Nanamika Thakur1, Rajeev Kumar Pandey2, Sanjana Mehrotra3. 1. Department of Human Genetics, Guru Nanak Dev University, Amritsar, Punjab, 143005, India. 2. Thermo Fisher Scientific, Bangalore, Karnataka, 560066, India. 3. Department of Human Genetics, Guru Nanak Dev University, Amritsar, Punjab, 143005, India. sanjana.bhu@gmail.com.
Abstract
BACKGROUND: Hypoxic injury to retinal ganglionic cells and adjoining glia is implicated in glaucomatous optic neuropathy. The present study evaluates the effect of IL-6 on R28 retinal precursor cell line exposed to hypoxic injury. METHODS AND RESULTS: Apoptotic cell death induced by hypoxia mimetic CoCl2 in R28 cells with or without IL-6 treatment was measured using cell viability assays and apoptotic markers. Oxidative stress was also measured. Hypoxia induced by mimetic CoCl2 led to a time and concentration dependent apoptosis of cells mediated by disruption of mitochondrial membrane potential and activation of caspase 3. Cells pre-treated with IL-6 demonstrated significantly higher viability and mitochondrial integrity under hypoxic conditions. A critical role of STAT3 was observed in mediating the cytoprotective effects of IL-6. Treatment of cells with IL-6 led to STAT3-mediated expression of the Bcl-2 family proteins and MnSOD. CONCLUSIONS: The data from the present study indicate cytoprotective role of IL-6 and suggest a previously unreported mechanism of neuroprotection via STAT3 mediated signaling.
BACKGROUND: Hypoxic injury to retinal ganglionic cells and adjoining glia is implicated in glaucomatous optic neuropathy. The present study evaluates the effect of IL-6 on R28 retinal precursor cell line exposed to hypoxic injury. METHODS AND RESULTS: Apoptotic cell death induced by hypoxia mimetic CoCl2 in R28 cells with or without IL-6 treatment was measured using cell viability assays and apoptotic markers. Oxidative stress was also measured. Hypoxia induced by mimetic CoCl2 led to a time and concentration dependent apoptosis of cells mediated by disruption of mitochondrial membrane potential and activation of caspase 3. Cells pre-treated with IL-6 demonstrated significantly higher viability and mitochondrial integrity under hypoxic conditions. A critical role of STAT3 was observed in mediating the cytoprotective effects of IL-6. Treatment of cells with IL-6 led to STAT3-mediated expression of the Bcl-2 family proteins and MnSOD. CONCLUSIONS: The data from the present study indicate cytoprotective role of IL-6 and suggest a previously unreported mechanism of neuroprotection via STAT3 mediated signaling.
Authors: Gail M Seigel; Wei Sun; Jian Wang; David H Hershberger; Lorrie M Campbell; Richard J Salvi Journal: Curr Eye Res Date: 2004-04 Impact factor: 2.424
Authors: V Pernet; S Joly; N Jordi; D Dalkara; A Guzik-Kornacka; J G Flannery; M E Schwab Journal: Cell Death Dis Date: 2013-07-18 Impact factor: 8.469