Calcaneal tendon plasticity following gastrocnemius muscle injury in rat
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE131884 | GEO | 2019/09/30
REPOSITORIES: GEO
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Project description:Calcaneal tendon plasticity following gastrocnemius muscle injury in rat
| PRJNA545233 | ENA
Project description:Partial tendon-to-bone interface (TBI) injuries heal in a mechanically inferior manner and redevelop healthy uninjured tissue morphology. The origin of the cells involved in tendon-to-bone healing remains unknown. We employed a rigorous approach to evaluate if mouse skeletal stem cells (mSSC) play a role in tendon-to-bone healing after partial-injury. Using fluorescence-activated cell sorting we identified that found that they are present within the TBI. Using a TBI-injury rainbow lineage tracing mouse model, we demonstrated that injury-responsive cells within the TBI and calcaneus proliferate polyclonally following partial-tendon injury at the TBI. These injury-responsive clonal cells express skeletal marker SP7. We quantified the differences in mSCC frequency after TBI-injury and found that mSSC respond to injury with a higher frequency and have associated changes in gene expression, with the specific down-regulation of the TGFβ signaling pathway. Exogenous delivery of TGFβ after injury was found to reduce the mSSC response after injury. These findings suggest that mSSC may facilitate tendon-to-bone healing by downregulating TGFβ signaling within the mSSC niche.
2022-02-14 | GSE167080 | GEO
Project description:Tendon degeneration and injury often result in significant pain and functional impairment. Typically, tendon healing occurs through a scar-mediated response and may progress to chronic tendinopathy without timely intervention. However, the molecular mechanisms underlying early tendon repair remain poorly understood. Further investigation is also impeded by the limited availability of early tendon injury samples in clinical settings. In this study, we established a puncture-induced tendon injury model to investigate the molecular patterns and cellular subpopulations involved in early tendon injury across multiple time points. RNA sequencing identified seven gene sets with distinct expression profiles during the early stages of tendon injury. Single-cell RNA sequencing further revealed eight myeloid cell types and seven mesenchymal cell types participating in the tendon repair process. Together, these findings illuminate the molecular and cellular dynamics coordinating early tendon repair, providing insights that could inform future clinical treatments for tendinopathy and tendon injury.
2025-04-23 | GSE288444 | GEO
Project description:Tendon is a hypocellular tissue that contains functional cable-like units of type I collagen responsible for the transmission of force from muscle to bone. In the setting of injury or disease, patients can develop chronic tendinopathies that are characterized by pain, loss of function and persistent inflammatory changes that are often difficult to treat. Platelet-rich plasma (PRP) has shown promise in the treatment of chronic tendinopathy, but little is known about the mechanisms by which PRP can improve tendon healing. PRP contains many different growth factors and cytokines, and since these proteins can both activate and inhibit various signaling pathways it has been challenging to determine precisely which signaling pathways and cellular responses are most important. Using state-of-the-art bioinformatics tools and genome wide-expression profiling, the purpose of this study was to determine the signaling pathways activated within cultured tendon fibroblasts in response to PRP treatment. Tendon fibroblasts were isolated from rat tail tendons and embedded in 3D type I collagen gels. Cells were treated with PRP or PPP for 24 hours, and total RNA was extracted for hybridization on Affymetrix arrays.
2016-01-12 | E-GEOD-70918 | biostudies-arrayexpress
Project description:Tendon degeneration and injury often result in significant pain and functional impairment. Typically, tendon healing occurs through a scar-mediated response and may progress to chronic tendinopathy without timely intervention. However, the molecular mechanisms underlying early tendon repair remain poorly understood. Further investigation is also impeded by the limited availability of early tendon injury samples in clinical settings. In this study, we established a puncture-induced tendon injury model to investigate the molecular patterns and cellular subpopulations involved in early tendon injury across multiple time points. RNA sequencing identified seven gene sets with distinct expression profiles during the early stages of tendon injury. Single-cell RNA sequencing further revealed eight myeloid cell types and seven mesenchymal cell types participating in the tendon repair process. Together, these findings illuminate the molecular and cellular dynamics coordinating early tendon repair, providing insights that could inform future clinical treatments for tendinopathy and tendon injury.
2025-04-23 | GSE288443 | GEO
Project description:Background: Tendon is a major component of musculoskeletal system connecting the muscles to the bone. Tendon injuries are very common orthopedics problems leading to impeded motion. Up to now, there still lacks effective treatments for tendon diseases. Methods: Tendon stem/progenitor cells (TSPCs) were isolated from the patellar tendons of SD rats. The expression levels of genes were evaluated by quantitative RT-PCR. Immunohistochemistry staining was performed to confirm the presence of tendon markers in tendon tissues. Bioinformatics analysis of data acquired by RNA-seq was used to find out the differentially expressed genes. Rat patellar tendon injury model was used to evaluate the effect of U0126 on tendon injury healing. Biomechanical testing was applied to evaluate the mechanical properties of newly formed tendon tissues. Results: In this study, we have shown that ERK inhibitor U0126 rather PD98059 could effectively increase the expression of tendon-related genes and promote the tenogenesis of TSPCs in vitro. To explore the underlying mechanisms, RNA sequencing was performed to identify the molecular difference between U0126-treated and control TSPCs. The result showed that GDF6 was significantly increased by U0126, which is an important factor of the TGFβ superfamily regulating tendon development and tenogenesis. In addition, NBM (nonwoven-based gelatin/polycaprolactone membrane) which mimics the native microenvironment of the tendon tissue was used as an acellular scaffold to carry U0126. The results demonstrated that when NBM was used in combination with U0126, tendon healing was significantly promoted with better histological staining outcomes and mechanical properties. Conclusion: Taken together, we have found U0126 promoted tenogenesis in TSPCs through activating GDF6, and NBM loaded with U0126 significantly promoted tendon defect healing, which provides a new treatment for tendon injury.
2022-12-10 | GSE190685 | GEO
Project description:Self-renewal of tendons is rare since the vascular formation inside is extremely poor, thus reconstructive surgery using autologous tendons has been often taken place in the case of severe injury. However, the rate of re-injury after surgery is relatively high, and collection of autologous tendons leads muscle weakness which results in prolonged rehabilitation. Here, we introduce the induced pluripotent stem cells (iPSCs)-based technology aiming at developing a new therapeutic option after tendon injury. Firstly, we derived tenocytes from human iPSCs by recapitulating the normal progression of step-wise narrowing fate decisions in the vertebrate embryo. We used single-cell RNA sequencing to analyze the developmental trajectory of iPSCs-derived tenocytes. We then demonstrated that grafting iPSCs-tenocytes contributed to recovery of motor function after Achilles tendon injury in rat via engraftments and paracrine effects. The biomechanical strength of regenerated tendons recovered comparable to that of healthy tendons. We propose that the iPSCs-tenocytes will provide a novel therapeutic option in tendon injury.
2021-07-01 | PXD020887 | JPOST Repository
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:Rotator cuff injuries result in over 500,000 surgeries performed annually, an alarmingly high number of which fail. These procedures typically involve repair of the injured tendon and removal of the subacromial bursa. However, recent identification of a resident population of mesenchymal stem cells and inflammatory responsiveness of the bursa to tendinopathy indicate an unexplored biological role of the bursa in the context of rotator cuff disease. Therefore, we aimed to understand the clinical relevance of bursa-tendon crosstalk, characterize the biologic role of the bursa within the shoulder, and test the therapeutic potential for targeting the bursa. Proteomic profiling of patient bursa and tendon samples demonstrated that the bursa is activated by tendon injury. Using a rat to model rotator cuff injury and repair, tenotomy-activated bursa protected the intact tendon adjacent to the injured tendon and maintained the morphology of the underlying bone. The bursa also promoted an early inflammatory response in the injured tendon, initiating key players in wound healing. In vivo results were supported by targeted organ culture studies of the bursa. To examine the potential to therapeutically target the bursa, dexamethasone was delivered to the bursa, prompting a shift in cellular signaling towards modulating inflammation in the healing tendon. In conclusion, contrary to current clinical practice, the bursa should be retained to the greatest extent possible and provides a new therapeutically target for improving tendon healing outcomes.
2023-07-07 | GSE235861 | GEO