Activation of the Mitochondrial Apoptotic Pathway in a Rat Model of Central Retinal Artery Occlusion

Zhang, Yi; Cho, Chang-Ho; Atchaneeyasakul, La-ongsri; McFarland, T.J.; Appukuttan, Binoy; Stout, J. Timothy

doi:10.1167/iovs.04-1235

Cited by 59 publications

(38 citation statements)

References 40 publications

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“…A previous study on animals showed that the correlation of the ERGs and histological changes with the residual retinal circulation variables was not significant [8]. However, in good agreement with the report by Machida et al [11], who found that the PhNR was the most affected wave following a CRAO, our results showed that the PhNR was significantly reduced in eyes with CRAO.…”

Section: Discussionsupporting

confidence: 91%

“…The RGCs are more vulnerable to ischemia and suffer irreversible damage soon after an occlusion, which is supported by histopathologic findings showing apoptotic changes in this layer [8]. The photopic negative response (PhNR) of the photopic ERG which originates from the neural activity of the RGCs has been used to assess the function of RGCs in experimental animals [9, 10] and in humans with retinal and optic nerve pathology [10,11,12,13,14,15].…”

Section: Introductionmentioning

confidence: 78%

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Photopic Negative Response Reflects Severity of Ocular Circulatory Damage after Central Retinal Artery Occlusion

et al. 2009

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Purpose: To determine the relationship of the photopic negative response (PhNR) of the photopic electroretinogram (ERG) with the degree of circulatory disturbances in eyes following central retinal artery occlusion (CRAO). Methods: The circulatory disturbance was graded as mild (group 1) when the arm-to-retina transmission time was <30 s, moderate (group 2) when the time was >30 s and severe (group 3) when concurrent choroidal circulatory damage was found. For statistical analysis, groups 1, 2 and 3 were scored as 1, 2 and 3, respectively. Photopic ERGs were elicited by either short-flash (SF) or long-flash (LF) stimuli. Results: Both the SF and LF PhNR were significantly reduced in groups 2 and 3. The PhNR amplitude was negatively correlated with the severity of the ocular circulatory disturbances (p = 0.0498, ρ = –0.507 for SF PhNR; p = 0.0050, ρ = –0.750 for LF PhNR). Conclusion: The amplitude of the PhNR became more reduced as the severity of the circulatory disturbances increased in eyes with CRAO.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 78%

Photopic Negative Response Reflects Severity of Ocular Circulatory Damage after Central Retinal Artery Occlusion

et al. 2009

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“…One study revealed that cells in the inner retina especially RGCs are more vulnerable to ischemic damage compared to cells of the outer retina (19). Apoptosis, as detected by TUNEL staining, has been observed in the GCL, INL, and outer nuclear layer of the retina (20). Apoptosis of the ganglion cells is progressive and irreversible (20); therefore, anti-apoptosis therapy in retinal ischemic diseases may be beneficial to improve retinal functions.…”

Section: Discussionmentioning

confidence: 99%

“…Apoptosis, as detected by TUNEL staining, has been observed in the GCL, INL, and outer nuclear layer of the retina (20). Apoptosis of the ganglion cells is progressive and irreversible (20); therefore, anti-apoptosis therapy in retinal ischemic diseases may be beneficial to improve retinal functions. ReIran Red Crescent Med J.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-33 Prevents Retinal Ischemia Reperfusion Injury in Rats by Preventing Apoptosis

Xing

Yang

et al. 2016

Iran Red Crescent Med J

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Background: Retinal ischemia reperfusion (RIR) injury is a common pathological process that can result in visual impairment in many ophthalmic diseases. Inflammation and apoptosis play an important role in RIR injury. Objectives: This experimental study was designed to explore the ability of a new cytokine, IL-33, to attenuate RIR injury via an apoptosis-inhibitory mechanism. Methods: From June, 2015 to October, 2015, 40 Sprague-Dawley (SD) rats from Wuhan university in China were divided into the following four groups: normal control group (NCG), RIR injury model group (MG), IL-33 pretreatment group (IL-33), and PBS group

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“…[9][10][11] Other common mechanisms include altered aquaporin expression, 12,13 oxidative stress, 14,15 and increases in proapoptotic and decreases in antiapoptotic markers. 16,17 Increased inflammation occurs in both conditions, including increased activation of glial cells and macrophages, 18,19 increased levels of inflammatory cytokines (IL-6, TNF-a, and so on), 20,21 and nuclear factor kappa-light-chain-enhancer of active B cells (NF-jB) pathway activation. 22,23 The high degree of mechanistic overlap, as well as the presence of central nervous system tissue in both cerebral and retinal/optic nerve ischemia, could allow for treatment crossover between diseases.…”

mentioning

confidence: 99%

Progesterone Treatment in Two Rat Models of Ocular Ischemia

Allen

Olsen

Sayeed

et al. 2015

Invest. Ophthalmol. Vis. Sci.

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Citation: Allen RS, Olsen TW, Sayeed I, et al. Progesterone treatment in two rat models of ocular ischemia. Invest Ophthalmol Vis Sci. 2015;56:2880-2891. DOI:10.1167/iovs.14-16070 PURPOSE. To determine whether the neurosteroid progesterone, shown to have protective effects in animal models of traumatic brain injury, stroke, and spinal cord injury, is also protective in ocular ischemia animal models.METHODS. Progesterone treatment was tested in two ocular ischemia models in rats: a rodent anterior ischemic optic neuropathy (rAION) model, which induces permanent monocular optic nerve stroke, and the middle cerebral artery occlusion (MCAO) model, which causes transient ischemia in both the retina and brain due to an intraluminal filament that blocks the ophthalmic and middle cerebral arteries. Visual function and retinal histology were assessed to determine whether progesterone attenuated retinal injury in these models. Additionally, behavioral testing and 2% 2,3,5-triphenyltetrazolium chloride (TTC) staining in brains were used to compare progesterone's neuroprotective effects in both retina and brain using the MCAO model. RESULTS.Progesterone treatment showed no effect on visual evoked potential (VEP) reduction and retinal ganglion cell loss in the permanent rAION model. In the transient MCAO model, progesterone treatment reduced (1) electroretinogram (ERG) deficits, (2) MCAO-induced upregulation of glutamine synthetase (GS) and glial fibrillary acidic protein (GFAP), and (3) retinal ganglion cell loss. As expected, progesterone treatment also had significant protective effects in behavioral tests and a reduction in infarct size in the brain. CONCLUSIONS.Progesterone treatment showed protective effects in the retina following MCAO but not rAION injury, which may result from mechanistic differences with injury type and the therapeutic action of progesterone.

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Activation of the Mitochondrial Apoptotic Pathway in a Rat Model of Central Retinal Artery Occlusion

Cited by 59 publications

References 40 publications

Photopic Negative Response Reflects Severity of Ocular Circulatory Damage after Central Retinal Artery Occlusion

Photopic Negative Response Reflects Severity of Ocular Circulatory Damage after Central Retinal Artery Occlusion

Interleukin-33 Prevents Retinal Ischemia Reperfusion Injury in Rats by Preventing Apoptosis

Progesterone Treatment in Two Rat Models of Ocular Ischemia

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