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AuthorRavindran, Sreenithya
AuthorPasha, Mazhar
AuthorAgouni, Abdelali
AuthorMunusamy, Shankar
Available date2019-08-27T08:20:09Z
Publication Date2019-08-01
Publication NameBiomolecules
Identifierhttp://dx.doi.org/10.3390/biom9080348
CitationRavindran, Sreenithya; Pasha, Mazhar; Agouni, Abdelali; Munusamy, Shankar. 2019. "Microparticles as Potential Mediators of High Glucose-Induced Renal Cell Injury." Biomolecules 9, no. 8: 348.
ISSN2218-273X
URIhttp://hdl.handle.net/10576/11732
AbstractDiabetic nephropathy (DN) is the most common cause of chronic kidney disease worldwide. Activation of signaling pathways such as the mammalian target of rapamycin (mTOR), extracellular signal-regulated kinases (ERK), endoplasmic reticulum (ER) stress, transforming growth factor-beta (TGF-β), and epithelial-mesenchymal transition (EMT), are thought to play a significant role in the etiology of DN. Microparticles (MPs), the small membrane vesicles containing bioactive signals shed by cells upon activation or during apoptosis, are elevated in diabetes and were identified as biomarkers in DN. However, their exact role in the pathophysiology of DN remains unclear. Here, we examined the effect of MPs shed from renal proximal tubular cells (RPTCs) exposed to high glucose conditions on naïve RPTCs in vitro Our results showed significant increases in the levels of phosphorylated forms of 4E-binding protein 1 and ERK1/2 (the downstream targets of mTOR and ERK pathways), phosphorylated-eIF2α (an ER stress marker), alpha smooth muscle actin (an EMT marker), and phosphorylated-SMAD2 and nuclear translocation of SMAD4 (markers of TGF-β signaling). Together, our findings indicate that MPs activate key signaling pathways in RPTCs under high glucose conditions. Pharmacological interventions to inhibit shedding of MPs from RPTCs might serve as an effective strategy to prevent the progression of DN.
Languageen
PublisherMDPI
SubjectERK1/2
TGF-β
diabetic nephropathy
endoplasmic reticulum stress
epithelial-mesenchymal transition
mTOR
microparticles
TitleMicroparticles as Potential Mediators of High Glucose-Induced Renal Cell Injury.
TypeArticle
Issue Number8 : 348
Volume Number9
ESSN2218-273X
dc.accessType Open Access


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