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Cannabidiol ameliorates mitochondrial disease via PPARg activation

ABSTRACT: Cannabidiol ameliorates mitochondrial disease via PPARg activation

PROVIDER: PRJNA1105908 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28830100_1.fastq.gz	Fastqsanger.gz
	SRR28830100_2.fastq.gz	Fastqsanger.gz
	SRR28830101_1.fastq.gz	Fastqsanger.gz
	SRR28830101_2.fastq.gz	Fastqsanger.gz
	SRR28830102_1.fastq.gz	Fastqsanger.gz

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Cannabidiol ameliorates mitochondrial disease via PPARg activation

Project description:Mutations in mitochondrial energy-producing genes lead to a heterogeneous group of untreatable disorders known as primary mitochondrial diseases (MD). Leigh syndrome (LS) is the most common pediatric MD and is characterized by progressive neuromuscular affectation and premature death. Here, we show that daily cannabidiol (CBD) administration significantly extends lifespan and ameliorates pathology in two LS mouse models, and cellular function in fibroblast from LS patients. CBD delays motor decline and neurodegenerative signs, improves social deficits and breathing abnormalities, decreases thermally induced seizures, and improves neuropathology in affected brain regions. Mechanistically, we identify peroxisome proliferator-activated receptor gamma (PPARg) as a key contributor to CBD’s beneficial effects, and provide proof of dysregulated PPARg expression and activity as a common feature in both mouse neurons and fibroblasts from LS patients. Taken together, our results provide the first evidence for CBD as a potential treatment for LS.

2024-08-03 | GSE266113 | GEO

Linezolid prevents fibroblast activation and ameliorates tissue fibrosis by inhibition of mitochondrial translation

Project description:Background: Beyond its role as a ribosome-targeting antibiotic, linezolid was recently shown to modulate immune responses by inhibiting mitochondrial translation. Since mitochondrial dysfunction is implicated in various fibrotic diseases, including systemic sclerosis (SSc), this study aimed to evaluate the antifibrotic potential of linezolid and delineate its underlying mechanisms in SSc. Methods: The effects of linezolid on fibrotic tissue remodeling were assessed using multiple experimental systems: human dermal fibroblasts, human macrophages, three-dimensional SSc skin equivalents (SScSE), the murine model of sclerodermatous chronic graft-versus-host disease (sclGvHD) and precision-cut skin slices (PCSS) obtained from SSc patients, by RNA sequencing, immunofluorescence, Western Blot and histology. Mitochondrial function was evaluated using Seahorse assays alongside mitochondrial protein synthesis assessments. Results: Linezolid inhibited TGFβ-induced fibroblast activation in cultured human fibroblasts, SScSE, sclGvHD mice and SSc PCSS, as demonstrated by reversal of profibrotic gene expression programs, downregulation of TGFβ, WNT, and JAK-STAT signaling and by reductions in αSMA expression or stress fiber formation, which led to reduced collagen deposition and ameliorated skin or lung fibrosis in vivo. Mechanistically, linezolid induced metabolic alterations by inhibiting mitochondrial translation in fibroblasts to hamper the oxidative phosphorylation, reduce the NAD⁺/NADH ratio and downregulate glycolysis, an essential metabolic pathway for fibroblast activation. Conclusions: This study provides first evidence that inhibiting mitochondrial translation with linezolid ameliorates fibrotic tissue remodeling. Since linezolid is already clinically approved as a reserve antibiotic, these findings hold translational promise and support the use of linezolid as a novel treatment for fibrotic disorders after further validation.

2026-01-29 | GSE310202 | GEO

Linezolid prevents fibroblast activation and ameliorates tissue fibrosis by inhibition of mitochondrial translation

Project description:Linezolid prevents fibroblast activation and ameliorates tissue fibrosis by inhibition of mitochondrial translation

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Cannabidiol ameliorates mitochondrial disease via PPARγ activation in preclinical models.

Project description: Not available

| S-EPMC11375224 | biostudies-literature

PPARg activation enhances myelination and neurological recovery in premature rabbits with intraventricular hemorrhage

Project description:We hypothesized that activation of PPARg would enhance myelination, reduce hydrocephalus, and promote neurological recovery in newborns with IVH. These hypotheses were tested in preterm rabbit model of IVH; autopsy brain samples from premature infants with and without IVH were analyzed. We found that IVH augmented PPARg expression in microglia of both preterm human infants and rabbit kits. The treatment with PPARg agonist or PPARg overexpression by adenovirus delivery further elevated PPARg levels in microglia, reduced pro-inflammatory cytokines, increased microglial phagocytosis, and improved oligodendrocyte progenitor cell (OPC) maturation in kits with IVH. Transcriptomic analyses of OPCs identified previously unrecognized PPARg-induced novel genes for purinergic signaling, cAMP generation, and antioxidant production, which would reprogram these progenitors toward promoting myelination. RNA-seq analyses of microglia revealed PPARg-triggered downregulation of several pro-inflammatory genes and transcripts having roles in Parkinson’s disease and amyotrophic lateral sclerosis, contributing to neurological recovery in kits with IVH. Accordingly, PPARg activation enhanced myelination and neurological function in kits with IVH.

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Project description:Conditional macrophage-specific PPARg knockout mice were generated on C57Bl/6 background by breeding PPARg fl/- (one allele is floxed, the other is null) and lysozyme Cre transgenic mice. PPARg and IL-4 signaling was analyzed on bone marrow-derived macrophages. Bone marrow of 3 mice per group was isolated and differentiated to macrophages with M-CSF (20 ng/ml). 20 ng/ml IL-4 was used to induce alternative macrophage activation and 1 uM Rosiglitazone (RSG) was used to activate PPARg. From each mouse 4 samples were generated: 1. M-CSF, 2. M-CSF+RSG, 3. IL-4 and 4. IL-4+RSG. All compounds were added throughout the whole differentiation process, and fresh media was added every other day. Control cells were treated with vehicle (DMSO:ethanol). After 10 days, RNA was isolated and gene expression profiles were analyzed using Mouse Genome 430 2.0 microarrays from Affymetrix. 3 PPARg +/- LysCre and 3 PPARg fl/- LysCre mice were used to isolate bone marrow and from each macrophages were differentiated with or without IL-4 and simultaneously treated with vehicle or RSG. Altogether we analyzed 24 samples with 3 biological replicates as below.

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Licensing of PPARg-regulated gene expression by IL-4-induced alternative macrophage activation

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Pioglitazone induces extensive PPARg-dependent hepatic expression of nuclear-mitochondrial genes

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