ArticleBiochemistry and biophysics reports2018
Proteomic analysis of AQP11-null kidney: Proximal tubular type polycystic kidney disease.
Article in Biochemistry and biophysics reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Mechanistic complement of autosomal dominant polycystic kidney disease: the role of aquaporins.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Aquaporins in Urinary System.Advances in experimental medicine and biology · 2023Article
- Emerging roles for AQP in mammalian extracellular vesicles.Biochimica et biophysica acta. Biomembranes · 2022Review
- Abnormal expression and the significant prognostic value of aquaporins in clear cell renal cell carcinoma.PloS one · 2022Article
- Aquaporins in insulin resistance and diabetes: More than channels!Redox biology · 2021Review
- Heterogeneity of cell composition and origin identified by single-cell transcriptomics in renal cysts of patients with autosomal dominant polycystic kidney disease.Theranostics · 2021Article
- A Multitubular Kidney-on-Chip to Decipher Pathophysiological Mechanisms in Renal Cystic Diseases.Frontiers in bioengineering and biotechnology · 2021Article
- Association of Serum PSP/REG IJournal of diabetes research · 2020Article
- Involvement of the NADPH oxidase 2 pathway in renal oxidative stress inBiochemistry and biophysics reports · 2019Article
- Aquaporins in Renal Diseases.International journal of molecular sciences · 2019Review
- Association of Serum PSP/REG Iα with Renal Function in Pregnant Women.BioMed research international · 2019Article
- Arginine reprogramming in ADPKD results in arginine-dependent cystogenesis.American journal of physiology. Renal physiology · 2018Article
- Prognostic values ofBioscience reports · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is caused by the mutation of polycystins (PC-1 or PC-2), in which cysts start from the collecting duct to extend to all nephron segments with eventual end stage renal failure. The cyst development is attenuated by a vasopressin V2 receptor antagonist tolvaptan which, however, will not affect proximal tubule cysts devoid of V2 receptor. Aquaporin-11 (AQP11) is expressed selectively in the proximal tubule of the kidney and AQP11-null kidneys have a disruptive PC-1 trafficking to the plasma membrane to develop polycystic kidneys. Here, we analyzed AQP11-null kidneys at the beginning of cyst formation by quantitative proteomic analysis using Tandem Mass Tag (TMT). Among ~ 1200 identified proteins, 124 proteins were differently expressed by > 1.5 or < 0.8 fold change. A pancreatic stone inhibitor or a growth factor, lithostathine-1 (Reg1) was most enhanced by 5 folds which was confirmed by western blot, while mitochondria-related proteins were downregulated. The identified proteins will be new target molecules for the treatment of proximal tubular cysts and helpful to explore the functional roles of AQP11 in the kidney.
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