Changes and expressions of Redd1 in neurons and glial cells in the gerbil hippocampus proper following transient global cerebral ischemia

Molecular Medicine Reports

Lee

et al. 2017

Self Cite

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.

“…Immunohistochemistry was performed out according to a previously published procedure (28). In brief, sections were incubated with mouse anti-neuronal nuclear antigen (NeuN; cat.…”

Section: Methodsmentioning

confidence: 99%

“…To examine the colocalization of CD74 and I1, the sections were processed by double immunofluorescence staining according to a previously published procedure (28). Briefly, sections were incubated with mouse anti-CD74 (cat.…”

Section: Methodsmentioning

confidence: 99%

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

Hwang

Molecular Medicine Reports

Lee

et al. 2017

Self Cite

“…The surgical procedure for transient cerebral ischemia was performed as previously described (22). In brief, the animals were anesthetized with a mixture of 2.5% isoflurane in 33% oxygen and 67% nitrous oxide.…”

Section: Methodsmentioning

confidence: 99%

“…Sections were prepared from the sham and ischemia-operated animals (n=7 at each time-point) at 2 and 4 days after reperfusion, according to the previously published procedure (22). In brief, the animals were perfused transcardially with 4% paraformaldehyde in 0.1 M phosphate-buffer (pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

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Transient cerebral ischemia induces albumin expression in microglia only in the CA1 region of the gerbil hippocampus

Molecular Medicine Reports

Ahn

et al. 2017

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Albumin, the most abundant plasma protein, is known to exhibit a neuroprotective effect in animal models of focal and global cerebral ischemia. In the present study, the expression and immunoreactivity of albumin was examined in the hippocampus following 5 min of transient cerebral ischemia in gerbils. Albumin immunoreactivity was observed in microglia of the CA1 hippocampal region 2 days post-ischemic insult, and it was significantly increased at 4 days following ischemia-reperfusion. In addition, at 4 days post-ischemic insult, albumin-immunoreactive microglia were abundant in the stratum pyramidale of the CA1 region. The present results demonstrated that albumin was newly expressed post-injury in microglia in the CA1 region, suggesting ischemia-induced neuronal loss. Albumin expression may therefore be associated with ischemia-induced delayed neuronal death in the CA1 region following transient cerebral ischemia.

Early IV-injected human dermis-derived mesenchymal stem cells after transient global cerebral ischemia do not pass through damaged blood-brain barrier

Ahn

Chen

et al. 2018

J Tissue Eng Regen Med

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There is lack of researches on effects of intravenously injected mesenchymal stem cells (MSCs) against transient cerebral ischemia (TCI). We investigated the disruption of the neurovascular unit (NVU), which comprises the blood-brain barrier and examined entry of human dermis-derived MSCs (hDMSCs) into the damaged hippocampal CA1 area in a gerbil model of TCI and their subsequent effects on neuroprotection and cognitive function. Impairments of neurons and blood-brain barrier were examined by immunohistochemistry, electron microscopy, and Evans blue and immunoglobulin G leakage. Neuronal death was observed in pyramidal neurons 5-day postischemia. NVU were structurally damaged; in particular, astrocyte end-feet were severely damaged from 2-day post-TCI and immunoglobulin G leaked out of the CA1 area 2 days after 5 min of TCI; however, Evans blue extravasation was not observed. On the basis of the results of NVU damages, ischemic gerbils received PKH2-transfected hDMSCs 3 times at early times (3 hr, 2, and 5 days) after TCI, and fluorescence imaging was used to detect hDMSCs in the tissue. PKH2-transfected hDMSCs were not found in the CA1 from immediate time to 8 days after injection, although they were detected in the liver. Furthermore, hDMSCs transplantation did not protect CA1 pyramidal neurons and did not improve cognitive impairment. Intravenously transplanted hDMSCs did not migrate to the damaged CA1 area induced by TCI. These findings suggest no neuroprotection and cognitive improvement by intravenous hDMSCs transplantation after 5 min of TCI.