Background: This research aimed at investigating the cyclosporine A intake impact with/without curcumin on podocyte protein gene expressions and matrix metalloproteins (MMPs) changes in rat kidney.
Methods: Thirty-two Wistar male rats were assigned to the control, sham, cyclosporine A, and cyclosporine A with curcumin groups.
Results: A significant increase was observed in CD2AP, ACTN4, podocin and also MMP9 and 2, cystatin C levels in the cyclosporine A group following treatment for four weeks, whereas a decrease was found in nephrin gene expression than the control group. In addition, a significant reduction was observed in the cyclosporine A group in glomerular filtration rate (GFR), urine creatinine, and increased plasma creatinine levels than the control group. Using curcumin plus cyclosporine A ameliorated gene expression alterations and increased the reduced amount of GFR, urine urea, and creatinine while reducing the increased plasma cystatine C, urea, and creatinine levels compared with the cyclosporine A group.
Conclusion: Accordingly, cyclosporine A-induced kidney abnormalities are possibly associated with changes in podocyte intra- and extra-cellular protein gene expression that influence the quality of filtrated fluid via altering the foot process shape and slit diaphragm size. Finally, such impacts are reduced via curcumin as an antioxidant and anti-inflammatory compound.
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http://dx.doi.org/10.1080/17425255.2020.1822323 | DOI Listing |
Anim Cells Syst (Seoul)
January 2025
Department of Biochemistry, College of Natural Sciences, Chungnam National University, Daejeon, Korea.
Interferon gamma (IFNγ) is well-known for its ability to stimulate immune cells in response to pathogen infections and cancer. To develop an effective cancer therapeutic vaccine, CT26 colon carcinoma cells were genetically modified to express IFNγ either as a secreted form (sIFNγ) or as a membrane-bound form. For the membrane-bound expression, IFNγ was fused with Fas (mbIFNγ/Fas), incorporating the extracellular cysteine-rich domains, transmembrane, and cytoplasmic domains of Fas.
View Article and Find Full Text PDFMol Clin Oncol
February 2025
Department of Urology Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Disulfidptosis, which was recently identified, has shown promise as a potential cancer treatment. Nonetheless, the precise role of long non-coding RNAs (lncRNAs) in this phenomenon is currently unclear. To elucidate their significance in bladder cancer (BLCA), a signature of disulfidptosis-related lncRNAs (DRlncRNAs) was developed and their potential prognostic significance was explored.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Medical Oncology, The First Hospital of China Medical University, Shenyang, Liaoning, China.
Background: Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with the worst prognosis among all subtypes. The impact of distinct cell subpopulations within the tumor microenvironment (TME) on TNBC patient prognosis has yet to be clarified.
Methods: Utilizing single-cell RNA sequencing (scRNA-seq) integrated with bulk RNA sequencing (bulk RNA-seq), we applied Cox regression models to compute hazard ratios, and cross-validated prognostic scoring using a GLMNET-based Cox model.
Front Immunol
December 2024
Molecular Immunology and Gene Therapy, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany.
Generation of high avidity T cell receptors (TCRs) reactive to tumor-associated antigens (TAA) is impaired by tolerance mechanisms, which is an obstacle to effective T cell therapies for cancer treatment. NY-ESO-1, a human cancer-testis antigen, represents an attractive target for such therapies due to its broad expression in different cancer types and the restricted expression in normal tissues. Utilizing transgenic mice with a diverse human TCR repertoire, we isolated effective TCRs against NY-ESO-1 restricted to HLA-A*02:01.
View Article and Find Full Text PDFFront Immunol
December 2024
Institute for Immunodeficiency, Center for Chronic Immunodeficiency, University Medical Center Freiburg, Freiburg, Germany.
Background: Hypomorphic mutations in the () gene cause a glycosylation disorder that leads to immunodeficiency. It is often associated with recurrent infections and atopy. The exact etiology of this condition remains unclear.
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