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Endothelial proliferation modulates neuron-glia survival and differentiation in ischemic stress.

Michael OO, Gbolahan BW, Ansa CE, Abdulbasitand A, Azeez IO - Ann Neurosci (2015)

Bottom Line: The increase in CD45 expression coupled with a reduced CD31/GFAP after the withdrawal phase was evident of vascular remodeling and neurosurvival.The VO-I showed a significant increase in vascular remodelling than the CN-I due to a more significant increase in monocytic expression (CD45) after the withdrawal of the occlusion.Generally, we found that degeneration was prominent in the parietal cortex and less in the periventricular zone for both forms of ischemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, College of Medicine and Health Sciences, AfeBabalola University, Ekiti State Ado-Ekiti, Nigeria.

ABSTRACT

Background: Recent studies have shown that endothelial proliferation and angiogenic response are characteristic of degenerative events, such that the magnitude of endothelial activation is reflective of the progression of neurodegeneration.

Purpose: This study sets out to, compare, the degenerative changes seen in the parietal cortex (PC) and periventricular zone (PVZ) after cyanide toxicity or vascular occlusion.

Methods: Global vascular occlusion (VO) and cyanide toxicity (CN) were induced in separate sets of male adult wistar rats for 10 days (treatment phase). Subsequently, the treatment was discontinued for another 10 days (withdrawal phase) (CN-I and VO-I). A separate group of control was maintained for 10 days and received normal saline for this duration. The animals were euthanized at day 10 (treatment and control) and day 20 (withdrawal) after which the tissue was processed for antigen retrieval immunohistochemistry to demonstrate; H&E (general histology) CD31/PECAM 1(endothelial proliferation), CD45 (monocyte/phagocyte), GFAP (glia), NSE (neuron), Ki-67 (cell proliferation) and NF (neurofilament). Total cell count, immunopositive cell counts, arterial wall thickness and lumen width were determined and plotted using ANOVA with significance set at P<0.05*.

Results: We observed an increase in endothelial proliferation (↑CD31), glia activation and a decrease in neuron count in vascular occlusion and cyanide toxicity after the treatment phase (degeneration). The neuron count increased (↑NSE) after withdrawal of cyanide treatment and vascular occlusion and was accompanied by a corresponding decrease in endothelial and glia activation (↓CD31/GFAP). Degenerative changes were more prominent in cyanide toxicity when compared with vascular occlusion. The increase in CD45 expression coupled with a reduced CD31/GFAP after the withdrawal phase was evident of vascular remodeling and neurosurvival.

Conclusion: We conclude that neuronal degeneration in cyanide toxicity or vascular occlusion is dependent on an increase in endothelial proliferation (↑CD31), glia activation (↑GFAP) and a decrease in monocyte expression (↓CD45); representing a pro-inflammatory response. Furthermore, cyanide toxicity induced more prominent degenerative changes when compared with the vascular occlusion due to a higher CD31/GFAP expression. Subsequent withdrawal of the ischemia facilitated a reduction in GFAP/CD31 with a corresponding increase in monocytes (↑CD45) for vascular remodeling and neurosurvival. The VO-I showed a significant increase in vascular remodelling than the CN-I due to a more significant increase in monocytic expression (CD45) after the withdrawal of the occlusion. Generally, we found that degeneration was prominent in the parietal cortex and less in the periventricular zone for both forms of ischemia.

No MeSH data available.


Related in: MedlinePlus

Distribution of NSE in the PC and PVZ. The γ-enolase was shown in IHC using anti rat-NSE to demonstrate the metabolic switch from α-enolase in oxidative stress or neurogenesis in the PC and PVZ (A) a reduction in NSE (+) cell count was observed after the treatment phase in vascular occlusion (P<0.001) when compared with the control (B) surprisingly, the withdrawal group of vascular occlusion (VO-I) showed no significant change in NSE (+) cell count in the PVZ and recorded a reduction in NSE (+) in the PC (P<0.05) versus the control (D) Cyanide treatment withdrawal group showed a good yield in NSE (+) cell count both in the PC (8) and the PVZ (29) (P<0.001) when compared with VO/ VO-I (E) Control group PVZ and PC showing the distribution of NSE positive cells in the molecular layer of the PC and the outer border of the PVZ (Magnification X400) (F) Bar chart representing the score for anti-NSE positive cell distribution in the PC and PVZ (Mean±SEM).
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fig_4: Distribution of NSE in the PC and PVZ. The γ-enolase was shown in IHC using anti rat-NSE to demonstrate the metabolic switch from α-enolase in oxidative stress or neurogenesis in the PC and PVZ (A) a reduction in NSE (+) cell count was observed after the treatment phase in vascular occlusion (P<0.001) when compared with the control (B) surprisingly, the withdrawal group of vascular occlusion (VO-I) showed no significant change in NSE (+) cell count in the PVZ and recorded a reduction in NSE (+) in the PC (P<0.05) versus the control (D) Cyanide treatment withdrawal group showed a good yield in NSE (+) cell count both in the PC (8) and the PVZ (29) (P<0.001) when compared with VO/ VO-I (E) Control group PVZ and PC showing the distribution of NSE positive cells in the molecular layer of the PC and the outer border of the PVZ (Magnification X400) (F) Bar chart representing the score for anti-NSE positive cell distribution in the PC and PVZ (Mean±SEM).

Mentions: The importance of neuronal metabolism in determining the significance of glia activation and other cellular changes associated with cyanide toxicity and vascular occlusion is important. Neuron specific enolase (NSE), a gamma enolase, expressed in immature neurons, early in neurogenesis, and adult neurons in oxidative stress was labelled in the PC to demonstrate neuron specific oxidative stress, and to distinguish neurons from glia cells. We observed a decrease in NSE immunopositive cell count after the treatment phase [VO (3; Figure 4A) and CN (2; Figure 4C)] and an increase after the withdrawal phase (Figure 4B; Table 1). The most significant change in NSE expression was observed in the cyanide treatment group, such that the withdrawal (CN-I; 8) recorded NSE scores four times the treatment (CN; 2) (Figure 4C, 4D and 4F). All the treatments and withdrawal groups recorded NSE scores significantly lower than the control value (10; Figure 4 E).


Endothelial proliferation modulates neuron-glia survival and differentiation in ischemic stress.

Michael OO, Gbolahan BW, Ansa CE, Abdulbasitand A, Azeez IO - Ann Neurosci (2015)

Distribution of NSE in the PC and PVZ. The γ-enolase was shown in IHC using anti rat-NSE to demonstrate the metabolic switch from α-enolase in oxidative stress or neurogenesis in the PC and PVZ (A) a reduction in NSE (+) cell count was observed after the treatment phase in vascular occlusion (P<0.001) when compared with the control (B) surprisingly, the withdrawal group of vascular occlusion (VO-I) showed no significant change in NSE (+) cell count in the PVZ and recorded a reduction in NSE (+) in the PC (P<0.05) versus the control (D) Cyanide treatment withdrawal group showed a good yield in NSE (+) cell count both in the PC (8) and the PVZ (29) (P<0.001) when compared with VO/ VO-I (E) Control group PVZ and PC showing the distribution of NSE positive cells in the molecular layer of the PC and the outer border of the PVZ (Magnification X400) (F) Bar chart representing the score for anti-NSE positive cell distribution in the PC and PVZ (Mean±SEM).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4481556&req=5

fig_4: Distribution of NSE in the PC and PVZ. The γ-enolase was shown in IHC using anti rat-NSE to demonstrate the metabolic switch from α-enolase in oxidative stress or neurogenesis in the PC and PVZ (A) a reduction in NSE (+) cell count was observed after the treatment phase in vascular occlusion (P<0.001) when compared with the control (B) surprisingly, the withdrawal group of vascular occlusion (VO-I) showed no significant change in NSE (+) cell count in the PVZ and recorded a reduction in NSE (+) in the PC (P<0.05) versus the control (D) Cyanide treatment withdrawal group showed a good yield in NSE (+) cell count both in the PC (8) and the PVZ (29) (P<0.001) when compared with VO/ VO-I (E) Control group PVZ and PC showing the distribution of NSE positive cells in the molecular layer of the PC and the outer border of the PVZ (Magnification X400) (F) Bar chart representing the score for anti-NSE positive cell distribution in the PC and PVZ (Mean±SEM).
Mentions: The importance of neuronal metabolism in determining the significance of glia activation and other cellular changes associated with cyanide toxicity and vascular occlusion is important. Neuron specific enolase (NSE), a gamma enolase, expressed in immature neurons, early in neurogenesis, and adult neurons in oxidative stress was labelled in the PC to demonstrate neuron specific oxidative stress, and to distinguish neurons from glia cells. We observed a decrease in NSE immunopositive cell count after the treatment phase [VO (3; Figure 4A) and CN (2; Figure 4C)] and an increase after the withdrawal phase (Figure 4B; Table 1). The most significant change in NSE expression was observed in the cyanide treatment group, such that the withdrawal (CN-I; 8) recorded NSE scores four times the treatment (CN; 2) (Figure 4C, 4D and 4F). All the treatments and withdrawal groups recorded NSE scores significantly lower than the control value (10; Figure 4 E).

Bottom Line: The increase in CD45 expression coupled with a reduced CD31/GFAP after the withdrawal phase was evident of vascular remodeling and neurosurvival.The VO-I showed a significant increase in vascular remodelling than the CN-I due to a more significant increase in monocytic expression (CD45) after the withdrawal of the occlusion.Generally, we found that degeneration was prominent in the parietal cortex and less in the periventricular zone for both forms of ischemia.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, College of Medicine and Health Sciences, AfeBabalola University, Ekiti State Ado-Ekiti, Nigeria.

ABSTRACT

Background: Recent studies have shown that endothelial proliferation and angiogenic response are characteristic of degenerative events, such that the magnitude of endothelial activation is reflective of the progression of neurodegeneration.

Purpose: This study sets out to, compare, the degenerative changes seen in the parietal cortex (PC) and periventricular zone (PVZ) after cyanide toxicity or vascular occlusion.

Methods: Global vascular occlusion (VO) and cyanide toxicity (CN) were induced in separate sets of male adult wistar rats for 10 days (treatment phase). Subsequently, the treatment was discontinued for another 10 days (withdrawal phase) (CN-I and VO-I). A separate group of control was maintained for 10 days and received normal saline for this duration. The animals were euthanized at day 10 (treatment and control) and day 20 (withdrawal) after which the tissue was processed for antigen retrieval immunohistochemistry to demonstrate; H&E (general histology) CD31/PECAM 1(endothelial proliferation), CD45 (monocyte/phagocyte), GFAP (glia), NSE (neuron), Ki-67 (cell proliferation) and NF (neurofilament). Total cell count, immunopositive cell counts, arterial wall thickness and lumen width were determined and plotted using ANOVA with significance set at P<0.05*.

Results: We observed an increase in endothelial proliferation (↑CD31), glia activation and a decrease in neuron count in vascular occlusion and cyanide toxicity after the treatment phase (degeneration). The neuron count increased (↑NSE) after withdrawal of cyanide treatment and vascular occlusion and was accompanied by a corresponding decrease in endothelial and glia activation (↓CD31/GFAP). Degenerative changes were more prominent in cyanide toxicity when compared with vascular occlusion. The increase in CD45 expression coupled with a reduced CD31/GFAP after the withdrawal phase was evident of vascular remodeling and neurosurvival.

Conclusion: We conclude that neuronal degeneration in cyanide toxicity or vascular occlusion is dependent on an increase in endothelial proliferation (↑CD31), glia activation (↑GFAP) and a decrease in monocyte expression (↓CD45); representing a pro-inflammatory response. Furthermore, cyanide toxicity induced more prominent degenerative changes when compared with the vascular occlusion due to a higher CD31/GFAP expression. Subsequent withdrawal of the ischemia facilitated a reduction in GFAP/CD31 with a corresponding increase in monocytes (↑CD45) for vascular remodeling and neurosurvival. The VO-I showed a significant increase in vascular remodelling than the CN-I due to a more significant increase in monocytic expression (CD45) after the withdrawal of the occlusion. Generally, we found that degeneration was prominent in the parietal cortex and less in the periventricular zone for both forms of ischemia.

No MeSH data available.


Related in: MedlinePlus