Expression of the Na+-K+-2Cl(-)-cotransporter 2 in the normal and pressure-induced ischemic rat retina

• Published in: Korean journal of ophthalmology Vol. 26; no. 3; pp. 203 - 211
• Main Authors: Kim, Do Hyun, Ahn, Myung Douk
• Format: Journal Article
• Language: English
• Published: Korea (South) The Korean Ophthalmological Society 01.06.2012; 대한안과학회
• Subjects: Animals; Blotting, Western; Disease Models, Animal; Immunohistochemistry; Intraocular Pressure; Ischemia - etiology; Ischemia - metabolism; Male; Microscopy, Confocal; Ocular Hypertension - complications; Ocular Hypertension - metabolism; Ocular Hypertension - physiopathology; Original; Rats; Rats, Sprague-Dawley; Retinal Diseases - etiology; Retinal Diseases - metabolism; Retinal Ganglion Cells - metabolism; Retinal Ganglion Cells - pathology; Sodium-Potassium-Chloride Symporters - biosynthesis; Solute Carrier Family 12, Member 1; 안과학; Ischemia; Retinal ganglion cells; Na+-K+-2Cl > cotransporter 2
• ISSN: 1011-8942; 2092-9382
• DOI: 10.3341/kjo.2012.26.3.203

To evaluate the expression of the Na(+)-K(+)-2Cl(-)-cotransporter 2 (NKCC2) in the ischemic rat retina. Retinal ischemia was induced by pressures 90 to 120 mmHg, above systemic systolic pressure. Immunohistochemistry and western blot analysis were performed. NKCC2 is expressed in the normal retina and its expression is increased by ischemia caused by intraocular pressure elevation. NKCC2 immunoreactivity was observed mainly in axon bundles of ganglion cells and horizontal cell processes in the retina. NKCC2 expression continuously increased with a peak value 3 days (to 415% of normal levels) after ischemic injury, and then gradually decreased to 314% of controls until 2 weeks post injury. The mean density of NKCC2-labeled ganglion cells per mm(2) changed from 1,255 ± 109 in normal retinas to 391 ± 49 and 185 ± 37 at 3 days and 2 weeks after ischemia, respectively (p < 0.05), implying cell death of ganglion cells labeled with NKCC2. Taken together, these results suggest that NKCC2, which is expressed in retinal ganglion and horizontal cells, may contribute to cell death by ischemic injury in the retina, although the molecular mechanisms involved remain to be clarified.