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Tara Tovar-Vidales, Yang Liu, Eric B. Gonzales, Abbot F Clark; Expression of Acid-Sensing Ion Channels in Optic Nerve Astrocytes. Invest. Ophthalmol. Vis. Sci. 2017;58(8):4912.
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Ion channels have been associated in the pathology of fibrotic diseases including glaucoma. We examined the expression of acid-sensing ion channels (ASIC) 1a, 1b, 2a, and 2b in mouse optic nerve astrocytes (ONA). The purpose of this study was to determine: (a) whether ASIC channels are expressed in ONA, (b) whether expressions of these ASIC channels are regulated by TGF-β2, (c) whether the functional expression of ASIC1a are present in ONA.
Primary mouse ONA were obtained from C57BL/6 mice. ONA were treated with or without TGF-β2 (5ng/ml) for 24 hours. Immunocytochemistry was used to determine expression and localization of ASIC channels in ONA. Western blot analysis of cell lysate was used to determine if TGF-β2 increased expression of ASIC channels by primary mouse ONA. ONA were subjected to whole-cell patch-clamp electrophysiology to detect amiloride-sensitive ASIC currents.
ASIC1a and ASIC2a proteins are present in mouse ONA. ASIC1a was localized to the cytoplasm and perinucleus by immunocytochemistry. TGF-β2 increased ASIC1a protein expression by Western immunoblot. ASIC 2a was localized to the cytoplasm by immunocytochemistry. ASIC1b and ASIC2b were not detected in ONA by immunocytochemistry or Western blot. Whole-cell patch-clamp electrophysiology confirmed the presence of amiloride-sensitive ASIC currents in ONA.
These data indicate that ASIC channels are expressed by ONA and may be regulated by TGF-β2. Therefore, TGF-β2 may be involved in altered ASIC function and subsequently in ONA fibrosis.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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