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Original Article

Exp Neurobiol 2018; 27(4): 287-298

Published online August 16, 2018

© The Korean Society for Brain and Neural Sciences

Spatiotemporal Protein Atlas of Cell Death-Related Molecules in the Rat MCAO Stroke Model

Jeong Seon Yoon1,†, Darong Jo2,†, Hye-Sun Lee1, Seung-Wan Yoo1, Tae-Young Lee2, Woo Sup Hwang1, Jung-Mi Choi1, Eunhee Kim3, Sung-Soo Kim1*, and Haeyoung Suh-Kim1,2*

1Department of Anatomy, Ajou University School of Medicine, Suwon 16499, Korea.

2Department of Biomedical Sciences, Ajou Graduate School, Suwon 16499, Korea.

3Department of Biological Sciences and Graduate School of New Drug Discovery and Development, Chungnam National University, Daejeon 34134, Korea.

Correspondence to: *To whom correspondence should be addressed.
Haeyoung Suh-Kim, TEL: 82-31-219-5036, FAX: 82-31-219-5039
Sung-Soo Kim, TEL: 82-31-219-5036, FAX: 82-31-219-5034
These authors contributed equally to this work.

Received: April 26, 2018; Revised: July 25, 2018; Accepted: July 26, 2018

Ischemic stroke and cerebral infarction triggered by the blockage of blood supply can cause damage to the brain via a complex series of pathological changes. Recently, diverse therapies have emerged as promising candidates for the treatment of stroke. These treatments exert therapeutic effects by acting on diverse target molecules and cells in different time windows from the acute to chronic phases. Here, using immunohistochemistry, we show pathophysiological changes in the brain microenvironment at the hyperacute (within 6 h), acute (1~3 days), subacute (7 days), and chronic (1 month) phases following ischemic injury. Ischemic injury in rats was induced by occluding the middle cerebral artery and was validated by magnetic resonance imaging. The progression of damage to the brain was evaluated by immunohistochemistry for NeuN+ neurons, GFAP+ astrocytes, and Iba1+ microglia, and by the emergence of the cell death-related molecules such as AIF, FAF1, and activated caspase-3. Our data regarding the spatial and temporal information on pathophysiological changes may warrant the investigation of the timing of administration of therapeutic treatments in preclinical studies with an animal model of stroke.

Graphical Abstract

Keywords: Brain ischemia, Cell death, Stem cell therapy, Antibody staining, Chronic stroke