CD74-immunoreactive activated M1 microglia are shown late in the gerbil hippocampal CA1 region following transient cerebral ischemia

Abstract

Activated M1 microglia secrete proinflammatory cytokines into damaged brain areas. The present study examined activated M1 microglial morphology and expression in the hippocampal Cornu Ammonis (CA) 1 region, which is vulnerable to transient ischemia. Transient cerebral ischemia was performed for 5 min in gerbils, and neuronal death in the CA1 region following transient cerebral ischemia was confirmed using cresyl violet staining, neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescent staining. In addition, CA1 regions were stained for cluster of differentiation (CD) 74, a marker for activated M1 microglia and a ligand for macrophage migration inhibitory factor In sham-operated animals, no CD74 immunoreactivity was observed in the hippocampal CA1 region. CD74 immunoreactivity was not observed in the hippocampal CA1 region until 3 days post-ischemic insult; however, elevated CD74 immunoreactivity was detected in the CA1 region from 5 days post-ischemia. Double immunofluorescence staining for CD74 and ionized calcium-binding adapter molecule 1, a marker for M1 microglial cells, confirmed the expression of CD74 on this microglial subtype. These results indicated that M1 microglia are activated late in the hippocampal CA1 region following ischemic stroke. Therefore, optimizing the timing of therapeutic intervention may reduce activated M1 microglial-induced neuronal damage.

Comparative Transcriptome Analysis of the Regenerating Zebrafish Telencephalon Unravels a Resource With Key Pathways During Two Early Stages and Activation of Wnt/β-Catenin Signaling at the Early Wound Healing Stage

“…There were 15 KEGG pathways significantly enriched in Y1 ( Figure 3F and Supplementary Table S5 ). The qPCR results confirmed that the regeneration-related DEGs csf1ra and cd74b ( Chitu et al, 2016 ; Hwang et al, 2017 ) were upregulated in the lesioned hemisphere ( Figure 3G ) and mpeg1.1 and gfap ( Kroehne et al, 2011 ; Paredes et al, 2015 ) in both hemispheres ( Figure 3H ). Moreover, we observed a remarkable increase in the number of proliferating cells at the ventricular zone of the telencephalon in the lesioned hemisphere, detected by proliferating cell nuclear antigen (PCNA) antibody staining ( Figures 3I,J ).…”

Modulators of microglia activation and polarization in ischemic stroke (Review)

“…These conclusions were further confirmed in both a bilateral common carotid artery ligation (Bcca) model and a photothrombotic (PT) stroke model. in the hippocampal ca1 region of the Bcca ligation mice, the M1 microglia marker CD74 was observed to be expressed from day 3 post-ischemic insult and elevated from day 5 post-ischemia (45). additionally, CD16 and iNOS expression levels were identified to be increased in infarct regions at day 42 following Bcca (46).…”

YES-10, A Combination of Extracts from Clematis mandshurica RUPR. and Erigeron annuus (L.) PERS., Prevents Ischemic Brain Injury in A Gerbil Model of Transient Forebrain Ischemia

“…The animals were randomly divided into eight groups (n = 7 in each group): (1) and 2were the vehicle/sham and ischemia group: each was treated with vehicle (sterilized normal saline; 0.85% w/v NaCl) and underwent sham and ischemia/reperfusion operation, (3) and (4) were the 50 mg/kg YES-10/sham and ischemia group: each was treated with 50 mg/kg YES-10 and given sham and ischemia/reperfusion operation, (5) and (6) were the 100 mg/kg YES-10/sham and ischemia group: each was treated with 100 mg/kg YES-10 and subjected to sham and ischemia/reperfusion operation and (7) and (8) were the 200 mg/kg YES-10/sham and ischemia group: each was treated with 200 mg/kg YES-10 and undergone sham and ischemia/reperfusion operation. The vehicle/sham group was designated as a control group.…”

“…With occurrence of the reactive gliosis, both pro-inflammatory and anti-inflammatory responses are triggered following ischemic insults [6]. Especially, pro-inflammatory M1 microglia are predominantly increased and distributed in the hippocampal CA1 field when reactive microgliosis occurs due to cerebral ischemia [7]. In addition, a number of studies have described that enhancement of anti-inflammatory responses can prevent neuronal damage following cerebral ischemic insults [8][9][10].…”