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

Chakravarthi, V. Praveen; Yerrathota, Sireesha; Radadiya, Priyanka S.; Bloomer, Clark; Gunewardhana, Sumedha; Sharma, Madhulika

doi:10.1016/j.dib.2020.105562

Cited by 2 publications

(8 citation statements)

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“…RNA sequencing was performed in four Notch4 d1 mice (2 females and 2 males) and six Notch3 d1 mice (3 females and 3 males) in an illumina NovaSeq 6000 sequencing machine (Illumina, San Diego, CA) at a strand specific 100 cycle paired-end resolution as described recently [3] . Sequencing generated between 28.0 to 32.1 million reads per sample.…”

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

“… These data will be of benefit to researchers who are interested in the role of Notch signaling in different renal diseases. These data can be compared to the data from wild type mice that we have recently published [3] . Together, this information can be used to compare renal genes that are altered in wildtype, Notch4 d1 and Notch3 d1 mice.…”

Section: Value Of the Datamentioning

confidence: 99%

“…These data can be compared to the data from wild type mice that we have recently published [3] . Together, this information can be used to compare renal genes that are altered in wildtype, Notch4 d1 and Notch3 d1 mice.…”

Section: Value Of the Datamentioning

confidence: 99%

“…While Notch1 or Notch2 deletion in mice is lethal, targeted deletion of Notch4 or Notch3 is not. This gives us the opportunity to learn more about the function and targets of Notch3 and Notch4 pathways, both of which are abnormally expressed in many diseases including cancers and kidney diseases [3] , [4] , [5] , [6] , [7] , [8] , [9] . The homozygous Notch4 d1 mice exhibit deletion of exon 21 and 22 which encode 186 amino acids of the extracellular domain of the Notch4 protein.…”

Section: Data Descriptionmentioning

confidence: 99%

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Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice

et al. 2021

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The Notch signaling pathway is an important conserved pathway for normal homeostasis during development. However, targeted deletion of Notch4 ( Notch4 d1 ) or Notch3 ( Notch3 d1 ) in mice is not lethal. In fact, both Notch4 d1 and Notch3 d1 mice develop normally and are fertile. Here we present RNA seq analysis of differential gene expression in the kidneys of Notch4 d1 mice versus the Notch3 d1 mice, all on FVB background. Kidneys were collected from Notch4 d1 and Notch3 d1 littermates at 3 months of age. RNA sequencing was carried out. 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 or greater to identify top upregulated and downregulated genes in Notch4 d1 mice compared to Notch3 d1 mice. The data provided will indentify targets of Notch3 and Notch4 signaling, specifically in kidney diseases where Notch3 or Notch4 are abberantly or redundantly expressed.

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Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

Section: Value Of the Datamentioning

confidence: 99%

Section: Value Of the Datamentioning

confidence: 99%

Section: Data Descriptionmentioning

confidence: 99%

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Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice

et al. 2021

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“…These genes were undifferentiated between Tg-N3KO and WT mouse kidneys (Fig: 4c). A list of genes comparing HIV-Tg26 versus WT has been shown by us before 37 . Genes that were most significantly downregulated in HIV-Tg-N3KO versus HIV-Tg26 kidneys are shown in figure 4d.…”

Section: Notch3 Deletion Inhibits Inflammatory Markers and Hiv-1 Genesmentioning

confidence: 99%

Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease

Thornton,

Sommer,

McGonigle

et al. 2023

Preprint

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Antiretroviral therapy (ART) has profoundly decreased HIV-1 associated morbidity. However, despite ART, immune cells remain latently infected and slowly release viral proteins, leading to chronic inflammation and HIV associated comorbidities. Thus, new strategies are needed to reduce the inflammatory effects of HIV-1. In previous studies we found that gamma secretase inhibitor (GSIXX) ameliorated renal lesions of HIV-Tg26 mice carrying replication defective HIV-1 PNL4-3 by inhibiting Notch activation. Since gamma secretase inhibition is not a safe strategy in humans, here we examined the specific role of the Notch3 pathway in the pathogenesis of the renal lesions and outcome of HIV-Tg26 mice. We found that Notch3 is activated in podocytes and other renal cells in HIV-Tg26 mice and human biopsies with HIV-1 associated Nephropathy (HIVAN). Knockdown of Notch3 in HIV-Tg26 mice revealed a marked reduction in the mortality rate, improvement in renal injury and function. RNA sequencing and immunolabeling data revealed that Notch3 deletion drastically reduced infiltrating renal macrophages in HIV-Tg-N3KO mice in association with renal reduction of HIV-nefmRNA expression levels. In fact, bone marrow derived macrophages from HIV-Tg26 mice showed a significant activation of Notch3 signaling. Further, systemic levels of TNF-alpha and MCP-1 and other inflammatory chemokines and cytokines were reduced in Tg-N3KO mice as compared to HIV-Tg26 mice and this translated to a marked reduction of HIV-induced skin lesions. Taken together, these studies strongly point to a dual inhibitory/therapeutic effect of Notch3 inhibition on HIV-induced systemic, skin and renal lesions independently of ART.Translational statementNotch3 inhibition has been reported to be an anti-inflammatory strategy for glomerular diseases. Here, using an HIV-1 transgenic mouse model we show that global Notch3 deletion not only improves kidney phenotype but also renal expression of HIV gene, Nef and systemic inflammation which leads to a drastic increase of life span of these mice. Notch3 inhibition can thus play a dual protective role in HIV related chronic diseases.

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

Cited by 2 publications

References 8 publications

Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice

Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice

Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease

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