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Atg5 Deletion in Macrophages Protects Against Kidney Fibrosis in Mice

ABSTRACT: To identify the factors or genes associated with macrophages in a condition of ATG5 deficiency, we isolated F4/80+ cells from kidney single-cell suspensions of MΦ Atg5 -/- and WT mice(10 mouse per group) by immunomagnetic positive selection. we performed RNA-seq and heatmap analysis to identify the expression of chemokine receptor genes in MΦ Atg5-/- and WT mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE215833 | GEO | 2023/10/15

REPOSITORIES: GEO

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ATG5-regulated MCP-1 production in myeloid cells selectively modulates anti-malarial CD4+ Th1 responses

Project description:Induction of parasite-specific CD4+ Th1 cell responses is a promising strategy for designing effective blood-stage malaria vaccines; however, the underlying regulatory mechanisms remain largely unknown. This study demonstrated that ATG5 deficiency in myeloid cells can significantly inhibit the growth of rodent blood-stage malarial parasites by enhancing parasite-specific CD4+ Th1 cell responses. This effect was independent of ATG5-mediated canonical and non-canonical autophagy. Mechanistically, ATG5 deficiency promoted myeloid cell (Ly6G-CD11b+F4/80-) survival and subsequently increased MCP-1 production in parasite-infected mice. Ly6G-CD11b+F4/80- cell-derived MCP-1 interacted with CCR2 on CD4+ Th1 cells for their optimized responses through the JAK2/STAT4 pathway. Notably, recombinant MCP-1 significantly improved parasite-specific CD4+ Th1 responses of the whole-killed blood-stage vaccine. Conclusively, our study highlights the previously unrecognized role of ATG5 in modulating myeloid cell survival via MCP-1 production, which selectively promotes CD4+ Th1 cell responses. Our findings provide new insights into the development of effective antimalarial vaccines.

2023-12-16 | GSE239405 | GEO

MCP-1 production regulated by ATG5 in inflammatory monocytes selectively modulates anti-malarial CD4+ Th1 response

Project description:A promising strategy to design effective malaria blood-stage vaccines is to induce parasite-specific CD4+ Th1 cell responses, but the regulatory mechanism of which is still largely unknown. Here, we showed that the ATG5-deficiency in myeloid cells significantly inhibit the growth of rodent blood-stage malaria parasites through specifically enhancing parasite-specific CD4+ Th1 cell responses. This effect was independent of ATG5-mediated canonical autophagy and non-canonical autophagy. Mechanistically, the deficiency of ATG5 promoted the survival of inflammatory monocytes (CD11b+F4/80- cells), and sequentially increased the generation of chemokine MCP-1 in parasite-infected mice. The interaction of CD11b+F4/80- cells-derived MCP-1 with CCR2 on CD4+ Th1 cells for its optimized differentiation dependent on Jak2/stat4 pathway. Therefore, we highlight the previously unrecognized role of ATG5 in the modulation of the survival of inflammatory monocytes to produce MCP-1, and the selective promoting effect of MCP-1 on CD4+ Th1 cell differentiation, which shed new lights on effective malaria vaccine designation.

2024-03-01 | GSE228461 | GEO

Microarray data of Atg5 WT and KO hematopoietic stem/progenitor cells

Project description:To comprehensively examine differences of gene expression patterns between WT and ATG5 KO HSCs/progenitors, we isolated LSK cells and conducted the microarray analysis.

2021-01-20 | GSE153613 | GEO

Global analysis of impact of Atg5 mutation on steady-state protein levels

Project description:This experiment analyzes the global impact of Atg5-/- mutation on steady-state protein levels by a standard SILAC experiment. WT+vector cells were grown in isotopically labeled media for multiple passages in order to fully label the proteome. Unlabeled Atg5-/- cells and labeled WT+vector cells were grown to confluency and protein extracts from quiescent cultures were combined at a 1:1 ratio and analyzed by LC-MS/MS. In this experiment, ratios of labeled to unlabeled spectra report on changes in steady-state expression levels of proteins induced by impairment of autophagy. Table of files Cells Fractionation Raw Data Filenames Wildtype & Atg5-/- Yes SILAC_(1-8).raw (8 fractions)

2016-06-14 | PXD003558 | Pride

Genome-wide expression analysis in Control and Atg5-deficient eosinophils.

Project description:Depletion of autophagy-associated protein 5 (Atg5), specifically within the eosinophil lineage in mice, resulted in increased body weight, impaired glucose metabolism, and structural alterations in adipose tissue. Our findings highlight that Atg5 influences the functional activity of eosinophils within adipose tissue rather than their quantity. To gain a deeper understanding of the molecular mechanisms underlying ATG5's role in eosinophils, we conducted total RNA-seq analyses on control and Atg5-deficient eosinophils isolated from both bone marrow and blood of mice.

2023-11-21 | GSE245134 | GEO

Next Generation Sequencing analysis atg5 gene expression in zebrafish model

Project description:Purpose: study of function of ATG5 protein on zebrafish larvae development Methods: Using morpholino oligos for atg5 gene knock down and overexpression, injected into one- to four-cell-stage embryos,extracted total RNA, then sending to RNA sequencing. Results: we compared to Wildtype, 5MO and atg5 mRNA groups, we analyza autophagy related gene mRNA expression, there are obvious different. Conclusion: our study showed the function of autophagy related gene 5 on zebrafish larvae, it has an important significant for understanding the affection of autophagy on embryo development

2019-04-30 | GSE120170 | GEO

Autophagy and alternative NF-kappaB inhibition by RNAi against RELB, ATG5 or ULK1 in A549 human cancer cells

Project description:In order to understand the contribution of autophagy and alternative NF-kappaB signalling to transcriptional output in A549 lung cancer cells, RNAi was used to knockdown the expression of core autophagy genes (ATG5, ULK1) or the key subunit of alternative NF-kappaB RELB. Seven samples were prepared for each biological replicate; two sequence independent non-targeting control siRNAs were transfected as a negative control. Three sequence independent siRNAs targeting the core autophagy machinery were transfected (ATG5 si, ATG5 si(2), ULK1 si). N.B. ATG5 si(2) only partially ablates Atg5 protein expression whereas ATG si has greater efficacy. Two sequence independent siRNAs targeting RELB were transfected (RELB si, RELB si(2) ). Three independent biological replicates of all conditions were obtained, by performance of the experiment on different days.

2015-09-18 | E-GEOD-73158 | biostudies-arrayexpress

Identification Atg5-related microRNAs involved in the regulation of tumor formation

Project description:Autophagy plays an important role in physiology and tumorigenesis. We and others have demonstrated that Ha-ras overexpression induces autophagy in NIH3T3 cells. Autophagic machinery is regulated by a family of autophagy associated genes (Atg). The inducible Ha-ras oncogene was introduced into mouse embryo fibroblast Atg5 wild type [MEF-Atg5(+/+)] and Atg5 knock-out [MEF-Atg5(-/-)] cells and the stable cell lines MR and M5R were established, respectively. Our results showed that M5R cell induced larger tumor formation compared with MR cells while these two cell lines were subcutaneously injected into SCID mice under Ha-ras overexpression conditions. It indicates that Atg5 is involved in the suppression of Ras-related tumor formation. MicroRNA (miRNA), approximately 22 nucleotide of non-coding RNA, regulates transcription and translation of the target genes and is involved in cell differentiation and tumorigenesis. A miRNA microarray (932 probes) screening was conducted to identify the autophagy-tumorigenesis-related miRNAs. Among the significant genes, miR-224 was highly expressed in autophagy deficient cell and it induced tumors. Overexpression miR-224 enhanced the activity of migration and invasion in vitro and tumor formation in vivo. In conclusion, this is the first report to demonstrate that autophagy suppresses tumor formation through down-regulation of microRNA in this case miR-224. MR and M5R cell lines were treated with IPTG for 48 hr. In addition, these cell lines were subcutaneously injected into mice to induce tumor formation. The RNA samples were extracted from above cell lines and tumors. In this research, BEL/ITRI 15K V1.0 miRNA microarray chips were used to evaluate the miRNA expression profile.

2012-06-25 | E-GEOD-38911 | biostudies-arrayexpress

Transcription profiling of mouse colonic goblet cells deficient in Atg5

Project description:Purpose of this experiment was to gain insight into the transcriptional changes resulting from Atg5 deficiency in colonic goblet cells.

2010-09-30 | E-TABM-815 | biostudies-arrayexpress

Expression in IFN-gamma treated control and Atg5-/- macrophages

Project description:Type-I (α/β) and -II (γ) interferons (IFN), through an incompletely understood combination of redundant and unique mechanisms, are essential for host resistance to viral infection. We report a requirement for the Atg5-Atg12/Atg16L1 autophagosome elongation complex in IFNγ-mediated control of murine norovirus in macrophages. We use microarrays to compare transcriptional changes induced in control and Atg5 deficient macrophages by IFNγ treatment. Bone marrow derived macrophages were generated from Atg5flox/flox and Atg5flox/flox+LysM cre mice and treated with media alone or 100U/ml of IFNγ for 14 hrs. RNA was extracted using Trizol (Invitrogen) and 10 µg of RNA hybridized to Affymetrix microarrays.

2012-01-05 | E-GEOD-34863 | biostudies-arrayexpress

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