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The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner

ABSTRACT: The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner

PROVIDER: PRJNA601160 | ENA |

REPOSITORIES: ENA

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The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner

Project description:The matricellular protein Fibulin-5 (Fbln5) is a secreted protein that is essential for elastic fiber formation, and pancreatic islets are usually surrounded by the extracellular matrix (ECM), which includes elastic fibers. However, much uncertainty remains regarding the function of the ECM and its components in β-cells. Here, we describe the role of Fbln5 in β-cell replication. Fbln5 expression was increased upon glucose stimulation in β-cells of mouse and human islets. β-Cell-specific Fbln5-knockout (βFbln5KO) mice exhibit significantly reduced β-cell proliferation in vivo but not in vitro. Secreted extracellular Fbln5 enhances β-cell replication. Fbln5-deficient β-cells exhibit downregulated expression of the gene encoding polo-like kinase 1 (PLK1), which is accompanied by ERK-mediated FoxM1 nuclear export. These data suggest that Fbln5 is secreted from β-cells in response to glucose and plays important roles in the appropriate maintenance of β-cell functions in an autocrine or paracrine manner.

2024-11-19 | GSE143633 | GEO

The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner.

Project description:The matricellular protein Fibulin-5 (Fbln5) is a secreted protein that is essential for elastic fiber formation, and pancreatic islets are usually surrounded by the extracellular matrix (ECM), which includes elastic fibers. However, much uncertainty remains regarding the function of the ECM and its components in β-cells. Here, we describe the role of Fbln5 in β-cell replication. Fbln5 expression was increased upon glucose stimulation in β-cells of mouse and human islets. β-Cell-specific Fbln5-knockout (βFbln5KO) mice exhibit significantly reduced β-cell proliferation in vivo but not in vitro. Secreted extracellular Fbln5 enhances β-cell replication. Fbln5-deficient β-cells exhibit the downregulated expression of the gene encoding Polo-like kinase 1 (PLK1), which is accompanied by ERK-mediated FoxM1 nuclear export. These data suggest that Fbln5 is secreted from β-cells in response to glucose and plays important roles in the appropriate maintenance of β-cell functions in an autocrine or paracrine manner.

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Fibulin-5, an integrin-binging matricellular protein, maintains epidermal stem cell heterogeneity during skin aging

Project description:The extracellular matrix (ECM) plays a crucial role in building the extracellular environment and translating extracellular information into biochemical signals that sustain organ functions. Fibulin-5 is a multifunctional ECM protein essential for the formation of elastic fibers and the regulation of cellular functions through integrin binding. Fibulin-5 expression decreases with aging in human skin; however, its functional significance remains unknown. To address the roles of fibulin-5 in regulating epidermal stem cells during skin aging, Fbln5 knockout mice were examined for changes in their cellular and molecular phenotypes. Loss of Fbln5 in mice results in early impairments of epidermal stem cell properties, similar to the chronological aging of the skin. Fibulin-5 deficiency results in the suppression of integrins and other cell junctional molecules, leading to the inactivation of YAP signaling in epidermal stem cells. The reduced YAP signal is associated with the down-regulation of the fast-cycling epidermal stem cell marker, SLC1A3, in human skin and primary keratinocytes. These findings underscore the important role of fibulin-5 in governing the balance of epidermal stem cell populations during skin aging via crosstalk between the extracellular environment and intracellular signaling.

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PyMINEr Finds Gene and Autocrine/Paracrine Networks from Human Islet scRNAseq

Project description:Toolsets available for in-depth analysis of scRNAseq datasets by biologists with little informatics experience is limited. Here we describe an informatics tool (PyMINEr) that fully automates cell type identification, cell type-specific pathway analyses, graph theory-based analysis of gene regulation, and detection of autocrine/paracrine signaling networks in silico. We applied PyMINEr to interrogate human pancreatic islet scRNAseq datasets and discovered several features of co-expression graphs including: concordance of scRNAseq-graph structure with both protein-protein interactions and 3D-genomic architecture; association of high connectivity and low expression genes with cell type-enrichment; and potential for graph-structure to clarify potential etiologies of enigmatic disease-associated variants. We further created a consensus co-expression network and autocrine/paracrine signaling networks within and across islet cell types from 7-datasets. PyMINEr correctly identified changes in BMP/WNT signaling associated with cystic fibrosis pancreatic acinar-cell loss. This proof-of-principle study demonstrates that the PyMINEr framework will be a valuable resource for scRNAseq analyses.

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Arginine utilization following mycobacteria infection in macrophages is dependent on autocrine-paracrine signaling

Project description:Nitric oxide (NO) produced by macrophages (MØs) is toxic to both host tissues and invading pathogens and its regulation is therefore essential to suppress host cytotoxicity. MØ arginase 1 (Arg1) inhibits NO production by competing with NO synthases for arginine, the common substrate of NO synthases and arginases. Two signal transduction pathways control Arg1 expression in MØs. First, a MyD88-dependent pathway induces Arg1 in intracellular infections, while a second Stat6-dependent pathway is required for Arg1 expression in alternativelyactivated MØs. We found that mycobacteria-infected MØs produce soluble factors that induce Arg1 in an autocrine-paracrine manner via Stat3. We identify these factors as IL-6, IL-10 and GCSF. We further establish that Arg1 expression is controlled by the MyD88-dependent production of IL-6, IL-10 and G-CSF rather than cell intrinsic MyD88 signaling to Arg1. Our data reveal the MyD88-dependent pathway of Arg1induction following BCG infection requires Stat3 activation and may result in the development of an immunosuppressive niche in granulomas due to the induced Arg1 production in surrounding uninfected MØs We used microarrays to perform genome wide expression analysis in mycobacteria-infected macrophages from C57Bl/6 WT and MyD88-knockout mice.

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Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications

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Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[BAT]

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Myostatin regulates energy homeostasis through autocrine- and paracrine-mediated microenvironment communications[gastrocnemius]

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Arginine utilization following mycobacteria infection in macrophages is dependent on autocrine-paracrine signaling

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