ArticlePloS one2019
Serum amyloid A and Janus kinase 2 in a mouse model of diabetic kidney disease.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 17 citations in OpenAlex.
- SOCS1 Mimetic Peptide Enhances Empagliflozin Improvement on Kidney Damage in the Type 2 Diabetes Mouse Model BTBR ob/ob.International journal of molecular sciences · 2026Article
- SAA3 deficiency exacerbates intestinal fibrosis in DSS-induced IBD mouse model.Cell death discovery · 2025Article
- Associations of serum amyloid A and 25-hydroxyvitamin D with diabetic nephropathy: A cross-sectional study.Journal of clinical laboratory analysis · 2022Article
- Serum Amyloid A3 Promoter-Driven Luciferase Activity Enables Visualization of Diabetic Kidney Disease.International journal of molecular sciences · 2022Article
- iTRAQ-based proteomic analysis of differentially expressed proteins in sera of seronegative and seropositive rheumatoid arthritis patients.Journal of clinical laboratory analysis · 2022Article
- Effect ofAnalytical cellular pathology (Amsterdam) · 2022Article
- Calcium dobesilate efficiency in the treatment of diabetic kidney disease through suppressing MAPK and chemokine signaling pathways based on clinical evaluation and network pharmacology.Frontiers in pharmacology · 2022Article
- Structural Basis for Vital Function and Malfunction of Serum Amyloid A: an Acute-Phase Protein that Wears Hydrophobicity on Its Sleeve.Current atherosclerosis reports · 2020Review
- Anti-inflammatory, antioxidant and renoprotective effects of SOCS1 mimetic peptide in the BTBR ob/ob mouse model of type 2 diabetes.BMJ open diabetes research & care · 2020Article
- Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- Distribution of serum amyloid A and establishment of reference intervals in healthy adults.Journal of clinical laboratory analysis · 2020Article
- Biological Characterization of Commercial Recombinantly Expressed Immunomodulating Proteins Contaminated with Bacterial Products in the Year 2020: The SAA3 Case.Mediators of inflammation · 2020Article
- Serum Amyloid A-Mediated Inflammasome Activation of Microglial Cells in Cerebral Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The serum amyloid A3 promoter-driven luciferase reporter mice is a valuable tool to image early renal fibrosis development and shows the therapeutic effect of glucosyl-hesperidin treatment.Scientific reports · 2019Article
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10 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSerum amyloid A (SAA), a potent inflammatory mediator, and Janus kinase 2 (JAK2), an intracellular signaling kinase, are increased by diabetes. The aims were to elucidate: 1) a JAK2-mediated pathway for increased SAA in the kidneys of diabetic mice; 2) a JAK2-SAA pathway for inflammation in podocytes.
methodsAkita diabetic mice (129S6) with podocyte JAK2 overexpression and angiotensin II infusion (4 weeks) were given a JAK1,2 inhibitor (LY03103801, 3 mg/kg/day orally for the last two weeks). Kidneys were immunostained for SAA isoform 3 (SAA3). SAA3 knockout and control mouse podocytes were exposed to advanced glycation end products (AGE) or exogenous SAA with JAK2 inhibition (Tyrphostin AG 490, 50μM). JAK2 activity (phosphorylation, Western blot, 1 hour) and mRNA for SAA3 and associated inflammatory genes (Cxcl5, Ccl2, and Ccl5) were measured by RT-PCR (20 hours).
resultsSAA3 protein was present throughout the diabetic kidney, and podocyte JAK2 overexpression increased tubulointerstitial SAA3 compared to wild type diabetic controls, 43% versus 14% (p = 0.007); JAK1,2 inhibition attenuated the increase in SAA3 to 15% (p = 0.003). Urine albumin-to-creatinine ratio (r = 0.49, p = 0.03), mesangial index (r = 0.64, p = 0.001), and glomerulosclerosis score (r = 0.51, p = 0.02) were associated with SAA3 immunostaining scores across mouse groups. Exposing podocytes to AGE or exogenous SAA increased JAK2 activity within one hour and mRNA for associated inflammatory genes after 20 hours. JAK2 inhibition reduced SAA3 mRNA expression in podocytes exposed to AGE or SAA. SAA3 knockout podocytes had >85% lower AGE-induced inflammatory genes.
conclusionJAK1,2 inhibition reduced SAA and histological features of DKD in podocyte JAK2-overexpressing mice. In podocytes exposed to a diabetes-like condition, JAK2 inhibition reduced expression of SAA, while SAA knockout blocked expression of associated pro-inflammatory mediators. SAA may promote JAK2-dependent inflammation in the diabetic kidney.
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