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PI3K-Akt signaling regulates Scx-lineage tenocytes and Tppp3-lineage tendon sheath synovial cells in physiological tendon regeneration

ABSTRACT: PI3K-Akt signaling regulates Scx-lineage tenocytes and Tppp3-lineage tendon sheath synovial cells in physiological tendon regeneration

PROVIDER: PRJNA989042 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25067714_1.fastq.gz	Fastqsanger.gz
	SRR25067714_2.fastq.gz	Fastqsanger.gz
	SRR25067715_1.fastq.gz	Fastqsanger.gz
	SRR25067715_2.fastq.gz	Fastqsanger.gz
	SRR25067716_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

PI3K-Akt signaling regulates Scx-lineage tenocytes and Tppp3-lineage tendon sheath synovial cells in physiological tendon regeneration

Project description:We identify a PI3K-Akt signaling pathway which is specifically upregulated in neonatal murine injured Achilles tendons. PI3K-Akt signaling inhibition in neonatal murine Achilles tendon rupture model decreases cell proliferation and cell migration to the regenerating tendons in both Scx-lineage intrinsic tenocytes and Tppp3-lineage extrinsic tendon sheath synovial cells. Moreover, PI3K-Akt signaling inhibition decreases stemness and promotes mature tenogenic differentiation in both Scx-lineage and Tppp3-lineage cells. Collectively, PI3K-Akt signaling plays an important role in physiological tendon regeneration.

2025-03-15 | GSE236106 | GEO

RNA-seq analysis of Scx-lineage cell depletion to investigate tendon cell functions during flexor tendon healing

Project description:Little is understood about the roles of tendon cells during flexor tendon healing. To better understand tendon cell functions, the Scx-Cre mouse was crossed to the DTR mouse model to facilitate scleraxis lineage cell depletion prior to acute flexor tendon injury and repair. WT (cre-) and experimental (cre+) mice underwent complete transection and repair of the flexor digitorum longus tendon. Repaired tendons were harvested at 14 and 28 days post-repair for bulk RNA-Seq analysis to examine possible mechanisms driving differential healing due to Scx lineage cell depletion.

2021-02-08 | GSE156157 | GEO

Genome-wide identification of Scx transcriptional target genes in tendon development II

Project description:Despite their important roles in the musculoskeletal system, tendon and ligaments are much less studied comparing to bone, cartilage and muscle. The lack of knowledge in tendon biology severely hinders the understanding of the etiologies of tendon related diseases and development of efficient clinical treatments. In mouse, Scx gene, encoding a Twist family bHLH transcription factor, is expressed in progenitors of all tendons and ligaments, as well as in mature tenocytes. Previous studies show that inactivation of Scx gene results in absence or severe hypoplastia of force transmitting tendons, with muscle anchoring tendons and ligaments are less affected. Here we report a set of ChIPseq data from E13.5 forelimbs of novel Scx-2xFlag tagged mice in which a Scx-Flag fusion protein is expressed recapitulating endogenous Scx expression, and a set of RNAseq data of Scx-GFP positive cells from E13.5 Scx wildtype, E15.5 Scx wildtype and homozygous mutant forelimbs. Using RNAseq and ChIPseq assays, we identify several genes exhibiting Scx-dependent tendon expression druing differentiation, with Scx binding peaks located within their promoter/enhancer regions. Thus these genes may play critical roles in mediating Scx regulated tendon cell differentiation. Our results provide new insights in the mechanisms of tendon development.

2021-06-28 | GSE173428 | GEO

RNA-seq analysis of equine tenocytes exposed to siRNA targeting scleraxis (Scx) to identify novel targets of Scx-mediated mechanotransduction

Project description:Equine tenocytes were exposed to an siRNA targeting the transcription factor scleraxis (Scx) or a scramble control and maintained under cyclic strain. The resulting transcriptomes were then used for RNA-seq analysis. The goal of this study was to identify novel ways in which Scx facilitates mechanotransduction in tenocytes in order to better understand tenocyte biology.

2018-08-02 | GSE110567 | GEO

A latent Axin2+/Scx+ progenitor pool is the central organizer of tendon healing

Project description:A tendon’s ordered extracellular matrix (ECM) is integral for transmitting force and highly prone to injury. Whether and how tendon cells, or tenocytes, embedded within this dense ECM mobilize and contribute to healing is unknown. Here, we identify a specialized Axin2+ tenocyte population in mouse and human tendons that remains latent in homeostasis yet serves as a major source of tendon progenitors during healing. We show that Axin2+ tenocytes readily expand in vitro and express stem cell markers. In vivo, Axin2+ cells are major functional contributors to repair: Axin2+ tenocytes de-differentiate, expand, and re-adopt a tenocyte fate post-injury. Specific loss of Wnt secretion in Axin2+ cells alters their stem cell identity and disrupts their activation upon injury, severely compromising healing. Our work highlights Axin2+ tenocytes as quiescent stem cells embedded in dense matrix, which are uniquely regulated in an autocrine manner and are central organizers of robust tendon healing.

2024-10-22 | GSE188598 | GEO

RNA Sequencing Facilitates Quantitative Analysis of Cont/Dicer KO/Scx HT mice Achilles Tendon Transcriptome

Project description:To investigate which mRNA and miRNA are involved in Dicer KO mouse tendon hypoplasticity, we performed RNA-seq and small RNA-seq using RNA from Achilles tendon of Cont (Dicer f/f), Scx HT (ScxCre/+ Knock In:Dicer +/+) and Dicer KO (ScxCre/+ Knock In:Dicer f/f) mice at 4 weeks of age. Achilles tendon from 4-week-old female mice was harvested, RNA was isolated using an RNA extraction kit. RNA libraries were generated and sequenced by K. K. DNAFORM (Tokyo, Japan). The libraries were sequenced by Illumina HISEQ4000 using Illumina provided protocol. Differential gene expression was analyzed with R Bioconductor DESeq2. We found that a large portion of tendon-fibroblast characteristic genes was downregulated in Dicer KO mice Achilles tendon compared to Cont and Scx HT.

2022-05-31 | GSE186353 | GEO

Scleraxis-lineage cells are required for tendon homeostasis and their depletion induces an accelerated extracellular matrix aging phenotype

Project description:Aged tendons have disrupted homeostasis, increased injury risk, and impaired healing capacity. Understanding mechanisms of homeostatic disruption is crucial for developing therapeutics to retain tendon health through the lifespan. Here, we developed a novel model of accelerated tendon extracellular matrix (ECM) aging via depletion of Scleraxis-lineage (ScxLin) cells in young mice (DTR). DTR recapitulates many aspects of tendon aging including comparable declines in cellularity, alterations in ECM structure, organization, and composition. Single cell RNA-sequencing demonstrated a conserved decline in tenocytes associated with ECM biosynthesis in aged and DTR tendons, identifying the requirement for ScxLin cells during homeostasis. However, the remaining cells in aged and DTR tendons demonstrate functional divergence. Aged tenocytes become pro-inflammatory and lose proteostasis. In contrast, DTR tenocytes demonstrate enhanced remodeling capacity. Collectively, this study defines DTR a novel model of accelerated tendon ECM aging and identifies novel biological intervention points to maintain tendon function through the lifespan.

2023-02-03 | PXD037230 | Pride

Expression data from mouse limb tendon cells during development.

Project description:We have undertaken a screen of mouse limb tendon cells in order to identify molecular pathways involved in tendon development. Mouse limb tendon cells were isolated based on Scleraxis (Scx) expression at different stages of development: E11.5, E12.5 and E14.5 Microarray comparisons were carried out between tendon progenitor and differentiated stages. Forelimbs from E11.5, E12.5 and E14.5 Scx-GFP embryos were collected and dissociated with trypsin to obtain cell suspensions. Scx-positive tendon cells were isolated by FACS. RNA was extracted and Fragmented biotin-labelled cRNA samples were hybridized on Affymetrix Gene Chip Mouse Genome 430 2.0 arrays.

2014-01-18 | E-GEOD-54207 | biostudies-arrayexpress

RNA-seq analysis of Scx-lineage cell depletion to investigate tendon cell functions during flexor tendon healing

Project description:RNA-seq analysis of Scx-lineage cell depletion to investigate tendon cell functions during flexor tendon healing

| PRJNA656853 | ENA

Differentially expressed transcriptomes of P7 mouse tendon cells with targeted deletion of TGF-beta signaling

Project description:Background: Our group has previously shown that disruption of TGFβ signaling in mouse limb mesenchyme resulted in arrested tendon formation (Pryce et at, 2007). To examine the role of TGFβ signaling in later stages of tendon development, the TGF-beta type II receptor gene (Tgfbr2) was targeted in the Scleraxis (Scx)-expressing cell lineage using the Cre-lox recombination system. We find that tendon development was not disrupted in mutant (Tgfbr2;ScxCre) embryos. However, shortly after birth tenocytes underwent dedifferentiation in which the cell lost differentiation markers and reverted to a more stem/progenitor state. Purpose: To determine gene expression changes in Tgfbr2;ScxCre mutant tendon cells. Methods: We performed scRNA-seq for transcriptome changes in P7 mutant tendon cells, a stage at which the majority of the mutant cells is dedifferentiated. Briefly, tendons from P7 mutant and wild-type (as a control) pups were harvested and enzymatically digested. The released cells were then subjected to scRNA-seq analysis using 10x Genomics platform. Results: Using unsupervised hierarchical clustering, we identified two major clusters corresponding to mutant (dedifferentiated) cells and wild-type tenocytes in the respective samples. Findings from the pairwise comparison of the gene set between the P7 wild-type tenocyte and mutant cell clusters do not only lend support to our notion that the mutant cells lost their differentiation state, but also suggest the possibility of induction of some developmental programs in these cells, a general feature in cellular dedifferentiation. Conclusions: TGF-beta signaling is critical for maintenance of the tendon cell fate.

2020-02-24 | GSE139558 | GEO

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