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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 for GKRP in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups following sham surgery and 1, 2 and 5 days post-ischemia-reperfusion. GKRP immunoreactivity was readily detected in the SP in the sham-group. GKRP immunoreactivity in the SP was marginally decreased 2 days after ischemia-reperfusion. At 5 days post-ischemia, GKRP immunoreactivity was almost undetectable in the SP. At 5 days post- ischemia-reperfusion, marked GKRP immunoreactivity was observed in non-pyramidal cells (arrows) of the SO and SR. In the IPC + sham and IPC + ischemia groups, GKRP immunoreactivity was similar to that in the sham group. Scale Bar=50 µm. GKRP, glucokinase regulatory protein; IPC, ischemic preconditioning; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum.
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f4-mmr-12-04-4939: Immunohistochemistry for GKRP in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups following sham surgery and 1, 2 and 5 days post-ischemia-reperfusion. GKRP immunoreactivity was readily detected in the SP in the sham-group. GKRP immunoreactivity in the SP was marginally decreased 2 days after ischemia-reperfusion. At 5 days post-ischemia, GKRP immunoreactivity was almost undetectable in the SP. At 5 days post- ischemia-reperfusion, marked GKRP immunoreactivity was observed in non-pyramidal cells (arrows) of the SO and SR. In the IPC + sham and IPC + ischemia groups, GKRP immunoreactivity was similar to that in the sham group. Scale Bar=50 µm. GKRP, glucokinase regulatory protein; IPC, ischemic preconditioning; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum.

Mentions: In the sham group, marked GKRP immunoreactivity was detected, predominantly in the SP of the CA1-3 regions. In this group, moderate GKRP immunoreactivity was observed in cells of the strata oriens and radiatum (Table II; Fig. 4A). In the ischemia groups, GKRP immunoreactivity was altered in the CA1 region, but notin the CA2/3 region. At 1 day post-ischemia-reperfusion, no change in GKRP immunoreactivity was observed in the SP of the CA1 region, compared with that in the sham group (Table II; Fig. 4B). However, GKRP immunoreactivity in the SP was marginally decreased 2 days after ischemia-reperfusion (Table II; Fig. 4C). At 5 days post-ischemia-reperfusion, GKRP immunoreactivity was notably decreased in the SP of the CA1 region; however, at this time-point, marked GKRP immunoreactivity was observed in several non-pyramidal cells in the strata oriens and radiatum (Table II; Fig. 4D). In the CA2/3 region, no significant changes were identified in GKRP immunoreactivity 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 for GKRP in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups following sham surgery and 1, 2 and 5 days post-ischemia-reperfusion. GKRP immunoreactivity was readily detected in the SP in the sham-group. GKRP immunoreactivity in the SP was marginally decreased 2 days after ischemia-reperfusion. At 5 days post-ischemia, GKRP immunoreactivity was almost undetectable in the SP. At 5 days post- ischemia-reperfusion, marked GKRP immunoreactivity was observed in non-pyramidal cells (arrows) of the SO and SR. In the IPC + sham and IPC + ischemia groups, GKRP immunoreactivity was similar to that in the sham group. Scale Bar=50 µm. GKRP, glucokinase regulatory protein; IPC, ischemic preconditioning; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4-mmr-12-04-4939: Immunohistochemistry for GKRP in the CA1 region of the (A–D) ischemia and (E–H) IPC + ischemia groups following sham surgery and 1, 2 and 5 days post-ischemia-reperfusion. GKRP immunoreactivity was readily detected in the SP in the sham-group. GKRP immunoreactivity in the SP was marginally decreased 2 days after ischemia-reperfusion. At 5 days post-ischemia, GKRP immunoreactivity was almost undetectable in the SP. At 5 days post- ischemia-reperfusion, marked GKRP immunoreactivity was observed in non-pyramidal cells (arrows) of the SO and SR. In the IPC + sham and IPC + ischemia groups, GKRP immunoreactivity was similar to that in the sham group. Scale Bar=50 µm. GKRP, glucokinase regulatory protein; IPC, ischemic preconditioning; SP, stratum pyramidale; SO; stratum oriens, SR; stratum radiatum.
Mentions: In the sham group, marked GKRP immunoreactivity was detected, predominantly in the SP of the CA1-3 regions. In this group, moderate GKRP immunoreactivity was observed in cells of the strata oriens and radiatum (Table II; Fig. 4A). In the ischemia groups, GKRP immunoreactivity was altered in the CA1 region, but notin the CA2/3 region. At 1 day post-ischemia-reperfusion, no change in GKRP immunoreactivity was observed in the SP of the CA1 region, compared with that in the sham group (Table II; Fig. 4B). However, GKRP immunoreactivity in the SP was marginally decreased 2 days after ischemia-reperfusion (Table II; Fig. 4C). At 5 days post-ischemia-reperfusion, GKRP immunoreactivity was notably decreased in the SP of the CA1 region; however, at this time-point, marked GKRP immunoreactivity was observed in several non-pyramidal cells in the strata oriens and radiatum (Table II; Fig. 4D). In the CA2/3 region, no significant changes were identified in GKRP immunoreactivity 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