Published Online
on June 5, 2003

A more recent version of this article appeared on July 1, 2003

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Submitted on January 13, 2003
Accepted on February 11, 2003

Different Expression Patterns of Bcl-2, Bcl-xl, and Bax Proteins After Sublethal Forebrain Ischemia in C57Black/Crj6 Mouse Striatum

Chaoran Wu MD^*; Hideyoshi Fujihara MD, PhD; Jian Yao MD, PhD; Sihua Qi MD, PhD; Huiping Li MD; Koki Shimoji MD, PhD; and Hiroshi Baba MD, PhD

From the Departments of Anesthesiology (C.W., H.B.), Cellular Physiology (J.Y.), Structural Pathology, and Institute of Nephrology (H.L.), Niigata University School of Medicine, Niigata; Department of Anesthesiology and Reanimatology, Fukui Medical University, Fukui (H.F.); Department of Anesthesiology, 2nd Affiliated Hospital, Harbin Medical University (S.Q.), Harbin; and Department of Human Sociology, Ube Frontier University (K.S.), Ube, Japan.

^* To whom correspondence should be addressed. E-mail: wcrmail{at}med.niigata-u.ac.jp.

Background and Purpose--Ischemic injury in neurons can be strongly reduced by a preceding sublethal ischemic episode, of which the mechanism is poorly understood. Although changes in the expression of apoptosis-related proteins (Bcl-2, Bcl-xl, and Bax) have been considered to be crucially important in ischemic injury, the roles these proteins play in ischemic preconditioning induced by sublethal forebrain ischemia have not been elucidated. Therefore, we investigated the transcription and expression of Bcl-2, Bcl-xl, and Bax in striatum of mice subjected to sublethal forebrain ischemia and lethal ischemia, with or without ischemic preconditioning.

Methods--Sublethal forebrain ischemia was induced in C57Black/Crj6 (C57BL/6) mice by 6 minutes of bilateral common carotid artery occlusion. The transcription and expression of Bcl-2 family genes were detected by reverse transcription-polymerase chain reaction, Western blot, and immunofluorescent staining.

Results--No detectable neuronal loss was induced in striatum by 6 minutes of bilateral common carotid artery occlusion. Transcription and expression of Bcl-2 and Bcl-xl were increased after sublethal forebrain ischemia, which attenuated the DNA fragmentation induced by lethal ischemia. The transcription and expression of Bax remained unchanged.

Conclusions--Upregulation of Bcl-2 and Bcl-xl but not Bax may have a role in protective ischemic preconditioning. This result indicates a potential strategy for further ischemic neuronal injury therapies.

Key words: cerebral ischemia • ischemic preconditioning • neuroprotection • proto-oncogene proteins c-bcl-2 • mice

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