Expression data from mouse limb tendon cells during development.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE54207 | GEO | 2014/01/18
SECONDARY ACCESSION(S): PRJNA235887
REPOSITORIES: GEO
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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
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
Project description:Laser capture microdissection mass spectrometry analysis on mouse embryonic tail tendon bundles, E12.5-E14.5 in half day steps.
2023-07-19 | PXD043811 | Pride
Project description:We report RNA sequencing data from the plantaris tendons of adult male mice in the C57Bl/6 background that either have the scleraxis gene (Scx+) or mice in which scleraxis has been deleted using CreERT2 driven from the Rosa26 locus (Scx-). Mice in which scleraxis was deleted were created by crossing scleraxis-floxed mice with Rosa26-CreERT2 mice. Rosa26-CreERT2 mice that did not have a floxed scleraxis allele served as controls. Mice were treated with tamoxifen for 5 days to induce recombination at the scleraxis locus, and then subjected to a synergist ablation procedure in which the Achilles tendon is removed, resulting in compensatory growth of the plantaris tendon. Mice were analyzed either 7 or 14 days after synergist ablation. Control mice that did not undergo tamoxifen treatment or synergist ablation were also studied (NOC).
2020-01-31 | GSE139493 | GEO
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
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
Project description:Tendons play fundamental role in the musculoskeletal system and locomotion by transferring forces generated by muscles to the skeleton. Tendon injuries can occur due to sports related incidents, as a result of trauma to overuse or during disease or ageing and are among the leading causes of musculoskeletal disability. Scleraxis is a marker of the tendon lineage and appears to be induced at the earliest stage of specification of this lineage, however little is known how scleraxis is modulating tendon growth activity. This study aimed to investigate how scleraxis modulates tendon cells activity.
2021-09-08 | PXD017944 | Pride
Project description:Tendons are composed of a heterogeneous cell environment, with Scleraxis-lineage (ScxLin) cells being the predominant population. Although ScxLin cells are required for maintenance of tendon homeostasis, their functions during tendon healing are unknown. To this end, we first characterized the spatiotemporal dynamics of ScxLin cells during tendon healing, and identified that the overall ScxLin pool continuously expands up to early remodeling healing phase. To better define the function of ScxLin cells during the late proliferative phase of healing, we inducibly depleted ScxLin cells from day 14-18 post-surgery using the Scx-Cre; Rosa-DTR mouse model, with local administration of diphtheria toxin inducing apoptosis of ScxLin cells in the healing tendon. At D28 post-surgery, ScxLin cell depleted tendons (DTRScxLin) had substantial impairments in structure and function, relative to WT, demonstrating the importance of ScxLin cells during tendon healing. Next, bulk RNAseq was utilized to identify the underlying mechanisms that were impaired with depletion and revealed that ScxLin depletion induced molecular and morphological stagnation of the healing process at D28. However, this stagnation was transient, such that by D56 tendon mechanics in DTRScxLin were not significantly different than wildtype repairs. Collectively, these data offer fundamental knowledge on the dynamics and roles of ScxLin cells during tendon healing.
2022-09-13 | GSE213033 | GEO
Project description:Purpose: Our lab has previously shown that Scleraxis (Scx) is require for proper valve development in vivo. In order to fully explore gene networks regulated by Scx during the vital stages of valve remodeling , high throughput RNA-squencing was performed. Results:There were a total of 18,810 genes were detected. A total of 864 genes were differentially expressed Scx null AVC regions: 645 being upregulated and 217 downregulated. In this data set, we include expression data from atrioventricular canal (AVC) regions from Scx null and wild-type littermate controls at embryonic day 15.5. A total of 6 samples were analyzed; 3 valve regions from E15.5 Scx-/- mice, and 3 from E15.5 Scx+/+ wild-type littermate controls. Differential expression read counts are ranked based on p-value (<0.05).
2014-05-14 | E-GEOD-57423 | biostudies-arrayexpress
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