Medicine, Seoul 136-705, Korea

³Department of Physical Therapy, Korea University College of Health Science, Seoul 136-703, Korea

⁴Divisions of Radiation Cancer Research and Korea Institute of Radiological and Medical Sciences, Seoul 139-706, Korea

Corresponding to: Junesun Kim, Department of Physical Therapy, Korea University College of Health Science, 1, Jungneung-3-dong, Sungbuk-gu, Seoul 136-703, Korea. (Tel) 82-2-940-2834, (Fax) 82-2-940-2830, (E-mail) junokim@korea.ac.kr

Received 6 May 2010 Revised 18 May 2010 Accepted 19 May 2010

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Heat shock proteins (HSPs) are specifically induced by various forms of stress. Hsp70.1, a member of the hsp70 family is known to play an important role in cytoprotection from stressful insults. However, the functional role of Hsp70 in motor function after spinal cord injury (SCI) is still unclear. To study the role of hsp70.1 in motor recovery following SCI, we assessed locomotor function in hsp70.1 knockout (KO) mice and their wild-type (WT) mice via the Basso, Beattie and Bresnahan (BBB) locomotor rating scale, before and after spinal hemisection at T13 level. We also examined lesion size in the spinal cord using Luxol fast blue/cresyl violet staining. One day after injury, KO and WT mice showed no significant difference in the motor function due to complete paralysis following spinal hemisection. However, when it compared to WT mice, KO mice had significantly delayed and decreased functional outcomes from 4 days up to 21 days after SCI. KO mice also showed significantly greater lesion size in the spinal cord than WT mice showed at 21 days after spinal hemisection. These results suggest that Hsp70 has a protective effect against traumatic SCI and the manipulation of the hsp70.1 gene may help improve the recovery of motor function, thereby enhancing neuroprotection after SCI.

Keywords: Spinal cord injury, Neuroprotection, Heat shock protein, Mice

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Fig. 1.

Motor recovery of hindlimb. Hindlimb motor function on the contralateral (A) and the ipsilateral side (B) was evaluated before SCI and on days 1, 4, 7, 10, 13, 17 and 21 after SCI. Asterisks indicate the values significantly different between the two groups (^∗p<0.05).

Fig. 2.

A representative section of spinal cord segment including epicenter in WT (A) and KO (B) mice. Longitudinal spinal cord sections double-stained with Luxol fast blue and cresyl violet show the injury and atrophy area. The lesion size is significantly different between WT and KO mice (C) (^∗p<0.05). Scale bars, 400 μm.

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