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E. C. Steele, Jr., P. Brooks, J. White, B. Bodo; Diabetes-Associated Hyperglycemia and Hyperosmolarity Do Not Adversely Affect Cell Growth or Viability of Immortalized Rat Retinal Müller (rMC-1) Cells. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1890.
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Retinal Müller glial cells provide many critical support functions for both neuronal and vascular cells in the retina. It has been proposed that loss of these support functions might precede and contribute to the progressive dysfunction and loss of neurons and vascular cells observed in later stages of diabetic retinopathy. Previously published data support the notion that such a loss of Müller glial cell functions might occur via hyperglycemia-mediated direct and acute apoptosis of retinal Müller glial cells. In this study, we re-tested this hypothesis directly using immortalized rat Müller (rMC-1) cells (kind gift of Dr. V. Sarthy).
The cell growth rate of rMC-1 cells was quantitatively compared over a 72 hour time course in three different media: euglycemic and normosmolar control (5mM glucose), hyperglycemic and hyperosmolar (25mM glucose), and euglycemic and hyperosmolar control (5mM glucose + 20mM mannose). The gross health status of rMC-1 cells was also compared in these same media over the same time course using the trypan blue exclusion assay.
rMC-1 cells grew with indistinguishable rates in all three media. No significant number of rMC-1 cells exhibited trypan blue staining in any media condition.
Our results challenge the parsimonious hypothesis that diabetes-associated hyperglycemia compromises Müller cell support functions simply via acute cell death. However, our data do not preclude nor discourage the possibility that hyperglycemia and/or hyperosmolarity may result in acute and direct changes in the expression or functional profiles of retinal Müller cells. The identification of such changes, which may play an important role in the progressive pathophysiology of diabetic retinopathy, is the focus of ongoing research in our laboratory.
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