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N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling

ABSTRACT: N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling

PROVIDER: PRJNA901966 | ENA |

REPOSITORIES: ENA

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N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling

Project description:N-acetyl-L-cysteine (NAC) is a potent antioxidant. However, how NAC affects the biological functions of tendon stem/progenitor cells (TSPCs) and tendon repair has not been clarified.The effect of NAC on gene transcription in TSPCs was analyzed by transcriptomes and bioinformatics.

2022-11-18 | GSE218038 | GEO

Transcription profiling of human N-Acetyl L-cysteine induced differentiation of NHEK cells in vitro

Project description:Gene expression analysis of N-Acetyl L-cysteine induced differentiation of NHEK cells in vitro.

2005-11-30 | E-MEXP-500 | biostudies-arrayexpress

N-Acetyl-L-cysteine facilitates tendon repair and promotes the tenogenic differentiation of tendon stem/progenitor cells by enhancing the integrin α5/β1/PI3K/AKT signaling.

Project description:BackgroundTendon injury is associated with oxidative stress, leading to reactive oxygen species (ROS) production and inflammation. N-acetyl-L-cysteine (NAC) is a potent antioxidant. However, how NAC affects the biological functions of tendon stem/progenitor cells (TSPCs) and tendon repair has not been clarified. METHOD: The impacts of NAC on the viability, ROS production, and differentiation of TSPCs were determined with the cell counting kit-8, fluorescence staining, Western blotting, and immunofluorescence. The effect of NAC on gene transcription in TSPCs was analyzed by transcriptomes and bioinformatics and validated by Western blotting. The potential therapeutic effect of NAC on tendon repair was tested in a rat model of Achilles tendon injury.ResultsCompared with the untreated control, treatment with 500 µM NAC greatly promoted the proliferation of TSPCs and significantly mitigated hydrogen peroxide-induced ROS production and cytotoxicity in vitro. NAC treatment significantly increased the relative protein expression of collagen type 1 alpha 1 (COL1A1), tenascin C (TNC), scleraxis (SCX), and tenomodulin (TNMD) in TPSCs. Bioinformatics analyses revealed that NAC modulated transcriptomes, particularly in the integrin-related phosphoinositide 3-kinase (PI3K)/AKT signaling, and Western blotting revealed that NAC enhanced integrin α5β1 expression and PI3K/AKT activation in TSPCs. Finally, NAC treatment mitigated the tendon injury, but enhanced the protein expression of SCX, TNC, TNMD, and COLIA1 in the injured tissue regions of the rats.ConclusionNAC treatment promoted the survival and differentiation of TSPCs to facilitate tendon repair after tendon injury in rats. Thus, NAC may be valuable for the treatment of tendon injury.

| S-EPMC9814204 | biostudies-literature

Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

Project description:Trichloroethylene (TCE) is a persistent and pervasive environmental contaminant. N-acetyl cysteine (NAC) is an antioxidant that may reduce TCE effects. Pregnant Wistar rats were exposed to 480 mg TCE mg/kg/day, 200 mg/kg/day NAC or co-exposure with both chemicals via ingestion (mini vanilla wafer) on gestation days 6-16 (tissue collection day). TCE- and/or NAC-induced changes to gene expression were evaluated in male and female rat placentae.

2022-06-01 | GSE168232 | GEO

Human Tendon-on-a-Chip for modeling vascular inflammatory fibrosis II

Project description:Vascular inflammation and myofibroblast activation by TGF-β1 are key, yet-to-be-fully-understood pathological processes in fibrosis. Here we report the development of a novel human Tendon-on-a-Chip (hToC) to elucidate the role of TGF-β1 in peritendinous adhesions, a debilitating fibrosis condition affecting flexor tendon, which currently lacks biological therapies. The hToC allows the crosstalk between a vascular compartment harboring endothelial cells and monocytes with a tissue hydrogel compartment containing tendon fibroblasts and macrophages. We find that the hToC replicates in vivo inflammatory and fibrotic phenotypes in preclinical and clinical samples, including myofibroblast differentiation and tissue contraction, excessive ECM deposition, and inflammatory cytokines secretion. We further show the fibrotic phenotypes are driven by the interactions between the vascular and tissue compartments, mediating the transmigration of monocytes. We demonstrate significant overlap in fibrotic transcriptional signatures in the hToC with human tenolysis samples, including the mTOR pathway, a regulatory nexus of fibrosis across various organs. Treatment with Rapamycin suppressed the fibrotic phenotype on the hToC, which validates the hToC as a preclinical alternative for investigating fibrosis and testing therapeutics.

2024-01-10 | GSE246391 | GEO

Tendon injury

Project description:Tendon injury

| PRJNA1027305 | ENA

Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

Project description:Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

| PRJNA706597 | ENA

Human Tendon-on-a-Chip for modeling vascular inflammatory fibrosis

Project description:Vascular inflammation and activation of myofibroblasts play crucial roles in the progression of fibrosis. Transforming growth factor beta 1 (TGF-β1) has been identified as a driver of adhesion formation in various tissues, including tendons. However, the mechanisms underlying fibrotic peritendinous adhesions remain poorly understood resulting in a lack of effective therapies. To address this, we developed a novel human Tendon-on-a-Chip (hToC) model, which combines a vascular compartment, with endothelial cells and monocytes, with a tissue compartment containing fibroblasts and tissue-resident macrophages, all in serum-free conditions. Our hToC successfully replicates inflammatory and fibrotic phenotypes observed in mouse models and clinical human samples including myofibroblast differentiation and senescence, tissue contraction, excessive extracellular matrix deposition, and secretion of inflammatory cytokines. We show that fibrosis-on-a-chip is driven by the interaction between the vascular and tissue compartments, including the infiltration of monocytes. Transcriptomics validate the hToC as disease model of diseased human tendon and shows the upregulation of the PI3K/AKT/mTOR pathway—a regulatory nexus of fibrosis in tendon injury. Consistent with this finding, treatment with the mTOR inhibitor Rapamycin suppresses the fibrotic phenotype. Our findings validate the hToC as a tool for investigating human fibrosis and illuminate the underappreciated vascular contribution to tendon pathophysiology.

2024-01-10 | GSE244543 | GEO

RNA-seq of achilles tendon from young and old donors to study age-related changes in tendon

Project description:Tendon from young and old donors was used for RNA-Seq analysis. The aim of the study was to identify differentially expressed tendon transcripts in ageing in order to to characterize molecular mechanisms associated with age-related changes in tendon.

2015-04-01 | E-MTAB-2449 | biostudies-arrayexpress

Collagen-derived prolyl-hydroxyproline dipeptide promotes cellular homeostasis and lamellipodia-driven cell motility through active β1-integrin in adult tendon cells

Project description:Collagen-derived hydroxyproline-containing peptides show a variety of biological properties in cells. However, no comprehensive study has yet explored the functional links between Hyp-containing peptides and cellular behavior. Here, we show that the dipeptide prolyl-hydroxyproline (Pro–Hyp) exhibits the most significant effect of a number of di- and tri-peptides on mouse tendon cells. We have shown that the cellular uptake of Pro-Hyp is a carrier-mediated process. In addition, Pro-Hyp promotes differentiation/maturation of tendon cells with modulation of lineage-specific factors, has profound effects on cellular phenotypes such as cell proliferation with significantly upregulated ERK-phosphorylation and extracellular matrix production with increased type I collagen network organization, and induced significant chemotactic activity in vitro. Proteomics analysis has identified cellular assembly and organizations, and movement as predicted linked-network pathways in response to Pro-Hyp. Mechanistically, cells treated with Pro-Hyp demonstrate increased directional persistence and significantly increased directed motility and migration velocity, which are accompanied by elongated lamellipodial protrusions with increased active β1-integrin-containing focal contacts and reorganizations of thicker peripheral F-actin fibrils. Thus, our findings document the molecular basis of the functional benefits of Pro-Hyp dipeptide in cellular behavior. Such dynamic properties of collagen-derived Pro-Hyp dipeptide could lead the way to its application to translational medicine.

2022-09-28 | PXD020374 | Pride

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