Caspase-Dependent Apoptosis of Retinal Ganglion Cells During the Development of Diabetic Retinopathy

Adamiec-Mroczek, Joanna; Zając-Pytrus, H; Misiuk-Hojło, Marta

doi:10.17219/acem/31805

Cited by 42 publications

(22 citation statements)

References 29 publications

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“…One group [33] found that this lack of arterial vasoconstrictor capacity was attributed to an alteration of nitric oxide production and bioavailability, whereas others [17] suggest that the overall reduced dilatory and constriction response could serve as an estimate of endothelial cell capacity to respond to a physiological stimulus. Furthermore, one study examining DM patients with varying severity of retinopathy demonstrated ganglion cell death with increasing severity of the retinopathy [35]. Our finding of more adverse endothelial markers in DM + CVD versus the other groups is in keeping with accepted pathophysiology [36, 37].…”

Section: Discussionsupporting

confidence: 85%

Retinal vessel diameters and reactivity in diabetes mellitus and/or cardiovascular disease

Heitmar

Lip

Ryder

et al. 2017

Cardiovasc Diabetol

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BackgroundRetinal vessel calibre and vascular dilation/constriction in response to flicker light provocation may provide a measure distinguishing patients suffering from diabetes mellitus and/or cardiovascular disease.MethodsOne hundred and sixteen age and sex matched patients with diabetes mellitus (DM), cardiovascular disease (CVD) and both DM and CVD (DM + CVD) underwent systemic and intraocular pressure measurements. Retinal vessel calibres were assessed using a validated computer-based program to compute central retinal artery and vein equivalents (CRVE) from monochromatic retinal images. Vessel dilation and constriction responses to flicker light provocation were assessed by continuous retinal vessel diameter recordings. Plasma endothelial markers von Willebrand factor (vWf) and soluble E selectin (sEsel) were measured by ELISA.ResultsRetinal vessel calibres were comparable across groups but CRVE correlated significantly with disease duration in DM patients (r = 0.57, p < 0.001). Patients suffering DM only exhibited reduced arterial vasomotion at rest and reduced arterial constriction following flicker light induced vessel dilation compared to patients with CVD and those suffering both CVD + DM (p = 0.030). Patients suffering from CVD + DM exhibited significant differences between each flicker cycle in regards to arterial maximum constriction (p = 0.006) and time needed to reach arterial maximum dilation (p = 0.004), whereas the other two groups did not show such inconsistencies between individual flicker cycles. vWf was raised in CVD + DM compared to the other two groups (p ≤ 0.02), whilst sEsel was raised in CVD + DM compared to DM alone (p = 0.044).ConclusionsDynamic retinal vascular calibres as obtained by continuous diameter measurements using flicker light provocation can reveal subtle differences between groups suffering from CVD with and without DM. This difference in reaction pattern and lack of arterial constriction in DM may provide a suitable marker to monitor progression.

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Section: Discussionsupporting

confidence: 85%

Retinal vessel diameters and reactivity in diabetes mellitus and/or cardiovascular disease

Heitmar

Lip

Ryder

et al. 2017

Cardiovasc Diabetol

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“…BCL family and caspases are prominent for the apoptosis. MCL-1 is one gene in BCL family, which inhibits caspase-3 and prohibits apoptosis [23]. In our study, we verified that hippocampal MCL-1 was down-regulated, while Caspase-3 was increased after diabetic modeling.…”

Section: Discussionsupporting

confidence: 71%

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

Wang

Fang

Zhen

et al. 2016

Cell Physiol Biochem

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Background/Aims: To explore the effects of sulforaphane (SFN) on neuronal apoptosis in hippocampus and memory impairment in diabetic rats. Methods: Thirty male rats were randomly divided into normal control, diabetic model and SFN treatment groups (N = 10 in each group). Streptozotocin (STZ) was applied to establish diabetic model. Water Morris maze task was applied to test learning and memory. Tunel assaying was used to detect apoptosis in hippocampus. The expressions of Caspase-3 and myeloid cell leukemia 1(MCL-1) were detected by western blotting. Neurotrophic factor levels and AKT/GSK3β pathway were also detected. Results: Compared with normal control, learning and memory were apparently impaired, with up-regulation of Caspase-3 and down-regulation of MCL-1 in diabetic rats. Apoptotic neurons were also found in CA1 region after diabetic modeling. By contrast, SFN treatment prevented the memory impairment, decreased the apoptosis of hippocampal neurons. SFN also attenuated the abnormal expression of Caspase-3 and MCL-1 in diabetic model. Mechanically, SFN treatment reversed diabetic modeling-induced decrease of p-Akt, p-GSK3β, NGF and BDNF expressions. Conclusion: SFN could prevent the memory impairment and apoptosis of hippocampal neurons in diabetic rat. The possible mechanism was related to the regulation of neurotropic factors and Akt/GSK3β pathway.

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“…These pathways promote oxidative stress [Gurler et al, ; Kowluru and Chan, ], vascular dysfunction and the appearance of pro‐inflammatory cytokines, such tumor necrosis factor (TNF‐ α), interleukin‐6 (IL‐6), and interleukin‐1 beta (IL‐1β). Curiously, changes of glial cells are also often connected with early stages of the disease [Adamiec‐Mroczek et al, ]. Therefore, diabetic retinopathy can be considered a neurovascular disease.…”

Section: Diabetic Retinopathymentioning

confidence: 99%

Angiogenesis and Inflammation Crosstalk in Diabetic Retinopathy

Capitão

Soares

2016

J of Cellular Biochemistry

263

190

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Diabetic retinopathy (DR) is one of the most prevalent microvascular complications of diabetes and one of the most frequent causes of blindness in active age. Etiopathogenesis behind this important complication is related to several biochemical, hemodynamic and endocrine mechanisms with a preponderant initial role assumed by polyol pathways, increment of growth factors, accumulation of advanced glycation end products (AGE), activation of protein kinase C (PKC), activation of the renin-angiotensin-aldosterone system (RAAS), and leukostasis. Chronic and sustained hyperglycemia works as a trigger to the early alterations that culminate in vascular dysfunction. Hypoxia also plays an essential role in disease progression with promotion of neovascularization and vascular dystrophies with vitreous hemorrhages induction. Thus, the accumulation of fluids and protein exudates in ocular cavities leads to an opacity augmentation of the cornea that associated to neurodegeneration results in vision loss, being this a devastating characteristic of the disease final stage. During disease progression, inflammatory molecules are produced and angiogenesis occur. Furthermore, VEGF is overexpressed by the maintained hyperglycemic environment and up-regulated by tissue hypoxia. Also pro-inflammatory mediators regulated by cytokines, such as tumor necrosis factor (TNF-α) and interleukin-1 beta (IL-1β), and growth factors leads to the progression of these processes, culminating in vasopermeability (diabetes macular edema) and/or pathological angiogenesis (proliferative diabetic retinopathy). It was found a mutual contribution between inflammation and angiogenesis along the process. J. Cell. Biochem. 117: 2443-2453, 2016. © 2016 Wiley Periodicals, Inc.

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Caspase-Dependent Apoptosis of Retinal Ganglion Cells During the Development of Diabetic Retinopathy

Cited by 42 publications

References 29 publications

Retinal vessel diameters and reactivity in diabetes mellitus and/or cardiovascular disease

Retinal vessel diameters and reactivity in diabetes mellitus and/or cardiovascular disease

Sulforaphane Prevents Neuronal Apoptosis and Memory Impairment in Diabetic Rats

Angiogenesis and Inflammation Crosstalk in Diabetic Retinopathy

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