Min Ji

Publications (2)9.58 Total impact

• Article: Group I mGluR-Mediated Inhibition of Kir Channels Contributes to Retinal Muller Cell Gliosis in a Rat Chronic Ocular Hypertension Model.

  Min Ji, Yanying Miao, Ling-Dan Dong, Jie Chen, Xiao-Fen Mo, Shi-Xiang Jiang, Xing-Huai Sun, Xiong-Li Yang, Zhongfeng Wang
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  ABSTRACT: Müller cell gliosis, which is characterized by upregulated expression of glial fibrillary acidic protein (GFAP), is a universal response in many retinal pathological conditions. Whether down-regulation of inward rectifying K(+) (Kir) channels, which commonly accompanies the enhanced GFAP expression, could contribute to Müller cell gliosis is poorly understood. We investigated changes of Kir currents, GFAP and Kir4.1 protein expression in Müller cells in a rat chronic ocular hypertension (COH) model, and explored the mechanisms underlying Müller cell gliosis. We show that Kir currents and Kir4.1 protein expression in Müller cells were reduced significantly, while GFAP expression was increased in COH rats, and these changes were eliminated by MPEP, a group I metabotropic glutamate receptors (mGluR I) subtype mGluR5 antagonist. In normal isolated Müller cells, the mGluR I agonist (S)-3,5-dihydroxyphenylglycine (DHPG) suppressed the Kir currents and the suppression was blocked by MPEP. The DHPG effect was mediated by the intracellular Ca(2+)-dependent PLC/IP(3)-ryanodine/PKC signaling pathway, but the cAMP-PKA pathway was not involved. Moreover, intravitreal injection of DHPG in normal rats induced changes in Müller cells, similar to those observed in COH rats. The DHPG-induced increase of GFAP expression in Müller cells was obstructed by Ba(2+), suggesting the involvement of Kir channels. We conclude that overactivation of mGluR5 by excessive extracellular glutamate in COH rats could contribute to Müller cell gliosis by suppressing Kir channels.
  Journal of Neuroscience 09/2012; 32(37):12744-55. · 7.11 Impact Factor
• Article: RGS2 and RGS4 modulate melatonin-induced potentiation of glycine currents in rat retinal ganglion cells.

  Min Ji, Wen-Jie Zhao, Ling-Dan Dong, Yanying Miao, Xiong-Li Yang, Xing-Huai Sun, Zhongfeng Wang
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  ABSTRACT: Regulator of G-protein signaling (RGS) proteins 2 (RGS2) and 4 (RGS4) play an important role in regulating G(i/o)- and G(q)-coupled receptors. In the present study, we investigated the possible impact of RGS2 and RGS4 on modulation of glycine currents of rat retinal ganglion cells (RGCs) mediated by the G(i/o)-coupled melatonin MT(2) receptor, using immunohistochemistry, Western blot analysis and whole-cell patch-clamp techniques. By immunofluorescence labeling the expression profiles of RGS2 and RGS4 proteins were basically similar. Both of them were widely expressed in the rat retina, particularly in the inner plexiform layer (IPL) and the ganglion cell layer (GCL). In addition, sparse signals of RGS2 and RGS4 were also detected in the inner nuclear layer (INL). Double immunofluorescence labeling further showed that all of RGCs retrogradely labeled expressed both RGS2 and RGS4. Western blot analysis confirmed the presence of RGS2 and RGS4 proteins in the rat retina. Intracellular dialysis of RGCs with the antibody against RGS2/RGS4 to block RGS2/RGS4 function gradually increased glycine current amplitudes of these cells. In the presence of the RGS2/RGS4 antibody melatonin-induced potentiation of glycine currents of RGCs was not observable. These results suggest that RGS2/RGS4 are coupled to melatonin receptor signaling in rat RGCs and these proteins may regulate the MT(2) receptor to change melatonin-induced modulation of glycine currents in rat RGCs.
  Brain research 09/2011; 1411:1-8. · 2.46 Impact Factor