Renal response to metabolic acidosis: Role of mRNA stabilization

摘要: The renal response to metabolic acidosis is mediated, in part, by increased expression of the genes encoding key enzymes glutamine catabolism and various ion transporters that contribute synthesis excretion ammonium ions net production release bicarbonate ions. resulting adaptations facilitate acid partially restore systemic acid–base balance. Much this may be mediated selective stabilization mRNAs encode responsive proteins. For example, glutaminase mRNA contains a direct repeat 8-nt AU sequences function as pH-response element (pHRE). This both necessary sufficient impart pH-responsive chimeric mRNAs. pHRE also binds multiple RNA-binding proteins, including ζ-crystallin (ζ-cryst), AU-factor 1 (AUF1), HuR. onset initiates an endoplasmic reticulum (ER)-stress leads formation cytoplasmic stress granules. ζ-cryst transiently recruited granules, concurrently, HuR translocated from nucleus cytoplasm. On basis cumulative data, mechanism for proposed. hypothesis suggests experiments should define better how cells kidney sense very slight changes intracellular pH mediate essential adaptive response.