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Silva-Aguiar, Rodrigo Pacheco; Bezerra, Nathália C.F.; Lucena, Miguel C.; Sirtoli, Gabriela M.; Sudo, Roberto T.; Zapata-Sudo, Gisele; Takiya, Christina M.; Pinheiro, Ana Acacia S.; Dias, Wagner Barbosa; Caruso-Neves, Celso
The Journal of biological chemistry, 08/2018, Letnik: 293, Številka: 33Journal Article
Hypertensive individuals are at greater risk for developing chronic kidney disease (CKD). Reducing proteinuria has been suggested as a possible therapeutic approach to treat CKD. However, the mechanisms underlying the development of proteinuria in hypertensive conditions are incompletely understood. Cardiac and vascular dysfunction is associated with changes in the O-GlcNAcylation pathway in hypertensive models. We hypothesized that O-GlcNAcylation is also involved in renal damage, especially development of proteinuria, associated with hypertension. Using the spontaneously hypertensive rat (SHR) model, we observed higher renal cortex O-GlcNAcylation, glutamine–fructose aminotransferase (GFAT), and O-GlcNAc transferase (OGT) protein expression, which positively correlated with proteinuria. Interestingly, this was observed in hypertensive, but not pre-hypertensive, rats. Pharmacological inhibition of GFAT decreased renal cortex O-GlcNAcylation, proteinuria, and albuminuria in SHR. Using a proximal tubule cell line, we observed that increased O-GlcNAcylation reduced megalin surface expression and albumin endocytosis in vitro, and the effects were correlated in vivo. Moreover, megalin is O-GlcNAcylated both in vitro and in vivo. In conclusion, our results demonstrate a new mechanism involved in hypertension-associated proteinuria.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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