Disease relevance of Slc26a4

• Regulation of the apical Cl-/HCO-3 exchanger pendrin in rat cortical collecting duct in metabolic acidosis [1].
• In this study, we investigated whether the abundance and subcellular localization of pendrin are regulated in response to experimental metabolic acidosis and alkalosis with maintained water and sodium intake [2].

High impact information on Slc26a4

• Recent work identified prestin, a protein with similarity to pendrin-related anion transporters, as the OHC motor molecule [3].
• The purpose of our study was to determine the regulation of Pds protein abundance during chronic changes in chloride balance [4].
• Conversely, NaCl depletion induced by furosemide was associated with increased Pds expression [4].
• Here, we examined the regulation of pendrin in metabolic acidosis, a condition known to decrease HCO(3)(-) secretion in CCD [1].
• These results indicate that changes in pendrin protein expression play a key role in the well-established regulation of HCO(3)(-) secretion in the CCD in response to chronic changes in acid-base balance and suggest that regulation of pendrin expression may be clinically important in the correction of acid-base disturbances [2].

Biological context of Slc26a4

• Adaptive downregulation of pendrin in metabolic acidosis indicates the important role of this exchanger in acid-base regulation in the CCD [1].

Anatomical context of Slc26a4

• Northern blot hybridizations indicated that the mRNA expression of pendrin in kidney cortex decreased by 68% in acidotic animals (P < 0.02 vs. control) [1].
• The anion exchanger pendrin is present in the apical plasma membrane of type B and non-A-non-B intercalated cells of the cortical collecting duct (CCD) and connecting tubule and is involved in HCO(3)(-) secretion [2].
• The protective effect of I2 was correlated with the highest expression of the I-/Cl- transporter pendrin and with the lowest levels of lipoperoxidation expression in mammary glands [5].

Associations of Slc26a4 with chemical compounds

• Regulated expression of pendrin in rat kidney in response to chronic NH4Cl or NaHCO3 loading [2].

Analytical, diagnostic and therapeutic context of Slc26a4

• Expression of pendrin protein was assessed by indirect immunofluorescence [1].
• Immunofluorescence labeling demonstrated significant reduction in pendrin expression in CCDs of acidotic rats [1].
• Pds protein abundance was estimated by semiquantitative immunoblotting in renal membrane fractions isolated from the cortex of treated and control rats [4].
• Moreover, double-label laser confocal microscopy revealed a reduction in the fraction of cells in the CCD exhibiting pendrin labeling to 65% of the control value (n = 6, P < 0.005) [2].

References