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Thrombospondin-1 promotes fibro-adipogenic stromal expansion and contractile dysfunction of the diaphragm in obesity

ABSTRACT: This study defines the impact of in vivo thrombospondin-1 (THBS1) ablation on diaphram stromal cell profile, histology and contractile funciton in a mosue model of diet-induced obesity

ORGANISM(S): Mus musculus

PROVIDER: GSE241005 | GEO | 2023/08/16

REPOSITORIES: GEO

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Thrombospondin-1 promotes fibro-adipogenic stromal expansion and contractile dysfunction of the diaphragm in obesity II

Project description:This study defines the impact of in vivo thrombospondin-1 (THBS1) ablation on diaphram stromal cell profile, histology and contractile funciton in a mosue model of diet-induced obesity

2023-08-18 | GSE241168 | GEO

Regulation of muscle mass by Thrombospondin-1

Project description:Loss of muscle mass is a pathological driver in both chronic illness and aging. We have discovered that skeletal muscle specific thrombospondin-1 (Thbs1) transgenic mice have profound muscle atrophy with age-dependent decreases in exercise capacity and premature lethality. Here, we compared the transcriptional profiles of skeletal muscle from control non-transgenic mice with those overexpressing Thbs1 in order to elucidate the transcriptional changes underlying the observed effects on skeletal muscle mass. The overall purpose was to identify new, effective targets to combat muscle atrophy and sarcopenia.

2024-04-18 | GSE245663 | GEO

O-fucosylation of Thrombospondin Type I Repeats on Thrombospondin 1 is dispensable for trafficking to Platelets

Project description:Thrombospondin 1 (THBS1) is a secreted extracellular matrix glycoprotein that regulates a variety of cellular and physiological processes. THBS1’s diverse functions are attributed to interactions between the modular domains of THBS1 with an array of proteins found in the extracellular matrix. THBS1’s three Thrombospondin Type 1 Repeats (TSRs) domains are modified with O-linked glucose-fucose disaccharide and C-mannose. It is unknown whether these modifications impact trafficking and/or function of THBS1 in vivo. The O-fucose is added by Protein O-fucosyltransferase 2 (POFUT2) and is sequentially extended to the disaccharide by β3glucosyltransferase (B3GLCT). The C-mannose is added by one or more of four C-mannosyltransferases. O-fucosylation by POFUT2/B3GLCT in the endoplasmic reticulum has been proposed to play a role in quality control by locking TSR domains into their 3-dimensional fold, allowing for proper secretion of many O-fucosylated substrates. Prior studies showed the siRNA knockdown of POFUT2 in HEK293T cells blocked secretion of TSRs 1-3 from THBS1. Here we demonstrated that secretion of THBS1 TSRs 1-3 was not reduced by CRISPR-Cas9-mediated knockout of POFUT2 in HEK293T cells and demonstrated that knockout of Pofut2 or B3glct in mice did not reduce trafficking of endogenous THBS1 to platelet secretory granules, a major site of THBS1 expression. Additionally, we demonstrated that all three TSRs from platelet THBS1 were highly C-mannosylated, which has been shown to stabilize TSRs in vitro. Combined these results suggested that POFUT2 substrates with TSRs that are also modified by C-mannose may be less susceptible to trafficking defects resulting from loss of the glucose-fucose disaccharide.

2023-02-02 | PXD037158 | Pride

Fibro-Adipogenic Remodeling of the Diaphragm in Obesity-Associated Respiratory Dysfunction.

Project description: Not available

| S-EPMC6302533 | biostudies-literature

Haloplasma contractile

Project description:Haloplasma contractile overview

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Proteome of Young and Old Murine Diaphragm and Associaated Changes in Contractile Properties

Project description:Proteomic analysis of young and old murine diaphragm and associated changed in contractile aproperties. Redox sensitive Cysteine residues from both adult and old diaphragm tissues examined.

2018-02-12 | PXD005014 | Pride

microRNA-222 Attenuates Mitochondrial Dysfunction Induced by Transmissible Gastroenteritis Virus via Targeting Thrombospondin-1 and Inhibiting Cluster of Differentiation 47

Project description:Transmissible gastroenteritis virus (TGEV) is a member of Coronaviridae family. Our previous research showed that TGEV infection could induce mitochondrial dysfunction and up-regulat miR-222 level. Therefore, we presumed that miR-222 might be implicated in regulating mitochondrial dysfunction induced by TGEV infection. To verify the hypothesis, the effect of miR-222 on mitochondrial dysfunction was detected and showed that miR-222 attenuated TGEV-induced mitochondrial dysfunction. To investigate the underlying molecular mechanism of miR-222 in TGEV-induced mitochondrial dysfunction, a quantitative proteomic analysis of PK-15 cells that were transfected with miR-222 mimics and infected with TGEV was performed. In total, 4151 proteins were quantified and 100 differentially expressed proteins were obtained (57 up-regulated, 43 down-regulated), among which thrombospondin-1 (THBS1) and cluster of differentiation 47 (CD47) were down-regulated. THBS1 was identified as the target of miR-222. Knockdown of THBS1 and CD47 increased mitochondrial Ca2+ level and decreased mitochondrial membrane potential (MMP) level. Together, our data establish a significant role of miR-222 in regulating mitochondrial dysfunction in response to TGEV infection.

2018-12-19 | PXD010927 | Pride

Haloplasma contractile SSD-17B

Project description:Haloplasma contractile SSD-17B genome sequencing

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Perivascular Fibro-Adipogenic Progenitor Tracing during Post-Traumatic Osteoarthritis.

Project description: Not available

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Metabolic reprogramming of fibro/adipogenic progenitors facilitates muscle regeneration.

Project description: Not available

| S-EPMC7003708 | biostudies-literature