ArticleBMC musculoskeletal disorders2017
Glutamate signaling through the NMDA receptor reduces the expression of scleraxis in plantaris tendon derived cells.
Article in BMC musculoskeletal disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 15 citations in OpenAlex.
- An overview in tendon's physiology, pathomorphology, and treatment options.Cell and tissue research · 2026Review
- Effects of glutaminase 1 inhibitor on rotator cuff derived cells: a preliminary report in 12 patients.BMC musculoskeletal disorders · 2025Article
- Dexamethasone alleviates etomidate-induced myoclonus by reversing the inhibition of excitatory amino acid transporters.Frontiers in neuroscience · 2024Article
- Novel insights into the pathogenesis of tendon injury: mechanotransduction and neuroplasticity.Neural regeneration research · 2022Article
- Reduction of mechanical loading in tendons induces heterotopic ossification and activation of the β-catenin signaling pathway.Journal of orthopaedic translation · 2021Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundA body of evidence demonstrating changes to the glutaminergic system in tendinopathy has recently emerged. This hypothesis was further tested by studying the effects of glutamate on the tenocyte phenotype, and the impact of loading and exposure to glucocorticoids on the glutamate signaling machinery.
methodsPlantaris tendon tissue and cultured plantaris tendon derived cells were immunohisto-/cytochemically stained for glutamate, N-Methyl-D-Aspartate receptor 1 (NMDAR1) and vesicular glutamate transporter 2 (VGluT2). Primary cells were exposed to glutamate or receptor agonist NMDA. Cell death/viability was measured via LDH/MTS assays, and Western blot for cleaved caspase 3 (c-caspase 3) and cleaved poly (ADP-ribose) polymerase (c-PARP). Scleraxis mRNA (Scx)/protein(SCX) were analyzed by qPCR and Western blot, respectively. A FlexCell system was used to apply cyclic strain. The effect of glucocorticoids was studies by adding dexamethasone (Dex). The mRNA of the glutamate synthesizing enzymes Got1 and Gls, and NMDAR1 protein were measured. Levels of free glutamate were determined by a colorimetric assay.
resultsImmunoreactions for glutamate, VGluT2, and NMDAR1 were found in tenocytes and peritendinous cells in tissue sections and in cultured cells. Cell death was induced by high concentrations of glutamate but not by NMDA. Scleraxis mRNA/protein was down-regulated in response to NMDA/glutamate stimulation. Cyclic strain increased, and Dex decreased, Gls and Got1 mRNA expression. Free glutamate levels were lower after Dex exposure.
conclusionsIn conclusion, NMDA receptor stimulation leads to a reduction of scleraxis expression that may be involved in a change of phenotype in tendon cells. Glutamate synthesis is increased in tendon cells in response to strain and decreased by glucocorticoid stimulation. This implies that locally produced glutamate could be involved in the tissue changes observed in tendinopathy.
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