Background And Aims: We undertook this study to investigate the effect of mesangial cells stimulated by immunoglobin A1 from IgAN on transforming growth factor-beta1 synthesis in podocytes.
Methods: Jacalin affinity chromatography and Sephacryl S-200 molecular sieve chromatography were used to isolate IgA1 from blood of IgAN patients, which was then used as aggregated IgA1 (aIgA1). Podocytes were incubated with special mesangial medium. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were used, respectively, to measure TGF-beta1 mRNA expression and its protein concentration in medium.
Results: TGF-beta1 mRNA and its protein concentration in the medium of podocytes increased when exposed to the medium of mesangial cells, which were stimulated by IgA1 from IgAN patients. Angiotensinogen and angiotensin-converting enzyme (ACE) mRNAs, as well as angiotensin II, were also increased by the medium (p <0.05). Enalaprilat and valsartan partly lowered overproduction of TGF-beta1 mRNA and excreted protein of podocytes, whereas enalaprilat plus valsartan completely restored them to the level as control.
Conclusions: These data suggest that mesangial cells stimulated by IgA1 from IgAN patients may excrete some material to facilitate TGF-beta1 synthesis in podocytes through activating renin-angiotensin system by cross-talk.
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http://dx.doi.org/10.1016/j.arcmed.2010.05.003 | DOI Listing |
Neurochem Int
December 2024
Master and PhD Programs in Pharmacology and Toxicology, School of Medicine, Tzu Chi University, Hualien, Taiwan 970; Department of Pharmacology, School of Medicine, Tzu Chi University, Hualien, Taiwan 970. Electronic address:
Previous studies have shown that celecoxib or NSAID may paradoxically induce cyclooxygenase-2 (COX-2) expression and trigger inflammation-like responses in airway smooth muscle cells and renal mesangial cells. Despite the extensive research on celecoxib, its atypical biological effect on the induction of COX-2 in astroglial cells within the central nervous system (CNS) remains unexplored. In the present study, we investigated the impact of celecoxib on COX-2 and Glial Fibrillary Acidic Protein (GFAP) expression and explored the mechanisms underlying celecoxib-regulated COX-2 expression in cortical astrocytes of rats.
View Article and Find Full Text PDFGenes Dis
March 2025
Department of Nephrology, China-Japan Friendship Hospital, Beijing 100029, China.
Diabetic nephropathy is a prevalent complication of diabetes and stands as the primary contributor to end-stage renal disease. The global prevalence of diabetic nephropathy is on the rise, however, due to its intricate pathogenesis, there is currently an absence of efficacious treatments to enhance renal prognosis in affected patients. The mammalian target of rapamycin (mTOR), a serine/threonine protease, assumes a pivotal role in cellular division, survival, apoptosis delay, and angiogenesis.
View Article and Find Full Text PDFVet Pathol
December 2024
Pfizer Inc., Cambridge, MA.
The kidney plays an important role in iron homeostasis and mesangial cells (MCs) are phagocytic cells important for glomerular homeostasis. Sickle hemoglobin (HbS) modulators are promising clinical candidates for treatment of sickle cell disease. Although they prevent disease pathophysiology of HbS polymerization and red blood cell (RBC) sickling by increasing hemoglobin oxygen affinity, higher oxygen affinity can also cause transient tissue hypoxia with compensatory increases in erythropoiesis and subsequent increases in RBC turnover.
View Article and Find Full Text PDFCell Mol Biol (Noisy-le-grand)
November 2024
Biology Department, College of Education for Pure Sciences, University of Anbar, Iraq.
This study aimed to evaluate the therapeutic effects of B6 in rats experimentally intoxicated by benzopyrene. Twenty-eight Male Sprague Dawley (white Swiss) rats weighing 170-210 g and 3-4 months old were utilized in this examination. Rats were divided into 4 control groups (G1), B[a]P 2 pmol/μL (G2), B6 only once per 2 days for a full month at 1000 mcg (15 dose per month) (G3), B6 + B[a]P (G4).
View Article and Find Full Text PDFKidney Int
December 2024
Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. Electronic address:
A common observation in diabetic kidney disease is lipid accumulation, but the mechanism(s) underlying this pathology is unknown. Inhibition of Vascular endothelial growth factor B (VEGF-B) signaling was shown to prevent glomerular lipid accumulation and ameliorated diabetic kidney disease in experimental models. Here, we examined kidney biopsies from patients with Type 2 (84 %) and Type 1 diabetes (16 %), combined with data mining of RNA-seq dataset analyses in patients with diabetic kidney disease.
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