Reaction of Müller cells after increased intraocular pressure in the rat retina

Kim, I.-B.; Kim, K.-Y.; Ck, Joo; Lee, M.-Y.; Oh, Su-Ja; Chung, Jin-Woong; Chun, Myung-Hoon

doi:10.1007/s002210050476

Cited by 81 publications

(33 citation statements)

References 16 publications

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“…Up to 3 days, strong immunoreactivity is appeared in some Mü ller cells, and then appeared in photoreceptor cells. Previous studies have shown that transient retinal ischemia results in progressive degeneration of retinal neurons over a period of several weeks which is more pronounced in the inner retina at earlier stages, while a marked loss of photoreceptors occurs at later stages (Bü chi et al, 1991;Kim et al, 1998;Ju et al, 2000). Thus, upregulation of clusterin expression follows the time course of retinal cell damage in the ischemic retina.…”

Section: Discussionmentioning

confidence: 86%

Expression of clusterin in Müller cells of the rat retina after pressure‐induced ischemia

Gwon¹,

Kim²,

Lee³

et al. 2004

Glia

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We have investigated the expression and cellular localization of clusterin in the rat retina following ischemia induced by transiently increasing the intraocular pressure. In the normal retina, weak clusterin immunoreactivity was visible in Müller cell profiles located in the inner nuclear layer. Following ischemia and reperfusion, strong immunoreactivity appeared in Müller cell somata and processes up to 3 days postlesion. Quantitative evaluation by immunoblotting confirmed that clusterin expression continuously increased and showed a peak value at 3 days after ischemic injury (to 1300% of control levels), and then decreased again to 400% of controls at 4 weeks postlesion. Immunocytochemistry using antisera against clusterin or glutamine synthase combined with the TUNEL method or immunocytochemistry using antisera activated caspase 3 and electron microscopy revealed that some clusterin-labeled Müller cells underwent apoptotic cell death. Our findings demonstrate that some Müller cells die by apoptosis, and suggest that clusterin produced and released by Müller cell may play an important role in the pathogenesis of ischemic injury in the rat retina.

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Section: Discussionmentioning

confidence: 86%

Expression of clusterin in Müller cells of the rat retina after pressure‐induced ischemia

Gwon¹,

Kim²,

Lee³

et al. 2004

Glia

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“…Neuronal cell death in the retinal ganglion cell layer (GCL) is observed as pyknotic nuclei in the GCL [25]. Glial activation is evident by up-regulation of glial fibrillary acidic protein (GFAP) in response to deleterious release of glutamate from over excited neurons after ischemia [6,7]. Retinal edema also occurs, because of the increased water transportation and accumulation as a result of increased extracellular fluid volume, increased aquaporin 4 (AQP4) immunoreactivity and swelling of retinal glial cells [8,9].…”

mentioning

confidence: 99%

Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

Liu

Yeung

Cheng

et al. 2015

Sci. China Life Sci.

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Ischemia occurs in diabetic retinopathy with neuronal loss, edema, glial cell reactivity and oxidative stress. Epacs, consisting of Epac1 and Epac2, are cAMP mediators playing important roles in maintenance of endothelial barrier and neuronal functions. To investigate the roles of Epacs in the pathogenesis of ischemic retinopathy, transient middle cerebral artery occlusion (tMCAO) was performed on Epac1-deficient (Epac1  ) mice, Epac2-deficient (Epac2  ) mice, and their wild type counterparts (Epac1 +/+ and Epac2). Two-hour occlusion and 22-hour reperfusion were conducted to induce ischemia/reperfusion injury to the retina. After tMCAO, the contralateral retinae displayed similar morphology between different genotypes. Neuronal loss, retinal edema and increase in immunoreactivity for aquaporin 4 (AQP4), glial fibrillary acidic protein (GFAP), peroxiredoxin 6 (Prx6) were observed in ipsilateral retinae. Epac2  ipsilateral retinae showed more neuronal loss in retinal ganglion cell layer, increased retinal thickness and stronger immunostaining of AQP4, GFAP, and Prx6 than those of Epac2 However, Epac1 ipsilateral retinae displayed similar pathology as those in Epac1 +/+ mice. Our observations suggest that Epac2-deficiency led to more severe ischemic retinopathy after retinal ischemia/reperfusion injury. Epac, retina, ischemia, retinopathyCitation: Liu J, Yeung PKK, Cheng L, Lo ACY, Chung SSM, Chung SK. Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy.

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“…5), and this effect was blocked by glibenclamide. Müller glial cell activation and increased GFAP expression are general phenomenon observed in ischemic-damaged neuronal tissues (28). Diazoxide, a K ATP -channel opener, reduced the activation of glial cells in brain ischemia.…”

Section: Discussionmentioning

confidence: 97%

KR-31378, a Potassium-Channel Opener, Induces the Protection of Retinal Ganglion Cells in Rat Retinal Ischemic Models

Choi¹,

Choi²,

Yoon³

et al. 2009

J Pharmacol Sci

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Abstract. KR-31378 is a newly developed K ATP -channel opener. To investigate the ability of KR-31378 to protect retinal ganglion cells (RGC), experiments were conducted using two retinal ischemia models. Retinal ischemia was induced by transient high intraocular pressure (IOP) for acute ischemia and by three episcleral vein occlusion for chronic retinal ischemia. KR-31378 was injected intraperitoneally and administered orally in the acute and chronic ischemia models, respectively. Under the condition of chronic ischemia, RGC density in the KR-31378-treated group was statistically higher than that in the non-treated group, and IOP was reduced. In the acute retinal ischemia model, 90% of RGC were degenerated after one week in non-treated retina, but, RGC in KR-31378-treated retina were protected from ischemic damage in a dosedependent manner and showed inhibited glial fibrillary acidic protein (GFAP) expression. Furthermore, the KR-31378 protective effect was inhibited by glibenclamide treatment in acute ischemia. These findings indicate that systemic KR-31378 treatment may protect against ischemic injury-induced ganglion cell loss in glaucoma.

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Reaction of Müller cells after increased intraocular pressure in the rat retina

Cited by 81 publications

References 16 publications

Expression of clusterin in Müller cells of the rat retina after pressure‐induced ischemia

Expression of clusterin in Müller cells of the rat retina after pressure‐induced ischemia

Epac2-deficiency leads to more severe retinal swelling, glial reactivity and oxidative stress in transient middle cerebral artery occlusion induced ischemic retinopathy

KR-31378, a Potassium-Channel Opener, Induces the Protection of Retinal Ganglion Cells in Rat Retinal Ischemic Models

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