alexa Matrix Metalloproteinase-9 Triggers the Gap Junction Im
ISSN: 2167-0501

Biochemistry & Pharmacology: Open Access
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Research Article

Matrix Metalloproteinase-9 Triggers the Gap Junction Impairment and Somatosensory Neuronal Dysfunction in Septic Encephalopathy

Huan Wang1#, Yukio Imamura2,3#*, Naoya Matsumoto2, Nao Yoshikawa4, Junichiro Nakagawa2, Kazuma Yamakawa2, Tomoki Yamada2, Yuki Murakami3, Satoko Mitani3, Takashi Jin5, Hiroshi Ogura2, Takeshi Shimazu2, and Akitoshi Seiyama4
1Institute of Pharmacology, Toxicology and Biochemical Pharmaceutics, Zhejiang University, Hangzhou, China
2Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, Japan
3Unit for Liveable Cities, Kyoto University of Graduate School of Engineering and Medicine, Kyoto, Japan
4Human Health Science, Kyoto University Graduate School of Medicine, Kyoto, Japan
5Laboratory for Nano-bio Probes, Quantitative Biology Center, Japan
#These authors equally contributed to the study
Corresponding Author : Yukio Imamura
Unit for liveable cities
Kyoto University Graduate School of Engineering
and Medicine, Japan
Tel: +81-75-751-3970
Fax: 81-75-751-3970
E-mail: [email protected]
Received November 21, 2012; Accepted December 14, 2012; Published December 17, 2012
Citation: Wang H, Imamura Y, Matsumoto N, Yoshikawa N, Nakagawa J, et al. (2013) Matrix Metalloproteinase-9 Triggers the Gap Junction Impairment and Somatosensory Neuronal Dysfunction in Septic Encephalopathy. Biochem Pharmacol 2:108. doi:10.4172/2167-0501.1000108
Copyright: © 2013 Wang H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Although septic encephalopathy leads to be the devastating neurological symptoms including sensory dysfunction, cognitive impairment and unconsciousness, potent substrates and their effects inducing the synaptic dysfunction remain obscure. In this study, we successfully characterized the sensory dysfunction with immunohistochemistry, immunoblotting and electrophysiology. A mouse model of septic encephalopathy was examined at 20 hrs after cecal ligation and puncture or intraperitoneal injection of lipopolysaccharide (1 mg). We found several effects of active enzyme of matrix metalloproteinases-9 (active MMP-9) on the somatosensory cortex, thalamus and prefrontal cortex related to the sensory functions in septic encephalopathy. At first, active MMP-9 was up-regulated. Second, both of the occludin, tight junction protein composing blood brain barrier, and the connexin-43, transmembrane protein of gap junction, which were potent substrate of active MMP-9, were disrupted. Third, the evoked local field potentials in cortical and thalamic neurons were impeded during sensory neuronal stimulation. Conversely, matrix metalloproteinase inhibitor GM6001 significantly protected the reduction of occludin, connexin-43 and the regression of neuronal activities. In conclusion, MMP-9 is a prerequisite candidate for protection of the junction proteins reduction and for the potent therapeutics in the sensory dysfunction in septic encephalopathy.

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