Publications by authors named "B S Kasinath"
The role played by anionic channels in diabetic kidney disease (DKD) is not known. Chloride channel accessory 1 (CLCA1) facilitates the activity of TMEM16A (Anoctamin-1), a Ca2+-dependent Cl- channel. We examined if CLCA1/TMEM16A had a role in DKD.
View Article and Find Full Text PDFArticle Synopsis
- The study investigates how high glucose levels in diabetes lead to kidney cell damage through the activation of a signaling pathway involving DJ-1 and PTEN.
- DJ-1 is found to be upregulated in kidney cells under high glucose conditions, which triggers the Akt/mTORC1 signaling pathway, resulting in cell growth and fibrosis.
- The research indicates that inhibiting DJ-1 can prevent glucose-induced cell growth and damage, while overexpressing DJ-1 replicates the harmful effects, highlighting its role in renal injury related to diabetes.
During the progression of diabetic kidney disease, proximal tubular epithelial cells respond to high glucose to induce hypertrophy and matrix expansion leading to renal fibrosis. Recently, a non-canonical PTEN has been shown to be translated from an upstream initiation codon CUG (leucine) to produce a longer protein called PTEN-Long (PTEN-L). Interestingly, the extended sequence present in PTEN-L contains cell secretion/penetration signal.
View Article and Find Full Text PDFReduced kidney AMPK activity is associated with nutrient stress-induced chronic kidney disease (CKD) in male mice. In contrast, female mice resist nutrient stress-induced CKD. The role of kidney AMPK in sex-related organ protection against nutrient stress and metabolite changes was evaluated in diabetic kidney tubule-specific AMPKγ2KO (KTAMPKγ2ΚΟ) male and female mice.
View Article and Find Full Text PDF