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. 2017 May 11;12(5):e0177362. doi: 10.1371/journal.pone.0177362

Fig 10. Schematic representation of the mechanisms involved in ALD-induced decrement of expression of cldn-5 in GL and, cldn-2 and occldn in PT, and increased expression of cldn-4 and -8 in DT.

Fig 10

(A) In GL, diabetes-induced ALD promotes glomerular damage, evaluated by decreased expression of nephrin and WT1, and oxidative stress, which may be associated to decreased cldn-5 expression and proteinuria. (B) In PT, diabetes-induced ALD promotes tubular damage, evaluated by increased expression of Kim-1 and Hsp72, and oxidative stress, which may be associated to decrements of occldn and cldn-2 expressions, this latter may explain increased natriuresis. (C) In DT, diabetes-induced ALD induces the expression of SGK1, which in turn phosphorylates serine (pSer) residues of WNK4 promoting its localization in the TJ. This latter phosphorylates threonine residues (pThr) of cldn-4 and -8, where both proteins constitute a paracellular Cl― channel and a Na+ barrier. In all nephron segments, blockade of ALD actions with SPL decreased oxidative stress in GL and PT and the expression, and phosphorylation of cldn-4 and -8 in DT.