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Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE205060 | GEO | 2024/05/27

REPOSITORIES: GEO

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Transcriptomic analysis of HIV-associated nephropathy (Tg26) mouse kidney [bulk RNA-seq]

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Transcriptomic data indicating differential expressed genes between HIV-1 Associated Nephropathy (HIVAN) mouse model (Tg26) and wildtype mice.

Project description:Tg26 mice are robust models of human immunodeficiency virus 1 associated nephropathy (HIVAN). These mice are useful for HIVAN pathology analysis, and recent studies suggest that the Tg26 mouse model is an excellent model of other chronic kidney diseases. We performed RNA seq analysis of differential gene expression in the kidneys of Tg26 mice. Kidneys were collected from Tg26 mice and wildtype (WT) littermates at 3 months of age. The raw data were analyzed for differential gene expression using a negative binomial generalized linear model in the DeSeq2 software package. We used P-Value ?0.05 and an absolute fold change of 1.5 to identify top 50 upregulated and top 50 downregulated differentially expressed genes between the WT and Tg26 mice. As expected inflammatory genes were among the top differentially regulated genes. Our data provides yet another level of information to help gain a more comprehensive understanding of disease progression and identify potential drug targets for HIVAN and chronic kidney diseases.

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ST3GAL1-Associated Transcriptomic Program in Glioblastoma Tumor Growth, Invasion, and Prognosis

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An HIV-Tat inducible mouse model system of childhood HIV-associated nephropathy.

Project description:Modern antiretroviral therapies (ART) have decreased the prevalence of HIV-associated nephropathy (HIVAN). Nonetheless, we continue to see children and adolescents with HIVAN all over the world. Furthermore, once HIVAN is established in children, it is difficult to revert its long-term progression, and we need better animal models of childhood HIVAN to test new treatments. To define whether the HIV-1 trans-activator (Tat) gene precipitates HIVAN in young mice, and to develop an inducible mouse model of childhood HIVAN, an HIV-Tat gene cloned from a child with HIVAN was used to generate recombinant adenoviral vectors (rAd-Tat). rAd-Tat and LacZ control vectors (2×109) were expressed in the kidney of newborn wild-type and HIV-transgenic (Tg26) FVB/N mice without significant proteinuria (n=5; 8 per group). Mice were sacrificed 7 and 35?days later to assess their renal outcome, the expression of HIV-genes and growth factors, and markers of cell growth and differentiation by RT-qPCR, immunohistochemistry and/or western blots. HIV-Tat induced the expression of HIV-1 genes and heparin-binding growth factors in the kidney of HIV-Tg26 mice, and precipitated HIVAN in the first month of life. No significant renal changes were detected in wild-type mice infected with rAd-Tat vectors, suggesting that HIV-Tat alone does not induce renal disease. This new mouse model of childhood HIVAN highlights the critical role that HIV-Tat plays in the pathogenesis of HIVAN, and could be used to study the pathogenesis and treatment of HIVAN in children and adolescents.

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