Distribution of thrombospondins and their neuronal receptor α2δ1 in the rat retina

Huang, Jufang; Zhou, Lihong; Wang, Hui; Luo, Jiayou; Zeng, Leping; Xiong, Kun; Chen, Dan

doi:10.1016/j.exer.2013.03.012

Cited by 21 publications

(18 citation statements)

References 41 publications

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“…This is in agreement with a recent study that showed that both retinal neurons and glial cells express TSP-1 [22]. As described recently [22], the overall retinal distribution of TSP-1 did not alter after ischemia-reperfusion of the rat retina (fig. 2b).…”

Section: Discussionsupporting

confidence: 81%

“…TSP-1 plays a central role in the immune privilege of the eye [19]. TSPs contribute to neuronal survival, synaptic remodeling, and tissue regeneration after retinal injury [20,21,22]. TSP-1 reduces the severity of retinal inflammation, suppresses microglia activation, and inhibits the formation of retinal neovascular membranes in animal models of retinal ischemia and inflammation [19,21,23,24].…”

Section: Introductionmentioning

confidence: 99%

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Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Yafai¹,

Eichler²,

Iandiev³

et al. 2014

Ophthalmic Res

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Background/Aims: By the release of antiangiogenic factors, Müller glial cells provide an angiostatic environment in the normal and ischemic retina. We determined whether Müller cells produce thrombospondin-1 (TSP-1), a known inhibitor of angiogenesis. Methods: Secretion of TSP-1 by cultured Müller cells was determined with ELISA. Slices of rat retinas and surgically excised retinal membranes of human subjects were immunostained against TSP-1 and the glial marker vimentin. The effects of TSP-1 on the growth of bovine retinal endothelial cells (BRECs) and activation of ERK1/2 were determined with DNA synthesis and migration assays, and Western blotting, respectively. Results: Cultured Müller cells secrete TSP-1 under normoxic and hypoxic (0.2% O₂) conditions. Secretion of TSP-1 was increased in hypoxia compared to normoxia. In rat retinal slices, glial, retinal ganglion, and possibly horizontal cells were stained for TSP-1. Retinal glial cells in preretinal membranes from human subjects with nonhypoxic epiretinal gliosis (macular pucker) and proliferative diabetic retinopathy, respectively, were immunopositive for TSP-1. Exogenous TSP-1 reduced the VEGF-induced proliferation and migration of BRECs and decreased the phosphorylation level of ERK1/2 in BRECs. Conclusion: The data suggest that Müller cells are one major source of TSP-1 in the normal and ischemic retina. Glia-derived TSP1 may inhibit angiogenic responses in the ischemic retina.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Yafai¹,

Eichler²,

Iandiev³

et al. 2014

Ophthalmic Res

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“…41 Previous researches showed that activation of glial cells contributed much to the loss of RGCs of glaucoma retina. [38][39][40][41][42] Inman et al found that in chronic glaucoma model of mice, microglial cell number increased by two-fold. 44 Moreover, minocycline treatment reduced the retina microglial activation in the DBA/2 J mouse model of glaucoma, corresponding to the improved optic nerve integrity.…”

Section: Discussionmentioning

confidence: 96%

“…After washing with 0.01 M phosphate buffered saline (PBS) for 10 min, sections were incubated in blocking solution (5% BSA and 0.3% Triton X-100 in 0.1 M PB) for 1 hr at room temperature. Then the sections were incubated in Age of Rats Affects the Degree of Retinal Damage 301 primary antibodies [36][37][38] (NeuN, 1:1000, Millipore, Billerica, MA; Iba-1, 1:1000, Wako Chemical, Richmond, MA; GFAP, 1:2000, Millipore) overnight at 4 C. On the second day, these sections were washed with 0.01 M PBS for three times and then incubated in the secondary antibodies labeled with fluorescent dyes (1:200, Jackson Immuno research) for 2 hours at room temperature. Through three washes of PBS, these sections were covered with mounting medium with DAPI (vector).…”

Section: Immunofluorescencementioning

confidence: 99%

Age of Rats Seriously Affects the Degree of Retinal Damage Induced by Acute High Intraocular Pressure

Tan

Peng

et al. 2014

Current Eye Research

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“…Correspondingly, it is suggested that under 100 mmHg there is more necrosis cells in RGC-5. In order to be consistent with the conditions in vivo [29], we believed that 100 mmHg insult condition was suitable for the next step of our experiment for necroptosis detection.…”

Section: Resultsmentioning

confidence: 97%

Calpain: a molecule to induce AIF-mediated necroptosis in RGC-5 following elevated hydrostatic pressure

et al. 2014

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BackgroundRIP3 (Receptor-interacting protein 3) pathway was mainly described as the molecular mechanism of necroptosis (programmed necrosis). But recently, non-RIP3 pathways were found to mediate necroptosis. We deliberate to investigate the effect of calpain, a molecule to induce necroptosis as reported (Cell Death Differ 19:245–256, 2012), in RGC-5 following elevated hydrostatic pressure.ResultsFirst, we identified the existence of necroptosis of RGC-5 after insult by using necrostatin-1 (Nec-1, necroptosis inhibitor) detected by flow cytometry. Immunofluorescence staining and western blot were used to detect the expression of calpain. Western blot analysis was carried out to describe the truncated AIF (tAIF) expression with or without pretreatment of ALLN (calpain activity inhibitor). Following elevated hydrostatic pressure, necroptotic cells pretreated with or without ALLN was stained by Annexin V/PI, The activity of calpain was also examined to confirm the inhibition effect of ALLN. The results showed that after cell injury there was an upregulation of calpain expression. Upon adding ALLN, the calpain activity was inhibited, and tAIF production was reduced upon injury along with the decreased number of necroptosis cells.ConclusionOur study found that calpain may induce necroptosis via tAIF-modulation in RGC-5 following elevated hydrostatic pressure.

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Distribution of thrombospondins and their neuronal receptor α2δ1 in the rat retina

Cited by 21 publications

References 41 publications

Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Thrombospondin-1 Is Produced by Retinal Glial Cells and Inhibits the Growth of Vascular Endothelial Cells

Age of Rats Seriously Affects the Degree of Retinal Damage Induced by Acute High Intraocular Pressure

Calpain: a molecule to induce AIF-mediated necroptosis in RGC-5 following elevated hydrostatic pressure

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