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Ischemic preconditioning maintains the immunoreactivities of glucokinase and glucokinase regulatory protein in neurons of the gerbil hippocampal CA1 region following transient cerebral ischemia.

Cho YS, Cho JH, Shin BN, Cho GS, Kim IH, Park JH, Ahn JH, Ohk TG, Cho BR, Kim YM, Hong S, Won MH, Lee JC - Mol Med Rep (2015)

Bottom Line: In the ischemia‑operated group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) at 5 days post‑ischemia; however, in the IPC+ischemia‑operated group, the neurons in the SP were well protected.Following immunohistochemical investigation, the immunoreactivities of GK and GKRP in the neurons of the SP were markedly decreased in the CA1, but not the CA2/3, from 2 days post‑ischemia, and were almost undetectable in the SP 5 days post‑ischemia.In brief, the findings of the present study demonstrated that IPC notably maintained the immunoreactivities of GK and GKRP in the neurons of the SP of CA1 following ischemia‑reperfusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.

ABSTRACT
Glucokinase (GK) is involved in the control of blood glucose homeostasis. In the present study, the effect of ischemic preconditioning (IPC) on the immunoreactivities of GK and its regulatory protein (GKRP) following 5 min of transient cerebral ischemia was investigated in gerbils. The gerbils were randomly assigned to four groups (sham‑operated group, ischemia‑operated group, IPC + sham‑operated group and IPC + ischemia‑operated group). IPC was induced by subjecting the gerbils to 2 min of ischemia, followed by 1 day of recovery. In the ischemia‑operated group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) at 5 days post‑ischemia; however, in the IPC+ischemia‑operated group, the neurons in the SP were well protected. Following immunohistochemical investigation, the immunoreactivities of GK and GKRP in the neurons of the SP were markedly decreased in the CA1, but not the CA2/3, from 2 days post‑ischemia, and were almost undetectable in the SP 5 days post‑ischemia. In the IPC + ischemia‑operated group, the immunoreactivities of GK and GKRP in the SP of the CA1 were similar to those in the sham‑group. In brief, the findings of the present study demonstrated that IPC notably maintained the immunoreactivities of GK and GKRP in the neurons of the SP of CA1 following ischemia‑reperfusion. This indicated that GK and GKRP may be necessary for neuron survival against transient cerebral ischemia.

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Immunohistochemistry to determine the expression of GK in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups 1, 2 and 5 days following ischemia-reperfusion. GK immunoreactivity was readily detected in the SP in the sham group. GK immunoreactivity in the SP was decreased from 2 days post-ischemia, and GK immunoreactivity was markedly decreased (*) 5 days post-ischemia. However, in the IPC-operated sham- and IPC + ischemia-operated groups, GK immunoreactivity was markedly increased in the SP of CA1, and was maintained until 5 days post-ischemia. Scale bar=50 µm. GK, glucokinase; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum; IPC, ischemic preconditioning.
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f3-mmr-12-04-4939: Immunohistochemistry to determine the expression of GK in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups 1, 2 and 5 days following ischemia-reperfusion. GK immunoreactivity was readily detected in the SP in the sham group. GK immunoreactivity in the SP was decreased from 2 days post-ischemia, and GK immunoreactivity was markedly decreased (*) 5 days post-ischemia. However, in the IPC-operated sham- and IPC + ischemia-operated groups, GK immunoreactivity was markedly increased in the SP of CA1, and was maintained until 5 days post-ischemia. Scale bar=50 µm. GK, glucokinase; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum; IPC, ischemic preconditioning.

Mentions: In the sham group, marked GK immunoreactivity was detected in neurons of the SP of the CA1-3 regions (Table II; Fig. 3A). In the ischemia group, GK immunoreactivity was altered in the CA1 region, but not in the CA2/3 region. At 1 day-post ischemia-reperfusion, GK immunoreactivity in the SP was not significantly different, compared with that in the sham group (Table II; Fig. 3B). However, GK immunoreactivity in the SP was distinctively decreased 2 days after ischemia-reperfusion (Table II; Fig. 3C). At 5 days-post ischemia-reperfusion, GK immunoreactivity was almost undetected in the pyramidal neurons of the SP (Table II; Fig. 3D). However, in the CA2/3 region, no significant changes in GK immunoreactivity were observed following ischemia-reperfusion (Table II).


Ischemic preconditioning maintains the immunoreactivities of glucokinase and glucokinase regulatory protein in neurons of the gerbil hippocampal CA1 region following transient cerebral ischemia.

Cho YS, Cho JH, Shin BN, Cho GS, Kim IH, Park JH, Ahn JH, Ohk TG, Cho BR, Kim YM, Hong S, Won MH, Lee JC - Mol Med Rep (2015)

Immunohistochemistry to determine the expression of GK in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups 1, 2 and 5 days following ischemia-reperfusion. GK immunoreactivity was readily detected in the SP in the sham group. GK immunoreactivity in the SP was decreased from 2 days post-ischemia, and GK immunoreactivity was markedly decreased (*) 5 days post-ischemia. However, in the IPC-operated sham- and IPC + ischemia-operated groups, GK immunoreactivity was markedly increased in the SP of CA1, and was maintained until 5 days post-ischemia. Scale bar=50 µm. GK, glucokinase; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum; IPC, ischemic preconditioning.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581829&req=5

f3-mmr-12-04-4939: Immunohistochemistry to determine the expression of GK in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups 1, 2 and 5 days following ischemia-reperfusion. GK immunoreactivity was readily detected in the SP in the sham group. GK immunoreactivity in the SP was decreased from 2 days post-ischemia, and GK immunoreactivity was markedly decreased (*) 5 days post-ischemia. However, in the IPC-operated sham- and IPC + ischemia-operated groups, GK immunoreactivity was markedly increased in the SP of CA1, and was maintained until 5 days post-ischemia. Scale bar=50 µm. GK, glucokinase; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum; IPC, ischemic preconditioning.
Mentions: In the sham group, marked GK immunoreactivity was detected in neurons of the SP of the CA1-3 regions (Table II; Fig. 3A). In the ischemia group, GK immunoreactivity was altered in the CA1 region, but not in the CA2/3 region. At 1 day-post ischemia-reperfusion, GK immunoreactivity in the SP was not significantly different, compared with that in the sham group (Table II; Fig. 3B). However, GK immunoreactivity in the SP was distinctively decreased 2 days after ischemia-reperfusion (Table II; Fig. 3C). At 5 days-post ischemia-reperfusion, GK immunoreactivity was almost undetected in the pyramidal neurons of the SP (Table II; Fig. 3D). However, in the CA2/3 region, no significant changes in GK immunoreactivity were observed following ischemia-reperfusion (Table II).

Bottom Line: In the ischemia‑operated group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) at 5 days post‑ischemia; however, in the IPC+ischemia‑operated group, the neurons in the SP were well protected.Following immunohistochemical investigation, the immunoreactivities of GK and GKRP in the neurons of the SP were markedly decreased in the CA1, but not the CA2/3, from 2 days post‑ischemia, and were almost undetectable in the SP 5 days post‑ischemia.In brief, the findings of the present study demonstrated that IPC notably maintained the immunoreactivities of GK and GKRP in the neurons of the SP of CA1 following ischemia‑reperfusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, Gangwon 200‑701, Republic of Korea.

ABSTRACT
Glucokinase (GK) is involved in the control of blood glucose homeostasis. In the present study, the effect of ischemic preconditioning (IPC) on the immunoreactivities of GK and its regulatory protein (GKRP) following 5 min of transient cerebral ischemia was investigated in gerbils. The gerbils were randomly assigned to four groups (sham‑operated group, ischemia‑operated group, IPC + sham‑operated group and IPC + ischemia‑operated group). IPC was induced by subjecting the gerbils to 2 min of ischemia, followed by 1 day of recovery. In the ischemia‑operated group, a significant loss of neurons was observed in the stratum pyramidale (SP) of the hippocampal CA1 region (CA1) at 5 days post‑ischemia; however, in the IPC+ischemia‑operated group, the neurons in the SP were well protected. Following immunohistochemical investigation, the immunoreactivities of GK and GKRP in the neurons of the SP were markedly decreased in the CA1, but not the CA2/3, from 2 days post‑ischemia, and were almost undetectable in the SP 5 days post‑ischemia. In the IPC + ischemia‑operated group, the immunoreactivities of GK and GKRP in the SP of the CA1 were similar to those in the sham‑group. In brief, the findings of the present study demonstrated that IPC notably maintained the immunoreactivities of GK and GKRP in the neurons of the SP of CA1 following ischemia‑reperfusion. This indicated that GK and GKRP may be necessary for neuron survival against transient cerebral ischemia.

Show MeSH
Related in: MedlinePlus