ArticleConnective tissue research2018
Substance P increases CCN2 dependent on TGF-beta yet Collagen Type I via TGF-beta1 dependent and independent pathways in tenocytes.
Article in Connective tissue research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Analysis of cranial tenocyte heterogeneity reveals a role for Wnt signaling in tendon attachments.Development (Cambridge, England) · 2026Article
- Potentiation of Collagen Deposition by the Combination of Substance P with Transforming Growth Factor Beta in Rat Skin Fibroblasts.International journal of molecular sciences · 2024Article
- Ultrasound-based assessment of the expression of inflammatory markers in the rectus femoris muscle of rats.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Blocking CCN2 Reduces Established Palmar Neuromuscular Fibrosis and Improves Function Following Repetitive Overuse Injury.International journal of molecular sciences · 2023Article
- Response to Mechanical Properties and Physiological Challenges of Fascia: Diagnosis and Rehabilitative Therapeutic Intervention for Myofascial System Disorders.Bioengineering (Basel, Switzerland) · 2023Review
- Key indicators of repetitive overuse-induced neuromuscular inflammation and fibrosis are prevented by manual therapy in a rat model.BMC musculoskeletal disorders · 2021Article
- Force dependent effects of chronic overuse on fibrosis-related genes and proteins in skeletal muscles.Connective tissue research · 2021Article
- TGF-β1-containing exosomes derived from bone marrow mesenchymal stem cells promote proliferation, migration and fibrotic activity in rotator cuff tenocytes.Regenerative therapy · 2020Article
- Sustained Exposure of Substance P Causes Tendinopathy.International journal of molecular sciences · 2020Article
- Blocking substance P signaling reduces musculotendinous and dermal fibrosis and sensorimotor declines in a rat model of overuse injury.Connective tissue research · 2020Article
- Blocking CTGF/CCN2 reduces established skeletal muscle fibrosis in a rat model of overuse injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- ISSLS Prize in Basic science 2019: Physical activity attenuates fibrotic alterations to the multifidus muscle associated with intervertebral disc degeneration.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2019Article
- The answer depends on the question: Optimal conditions for western blot characterization of muscle collagen type 1 depends on desired isoform.Journal of biological methods · 2019Article
- Fascial tissue research in sports medicine: from molecules to tissue adaptation, injury and diagnostics: consensus statement.British journal of sports medicine · 2018Article
- Development of Normal and Cleft Palate: A Central Role for Connective Tissue Growth Factor (CTGF)/CCN2.Journal of developmental biology · 2018Review
- Substance P-A neuropeptide regulator of periodontal disease pathogenesis and potential novel therapeutic entity: A narrative review.Journal of Indian Society of PeriodontologyReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor beta 1 (TGFbeta-1) and connective tissue growth factor (CCN2) are important mediators of tissue repair and fibrosis, with CCN2 functioning as a downstream mediator of TGFβ-1. Substance P (SP) is also linked to collagen production in tenocytes. A link between SP, TGFbeta-1 and CCN2 has yet to be established in tenocytes or fibrogenic processes. We sought to determine whether SP induces tenocyte proliferation, CCN2, or collagen production via TGFbeta-1 signaling or independently in rat primary tenocytes. Tenocytes were isolated from rat tendons, cultured and stimulated by SP and/or TGFbeta-1. Cultured cells expressed proteins characteristic of tenocytes (vimentin and tenomodulin) and underwent increased proliferation dose dependently after SP and TGFbeta-1 treatments, alone or combined (more than SP alone when combined). SP induced TGFbeta-1 expression in tenocytes in both dose- and time-dependent manners. SP and TGFbeta-1, alone or combined, stimulated CCN2 expression in tenocytes and their supernatants after both 24 and 48 h of stimulation; a response blocked with addition of a TGFbeta-1 receptor inhibitor. In contrast, SP potentiated collagen type I secretion by tenocytes, a response abrogated by the TGFbeta-1 receptor inhibitor after 48 h of stimulation, but not after the shorter 24 h of stimulation. Our findings suggest that both SP and TGFbeta-1 can stimulate tenocyte fibrogenic processes, albeit differently. TGFbeta-1 pathway signaling was involved in CCN2 production at all time points examined, while SP induced collagen type I production independently prior to the onset of signaling through the TGFbeta-1 pathway.
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Registered trials
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