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Targeting WIP1 phosphatase promotes partial remission in experimental collapsing glomerulopathy

ABSTRACT: Targeting WIP1 phosphatase promotes partial remission in experimental collapsing glomerulopathy

PROVIDER: PRJNA1051068 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27175683_1.fastq.gz	Fastqsanger.gz
	SRR27175683_2.fastq.gz	Fastqsanger.gz
	SRR27175684_1.fastq.gz	Fastqsanger.gz
	SRR27175684_2.fastq.gz	Fastqsanger.gz
	SRR27175685_1.fastq.gz	Fastqsanger.gz

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Targeting WIP1 phosphatase promotes partial remission in experimental collapsing glomerulopathy

Project description:Collapsing focal segmental glomerulosclerosis (FSGS), also known as collapsing glomerulopathy (CG), is the most aggressive variant of FSGS and is characterized by rapid progression to end-stage kidney disease (ESKD). Understanding CG pathogenesis represents a key step for the development of targeted therapies. Previous work implicated the telomerase protein component TERT in CG pathogenesis, as transgenic TERT expression in adult mice resulted in a CG resembling that seen in human primary CG and HIV-associated nephropathy (HIVAN). We used the telomerase-induced mouse model of CG (i-TERTci mice) to identify mechanisms to inhibit CG pathogenesis. We found that inactivation of WIP1 phosphatase, a p53 target acting in a negative feedback loop, blocks disease initiation in i-TERTci mice. Repression of disease initiation upon WIP1 deficiency is associated with senescence enhancement and requires TGF-b functions. We further assessed efficacy of a pharmacologic treatment to reduce disease severity in both i-TERTci mice and in a mouse model of HIVAN (Tg26 mice). We found that pharmacologic inhibition of WIP1 enzymatic activity in either telomerase mice with CG or in Tg26 mice promotes partial remission of proteinuria and ameliorates renal histopathologic features. Histological as well as high throughput sequencing methods further showed that selective inhibition of WIP1 does not promote kidney fibrosis or inflammation. Our findings suggest that targeting WIP1 may be an effective therapeutic strategy for patients with CG.

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Murine liver tissues: WT and Wip1 KO mice after Partial Hepatectomy at 24h and 36 h.

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Murine liver tissues: WT and Wip1 KO mice after Partial Hepatectomy at 24h and 36 h.

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Circulating small RNAs in transplant glomerulopathy

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Expression data from Wild type and Wip1 knockout Hematopoietic stem cell

Project description:Hematopoietic stem cell (HSC) aging underlies many age-related hematopoietic disorders. Accumulation of DNA damage is a hallmark of HSC aging. Wild-type p53-induced phosphatase 1 (Wip1) is a homeostatic regulator of DNA damage response. We used microarrays to detail the global programme of gene expression in Wip1 KO HSC Wild-type p53-induced phosphatase 1 (Wip1) knockout HSC and Wild type HSC were selected for RNA extraction and hybridization on Affymetrix microarrays.

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Transcriptional signatures that define Ulcerative Colitis in remission

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Plasma proteomics in children with new-onset type 1 diabetes: a strong tool to identify partial remission biomarkers

Project description:Partial remission (PR) occurs in only half of patients with new-onset type 1 diabetes (T1D) and correspond to a transient period characterized by low daily insulin needs, low glycemic fluctuations and increased endogenous insulin secretion. While identification of newly-onset T1D patients with significant residual beta-cell function may foster patient-specific interventions, reliable predictive biomarkers of PR occurrence currently lack. We analyzed the plasma of children with new-onset T1D to identify biomarkers present at diagnosis that predicted PR at 3 months post-diagnosis. We first performed an extensive shotgun proteomic analysis using Liquid Chromatography-Tandem-Mass-Spectrometry (LCMS/MS) on the plasma of 16 children with new-onset T1D and quantified nearly 1500 unique proteins with 98 significantly correlating with Insulin-Dose Adjusted glycated hemoglobin A1c score (IDAA1C). We next applied a series of both qualitative and statistical filters that yielded to the selection of 26 protein candidates that were associated to pathophysiological mechanisms related to T1D. Finally, we translationally validated several of the candidates using single-shot targeted proteomic (PRM method) on raw plasma. Taken together, we identified plasmatic biomarkers present at diagnosis that may predict the occurrence of PR in a single mass-spectrometry run. We believe that the identification of new predictive biomarkers of PR and β-cell function is key to stratify patients with new-onset T1D for β-cell preservation therapies

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