Selective accumulation of adiponectin in the cerebral cortex under chronic cerebral hypoperfusion in the rat

Yu Takahashi, Hideaki Wakita, Kenmei Mizutani, Atsushi Watanabe, Shigeru Sonoda, Hidekazu Tomimoto

研究成果: Article

抜粋

Adiponectin is a plasma protein predominantly derived from adipocytes. Adiponectin has beneficial properties against diabetes, cardiovascular diseases, and cancer. In experimental acute cerebral ischemia, adiponectin accumulates on vessels in ischemic lesions and has anti-inflammatory protective effects. Chronic cerebral hypoperfusion is associated with white matter lesions and risk of dementia. Chronic cerebral hypoperfusion induced by permanent occlusion of the bilateral common carotid artery can experimentally produce cerebrovascular white matter lesions in the rat brain. Microglia are activated shortly after ischemia and correlate with the severity of white matter and hippocampal tissue damage. These data suggest that the inflammatory response selectively increases white matter and hippocampal damage during chronic cerebral hypoperfusion. However, factors protecting the cerebral cortex have not been elucidated. To clarify the role of adiponectin, we investigated possible changes in adiponectin and adiponectin receptor 1 (ADR1) in the brains of rats under chronic cerebral hypoperfusion. Adiponectin accumulated on the vessels predominantly in the cerebral cortex under chronic cerebral hypoperfusion. Adiponectin accumulation was not detected in the white matter or hippocampus. In the cerebral cortex, the number of ADR1-immunopositive vessels was increased, and adiponectin was colocalized with ADR1. It is plausible that accumulation of adiponectin may be mediated by the binding of adiponectin to ADR1, and its accumulation in the cerebral cortex may protect tissue injury by inhibiting inflammation under chronic cerebral hypoperfusion.

元の言語English
ページ(範囲)148-155
ページ数8
ジャーナルNeuroreport
31
発行部数2
DOI
出版物ステータスPublished - 27-01-2020

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All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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