Hyperglycemia induces early upregulation of the calcium sensor KChIP3/DREAM/calsenilin in the rat retina

Chavira-Suárez, Erika; Sandoval, Alejandro; Quintero, Heberto; Bustamante, Prisca; Felix, Ricardo; Lamas, Marta

doi:10.1016/j.bbrc.2012.01.048

Cited by 5 publications

(3 citation statements)

References 35 publications

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“… 2012 ; Chavira-Suárez et al. 2012 ). The organelles in retinal Müller cells may be damaged under long-term hyperglycaemia, and changes in cell ultrastructure can stimulate Müller cell activation and cause dysfunction (Abu El-Asrar et al.…”

Section: Discussionmentioning

confidence: 99%

“…High glucose status is the basis for the occurrence and development of DR. The occurrence of DR is closely associated with the increase in blood sugar (Antonetti et al 2012;Chavira-Su arez et al 2012). The organelles in retinal M€ uller cells may be damaged under long-term hyperglycaemia, and changes in cell ultrastructure can stimulate M€ uller cell activation and cause dysfunction (Abu El-Asrar et al 2001;Wang et al 2010).…”

Section: Discussionmentioning

confidence: 99%

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Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway

Yin

Chen

2021

Pharmaceutical Biology

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Context Oxidative injury in a high-glucose (HG) environment may be a mechanism of diabetic retinopathy (DR) and edaravone can protect retinal ganglion cells by scavenging ROS. Objective To explore the effect of edaravone on HG-induced injury. Materials and methods First, Müller cells were cultured by different concentrations of glucose for different durations to obtain a suitable culture concentrations and duration. Müller cells were then divided into Control, HG + Vehicle, HG + Eda-5 μM, HG + Eda-10 μM, HG + Eda-20 μM, and HG + Eda-40 μM groups. Cells were cultured by 20 mM glucose and different concentrations of edaravone for 72 h. Results The IC 50 of glucose at 12–72 h is 489.3, 103.5, 27.92 and 20.71 mM, respectively. When Müller cells were cultured in 20 mM glucose for 72 h, the cell viability was 52.3%. Edaravone significantly increased cell viability compared to Vehicle (68.4% vs 53.3%; 78.6% vs 53.3%). The EC 50 of edaravone is 34.38 μM. HG induced high apoptosis rate (25.5%), while edaravone (20 and 40 μM) reduced it to 12.5% and 6.89%. HG increased the DCF fluorescence signal (189% of Control) and decreased the mitochondrial membrane potential by 57%. Edaravone significantly decreased the DCF fluorescence signal (144% and 132% of Control) and recovered the mitochondrial membrane potential to 68% and 89% of Control. Furthermore, HG decreased the expression of TRX1, PGC-1α, NRF1 and TFAM, which were restored by edaravone. Discussion and conclusion These findings provide a new potential approach for the treatment of DR and indicated new molecular targets in the prevention of DR.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway

Yin

Chen

2021

Pharmaceutical Biology

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“…The diversity of responses reflects the genotype of the cell and the mechanical demands of the resident tissue. It has been shown that hyperglycemia alters the tight control of intracellular calcium dynamics in retinal cells and may lead to the development of diabetic retinopathy [97]. Calcium signaling upon mechanical stimulation has been demonstrated in human corneal endothelial [98] and retinal pigment epithelial cells [99], rat retinal astrocytes, and Müller cells as well [100].…”

Section: Discussionmentioning

confidence: 99%

Functional and Molecular Characterization ofEx VivoCultured Epiretinal Membrane Cells from Human Proliferative Diabetic Retinopathy

Veréb

Lumi

Andjelić

et al. 2013

BioMed Research International

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Characterization of the cell surface marker phenotype of ex vivo cultured cells growing out of human fibrovascular epiretinal membranes (fvERMs) from proliferative diabetic retinopathy (PDR) can give insight into their function in immunity, angiogenesis, and retinal detachment. FvERMs from uneventful vitrectomies due to PDR were cultured adherently ex vivo. Surface marker analysis, release of immunity- and angiogenesis-pathway-related factors upon TNFα activation and measurement of the intracellular calcium dynamics upon mechano-stimulation using fluorescent dye Fura-2 were all performed. FvERMs formed proliferating cell monolayers when cultured ex vivo, which were negative for endothelial cell markers (CD31, VEGFR2), partially positive for hematopoietic- (CD34, CD47) and mesenchymal stem cell markers (CD73, CD90/Thy-1, and PDGFRβ), and negative for CD105. CD146/MCAM and CD166/ALCAM, previously unreported in cells from fvERMs, were also expressed. Secretion of 11 angiogenesis-related factors (DPPIV/CD26, EG-VEGF/PK1, ET-1, IGFBP-2 and 3, IL-8/CXCL8, MCP-1/CCL2, MMP-9, PTX3/TSG-14, Serpin E1/PAI-1, Serpin F1/PEDF, TIMP-1, and TSP-1) were detected upon TNFα activation of fvERM cells. Mechano-stimulation of these cells induced intracellular calcium propagation representing functional viability and role of these cells in tractional retinal detachment, thus serving as a model for studying tractional forces present in fvERMs in PDR ex vivo.

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Genomic and proteomic characterization of physiological and pathological angiogenesis in the human eye

Zoltán¹

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Hyperglycemia induces early upregulation of the calcium sensor KChIP3/DREAM/calsenilin in the rat retina

Cited by 5 publications

References 35 publications

Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway

Edaravone prevents high glucose-induced injury in retinal Müller cells through thioredoxin1 and the PGC-1α/NRF1/TFAM pathway

Functional and Molecular Characterization ofEx VivoCultured Epiretinal Membrane Cells from Human Proliferative Diabetic Retinopathy

Genomic and proteomic characterization of physiological and pathological angiogenesis in the human eye

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