Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Tolerogenic dendritic cells protect against acute kidney injury

ABSTRACT: We use tolDCs from syngeneic (C57BL6) and allogeneic (BALB/c) mice to show potent renoprotective abilities in a ischemia reperfusion AKI model. Dendritic cells were derived from mice bone marrow and cultured for 7 days with GM-CSF and IL-4. Tolerogenic DCs were cultured in the same DC media but with the addition of VitD3 and IL10. LPS was added on day 6 and cells harvested for use or analysis on day 7.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Nicholas Matigian

PROVIDER: E-MTAB-14618 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Tolerogenic dendritic cells protect against acute kidney injury.

Li Jennifer S Y JSY Robertson Harry H Trinh Katie K Raghubar Arti M AM Nguyen Quan Q Matigian Nicholas N Patrick Ellis E Thomson Angus W AW Mallett Andrew J AJ Rogers Natasha M NM

Kidney international 20230525 3

Ischemia reperfusion injury is a common precipitant of acute kidney injury that occurs following disrupted perfusion to the kidney. This includes blood loss and hemodynamic shock, as well as during retrieval for deceased donor kidney transplantation. Acute kidney injury is associated with adverse long-term clinical outcomes and requires effective interventions that can modify the disease process. Immunomodulatory cell therapies such as tolerogenic dendritic cells remain a promising tool, and her ...[more]

PMID: 37244471

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Project description:Telomere attrition ultimately leads to the activation of protective cellular responses such as apoptosis or senescence. Impairment of such mechanisms can allow continued proliferation despite the presence of dysfunctional telomeres. Under such conditions, high levels of genome instability are often engendered. Data from both mouse and human model systems indicate that a period of genome instability might facilitate tumorigenesis. Here, we employ a liposarcoma model system to assay telomere maintenance mechanism-specific genetic alterations. A multiassay approach was used to assess the telomere maintenance mechanism(s) active in tumors. Genomic DNA from these samples was then analyzed by high resolution DNA mapping array in order to identify genetic alterations. Our data reveal a higher level of genome instability in ALT-positive tumors as compared with telomerase-positive tumors, whereas tumors lacking both mechanisms have relatively low levels of genome instability. The bulk of the genetic changes are amplifications, regardless of the mode of telomere maintenance employed. We also identified genetic changes specific to the ALT mechanism, e.g., deletion of chromosome 1q32.2-q44, as well as changes that are underrepresented amongst ALT-positive tumors, such as amplification of chromosome 12q14.3-q21.2. Taken together, these studies provide insight into the molecular pathways involved in the regulation of ALT and reveal several loci that might be exploited either as prognostic markers or targets of chemotherapeutic intervention. Experiment Overall Design: Goal: To study telomere maintenance and genetic alterations in liposarcoma using Affymetrix Mapping 50K Xba 240 GeneChip. Experiment Overall Design: Brief description: Telomere attrition ultimately leads to the activation of protective cellular responses such as apoptosis or senescence. Impairment of such mechanisms, however, can allow continued proliferation despite the presence of dysfunctional telomeres. Under such conditions, high levels of genome instability are often engendered. Data from both mouse and human model systems indicate that a period of genome instability might facilitate tumorigenesis. The high-density SNP-based microarrays (e.g., Affymetrix 100K arrays) can detect deletions, amplifications, and loss-of-heterozygosity on a genome in the liposarcoma samples. Chromosomal alterations of liposarcoma should provide insight into the molecular pathways involved in the regulation of ALT and reveal several loci that might be exploited either as prognostic markers or targets of chemotherapeutic intervention. Experiment Overall Design: Quality control steps taken: Experiment Overall Design: a. PCR-based quality assessment of liposarcoma tissue genomic DNA Experiment Overall Design: b. Nanodrop analysis of preprocessed DNA prior to array hybridization Experiment Overall Design: c. Analysis of array call rates following hybridization (array experiments giving call rates of less than 80% were routinely repeated) Experiment Overall Design: Data extraction and processing protocols Experiment Overall Design: a. Image scanning hardware and software, and processing procedures and parameters: SNP array hybridization was detected using a GCS3000 scanner (Affymetrix). SNP calls and signal quantification were obtained with Gene Chip Operating System (GCOS) 1.2 and Affymetrix GDAS 3.0 with Dynamic Model Mapping Analysis by default settings (0.25) for both homozygote and heterozygote call thresholds. Copy number analyses were carried out using Affymetrix Chromosome Copy Number Analysis Tool (CNAT) 2.1 with a default genomic smoothing window setting of 0.5 Mb. Experiment Overall Design: b. Normalization, transformation and data selection procedures and parameters. Array data was normalized by a reference data set with CNAT. Experiment Overall Design: c. Definition of chromosomal aberration, amplification, deletion and LOH used for data interpretation: These definitions and their algorithms were described in detail by Huang, et al: Whole genome DNA copy number changes identified by high density oligonucleotide arrays. Hum Genomics. 2004 May;1(4):287-99.

Dataset Information

Tolerogenic dendritic cells protect against acute kidney injury

Publications

Tolerogenic dendritic cells protect against acute kidney injury.

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