Galectin-3 expression is induced in renal -intercalated cells during metabolic acidosis

Schwaderer, Andrew L., Soundarapandian Vijayakumar, Qais Al-Awqati, and George J. Schwartz. Galectin-3 expression is induced in renal -intercalated cells during metabolic acidosis. Am J Physiol Renal Physiol 290: F148–F158, 2006. First published August 30, 2005; doi:10.1152/ajprenal.00244.2005.—The adaptation of the cortical collecting duct (CCD) to metabolic acidosis requires the polymerization and deposition in the extracellular matrix of the novel protein hensin. HCO3 -secreting -intercalated cells remove apical Cl :HCO3 exchangers and may reverse functional polarity to secrete protons. Using intercalated cells in culture, we found that galectin-3 facilitated hensin polymerization, thereby causing their differentiation into the H -secreting cell phenotype. We examined the expression of galectin-3 in the rabbit kidney and its relationship to hensin during metabolic acidosis. In control kidneys, galectin-3 was expressed in the cortical and medullary collecting ducts. In the outer cortex 26 3% of CCD cells expressed galectin-3 compared with 64 3% of the cells of the inner cortex. In the CCD, galectin-3 was rarely expressed in -intercalated cells, being primarily present in -intercalated and principal cells. During metabolic acidosis, the intensity of cellular staining for galectin-3 increased and more cells began to express it; the percentage of CCD cells expressing galectin-3 increased from 26 3 to 66 3% in the outer cortex and from 64 3 to 78 4% in the inner cortex. This was particularly evident in -intercalated cells where expression was found in only 8 2% in control animals but in 75 2% during metabolic acidosis in the outer cortex and similarly for the inner cortex (26 6 to 90 7%). Importantly, both galectin-3 and hensin were found in the extracellular matrix of microdissected CCDs; and during metabolic acidosis, many more cells exhibited this extracellular colocalization. Thus galectin-3 may play several important roles in the CCD, including mediating the adaptation of -intercalated cells during metabolic acidosis.