ArticleJournal of the American Society of Nephrology : JASN2013
Rab38 modulates proteinuria in model of hypertension-associated renal disease.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
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- Tanshinone IIA is superior to paricalcitol in ameliorating tubulointerstitial fibrosis through regulation of VDR/Wnt/β-catenin pathway in rats with diabetic nephropathy.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The Critical Role of the Shroom Family Proteins in Morphogenesis, Organogenesis and Disease.Phenomics (Cham, Switzerland) · 2024Review
- Albumin uptake and processing by the proximal tubule: physiological, pathological, and therapeutic implications.Physiological reviews · 2022Review
- mRatBN7.2: familiar and unfamiliar features of a new rat genome reference assembly.Physiological genomics · 2022Review
- The adducin saga: pleiotropic genomic targets for precision medicine in human hypertension-vascular, renal, and cognitive diseases.Physiological genomics · 2022Review
- Emerging Insights Into Chronic Renal Disease Pathogenesis in Hypertension From Human and Animal Genomic Studies.Hypertension (Dallas, Tex. : 1979) · 2021Review
- Small Rab GTPases in Intracellular Vesicle Trafficking: The Case of Rab3A/Raphillin-3A Complex in the Kidney.International journal of molecular sciences · 2021Review
- Knockout ofThe Journal of pharmacology and experimental therapeutics · 2021Article
- Genetic susceptibility of hypertension-induced kidney disease.Physiological reports · 2021Review
- Gender Differences in Genetic Associations of RAB38 with Urinary Protein-to-Creatinine Ratio (UPCR) Levels in Diabetic Nephropathy Patients.Journal of personalized medicine · 2020Article
- Rat models of human diseases and related phenotypes: a systematic inventory of the causative genes.Journal of biomedical science · 2020Review
- A Mutation inJournal of the American Society of Nephrology : JASN · 2020Article
- Pulling the Hood off Genetic Susceptibility to Hypertensive Renal Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Combined deficiency of RAB32 and RAB38 in the mouse mimics Hermansky-Pudlak syndrome and critically impairs thrombosis.Blood advances · 2019Article
- Analysis of the genomic architecture of a complex trait locus in hypertensive rat models linkseLife · 2019Article
- Function and regulation of the Caenorhabditis elegans Rab32 family member GLO-1 in lysosome-related organelle biogenesis.PLoS genetics · 2018Article
- Chrm3 Gene and M3 Muscarinic Receptors Contribute to Salt-Sensitive Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018Article
- The transcriptome of theAmerican journal of physiology. Renal physiology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We previously reported that the fawn-hooded hypertensive (FHH) rat is a natural Rab38 knockout, supported by a congenic animal (FHH.BN-Rab38) having less proteinuria than FHH animals. Because these congenic animals contain Brown Norway (BN) alleles for five other named genes; however, a causal role for Rab38 in the FHH phenotype remains uncertain. Here, we used transgenic and knockout models to validate Rab38 and to exclude other genes within the 1.5 Mb congenic region from involvement in causing the FHH phenotype. Transgenic rats homozygous for the wild-type Rab38 BN allele on the FHH background exhibited phenotypic rescue, having 43% lower proteinuria and 75% lower albuminuria than nontransgenic FHH littermates. Conversely, knockout of the Rab38 gene on the FHH.BN-Rab38 congenic line recapitulated a proteinuric phenotype indistinguishable from the FHH strain. In addition, in cultured proximal tubule LLC-PK1 cells, knockdown of Rab38 mRNA significantly decreased endocytosis of colloidal gold-coupled albumin, supporting the hypothesis that Rab38 modulates proteinuria through effects on tubular re-uptake and not by altering glomerular permeability. Taken together, these findings validate Rab38 as a gene having a causal role in determining the phenotype of the FHH rat, which models hypertension-associated renal disease. Furthermore, our data suggest that Rab38 affects urinary protein excretion via effects in the proximal tubule.
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