Articles

  • the Korean Society for Brain and Neural Sciences

Article

Original Article

Exp Neurobiol 2016; 25(2): 64-71

Published online April 30, 2016

https://doi.org/10.5607/en.2016.25.2.64

© The Korean Society for Brain and Neural Sciences

Induction of Nerve Injury-Induced Protein 1 (Ninjurin 1) in Myeloid Cells in Rat Brain after Transient Focal Cerebral Ischemia

Hye-Kyung Lee1,2, Hahnbie Lee1,2, Lidan Luo1,2 and Ja-Kyeong Lee1,2*

1Department of Anatomy, Inha University School of Medicine, 2Medical Research Center, Inha University School of Medicine, Incheon, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-32-890-0913, FAX: 82-32-884-2105
e-mail: jklee@inha.ac.kr

Received: March 24, 2016; Revised: April 13, 2016; Accepted: April 15, 2016

Abstract

Nerve injury-induced protein-1 (Ninjurin-1, Ninj1) was initially identified as a novel adhesion molecule in rat sciatic nerve and to be up-regulated in neurons and Schwann cells of distal nerve segments after nerve transection or crush injury. Recently, Ninj1 was found to act as a modulator of cell migration, angiogenesis, and apoptosis. Accumulating evidence indicates that innate immune response plays beneficial and deleterious roles in brain ischemia, and the trans-endothelial migration of blood-derived immune cells is key initiator of this response. In the present study, we examined the expression profile and cellular distribution of Ninj1 in rat brain after transient focal cerebral ischemia. Ninj1 expression was found to be significantly induced in cortical penumbras 1 day after 60 min of middle cerebral artery occlusion (MCAO) and to increase gradually for 8 days and then declined. In infarction cores of cortices, patterns of Ninj1 expression were similar to those observed in cortical penumbras, except induction was maintained for 10 days. At 1 day post-MCAO, Ninj1 inductions were detected mainly in neutrophils and endothelial cells in both infarction cores and penumbras, but reactive macrophages were the major cellular expressers of Ninj1 at 4 days post-MCAO. Expressional induction in reactive macrophages was maintained in infarction cores after 12 days post-MCAO but not in penumbras. These dynamic expressions of Ninj1 in different immune cells at different times suggest that this protein performs various, critical roles in the modulation of acute and delayed immune responses in the postischemic brain.

Keywords: Ninjurin 1, MCAO, myeloid cells, induction