Interleukin 2 (IL-2) treatment is associated with proteinuria. A conditionally immortalized human podocyte cell line was used to investigate expression of the podocyte specific marker podocin, IL-2R alpha (IL-2Rα), apoptosis marker Bax, and autophagy markers LC3I AND LC3II, determined by quantitative immunoblotting, following 24, 48, and 72 hours of IL-2 stimulation, comparing them to unstimulated cells. Podocin was expressed at all time points. IL-2Rα expression was increased after 24 and 72 hrs ( 0.0014, 0.0139) and decreased after 48 hours ( 0.0445). Bax, LC3I, and LC3II were increased after 24 hrs ( 0.0094, 0.0016, 0.0004) and 48 hrs ( 0.0072, 0.0024, 0.0087). Human podocytes express the IL-2R and activation results in increased autophagy and apoptosis.
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http://dx.doi.org/10.1080/15513815.2019.1710793 | DOI Listing |
Theranostics
January 2025
Department of Nephrology, China-Japan Friendship Hospital (Institute of Clinical Medical Sciences), Beijing, 100029, China.
The tertiary structure of normal podocytes prevents protein from leaking into the urine. However, observing the complexity of podocytes is challenging because of the scale differences in their three-dimensional structure and the close proximity between neighboring cells in space. In this study, we explored podocyte-secreted angiopoietin-like 4 (ANGPTL4) as a potential morphological marker via super-resolution microscopy (SRM).
View Article and Find Full Text PDFSci Rep
January 2025
Department of Nephrology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chronic kidney disease (CKD) is a worldwide public health problem. Podocyte damage is a hallmark of glomerular diseases including focal segmental glomerulosclerosis (FSGS) and one of the leading causes of CKD. Lysine methylation is a crucial post-translational modification.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Medicine and Feinstein Institute for Medical Research, Zucker School of Medicine, Hempstead, NY 11549, USA.
Patients carrying APOL1 risk alleles (G1 and G2) have a higher risk of developing Focal Segmental Glomerulosclerosis (FSGS); we hypothesized that escalated levels of miR193a contribute to kidney injury by activating renin-angiotensin system (RAS) in the APOL1 milieus. Differentiated podocytes (DPDs) stably expressing vector (V/DPD), G0 (G0/DPDs), G1 (G1/DPDs), and G2 (G2/DPDs) were evaluated for renin, Vitamin D receptor (VDR), and podocyte molecular markers (PDMMs, including WT1, Podocalyxin, Nephrin, and Cluster of Differentiation [CD]2 associated protein [AP]). G0/DPDs displayed attenuated renin but an enhanced expression of VDR and Wilms Tumor [WT]1, including other PDMMs; in contrast, G1/DPDs and G2/DPDs exhibited enhanced expression of renin but decreased expression of VDR and WT1, as well as other PDMMs (at both the protein and mRNA levels).
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Unit of Nephrology, Dialysis and Transplantation and Laboratory of Molecular Nephrology, Core Facilities-Proteomics Laboratory, 16147 Genoa, Italy.
Historically, oxidants have been considered mechanisms of glomerulonephritis, but a direct cause-effect correlation has never been demonstrated. Several findings in the experimental model of autoimmune conditions with renal manifestations point to the up-regulation of an oxidant/anti-oxidant system after the initial deposition of autoantibodies in glomeruli. Traces of oxidants in glomeruli cannot be directly measured for their rapid metabolism, while indirect proof of their implications is derived from the observation that Superoxide Oxidase 2 (SOD2) is generated by podocytes after autoimmune stress.
View Article and Find Full Text PDFJ Bioenerg Biomembr
January 2025
Department of Endocrinology, Tianjin 4th Center Hospital, Tianjin, 300140, China.
To investigate the role of silent information regulator 6 (SIRT6) in regulating podocyte injury in diabetic nephropathy (DN) through autophagy mediated by Notch signaling pathway. A blank control group (group A), a diabetic nephropathy group (group B), and a Sirt6 intervention group (group C) were established. The group A cells were human normal glomerular podocyte cell lines (HGPCs) without any treatment.
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