2007NeuropathologyRequires access

Amplified expression of uncoupling proteins in human brain ischemic lesions

Taizen Nakase, Yasuji Yoshida, Ken Nagata

Open publisher page 44 citations

Abstract

Uncoupling proteins (UCPs) are reported to regulate mitochondrial respiration and energy metabolism during hibernation. Recently, it has been reported that UCP2 and UCP5 might reduce free radical stress in the ischemic condition in in vitro models, suggesting both as potential neuroprotective agents. We therefore investigated the levels of UCP2 and UCP5 expression in the lesion of human brain infarction. Brain slice sections were prepared from pathological samples collected at our hospital. Embolic stroke brains sectioned because of the stroke (n = 5) and multiple brain infarction with several stroke episodes (n = 4) were selected for this study. We observed the amount of UCP2 and UCP5 expression in both lesioned and intact areas, and compared them between embolic stroke and multiple infarction cases. The results showed that the expression of UCP2 and UCP5 was significantly elevated in the ischemic lesions compared to the intact area. UCP5 expression in the lesions was higher in multiple infarction cases than in embolic stroke cases. In conclusion, brains may respond to neuroprotection through the increased expression of UCP2 and UCP5 under ischemic conditions. Moreover, UCP5 may respond to repetitive ischemic stresses or have a long-term effect.

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What this paper is about

Uncoupling proteins (UCPs) are reported to regulate mitochondrial respiration and energy metabolism during hibernation. Recently, it has been reported that UCP2 and UCP5 might reduce free radical stress in the ischemic condition in in vitro models, suggesting both as potential neuroprotective agents. We therefore investigated the levels of UCP2 and UCP5 expression in the lesion of human brain infarction. Brain slice sections were prepared from pathological samples collected at our hospital. Embolic stroke brains sectioned because of the stroke (n = 5) and multiple brain infarction with several stroke episodes (n = 4) were selected for this study. We observed the amount of UCP2 and UCP5 expression in both lesioned and intact areas, and compared them between embolic stroke and multiple infarction cases. The results showed that the expression of UCP2 and UCP5 was significantly elevated in the ischemic lesions compared to the intact area. UCP5 expression in the lesions was higher in multiple infarction cases than in embolic stroke cases. In conclusion, brains may respond to neuroprotection through the increased expression of UCP2 and UCP5 under ischemic conditions. Moreover, UCP5 may respond to repetitive ischemic stresses or have a long-term effect.

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Available abstract

Uncoupling proteins (UCPs) are reported to regulate mitochondrial respiration and energy metabolism during hibernation. Recently, it has been reported that UCP2 and UCP5 might reduce free radical stress in the ischemic condition in in vitro models, suggesting both as potential neuroprotective agents. We therefore investigated the levels of UCP2 and UCP5 expression in the lesion of human brain infarction. Brain slice sections were prepared from pathological samples collected at our hospital. Embolic stroke brains sectioned because of the stroke (n = 5) and multiple brain infarction with several stroke episodes (n = 4) were selected for this study. We observed the amount of UCP2 and UCP5 expression in both lesioned and intact areas, and compared them between embolic stroke and multiple infarction cases. The results showed that the expression of UCP2 and UCP5 was significantly elevated in the ischemic lesions compared to the intact area. UCP5 expression in the lesions was higher in multiple infarction cases than in embolic stroke cases. In conclusion, brains may respond to neuroprotection through the increased expression of UCP2 and UCP5 under ischemic conditions. Moreover, UCP5 may respond to repetitive ischemic stresses or have a long-term effect.

Key concepts: Neuroprotection, Stroke (engine), Brain infarction, Medicine, Pathological, Infarction, Lesion, Ischemia

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