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Glutamate signaling through the NMDA receptor reduces the expression of scleraxis in plantaris tendon derived cells

Overview of attention for article published in BMC Musculoskeletal Disorders, May 2017
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Title
Glutamate signaling through the NMDA receptor reduces the expression of scleraxis in plantaris tendon derived cells
Published in
BMC Musculoskeletal Disorders, May 2017
DOI 10.1186/s12891-017-1575-4
Pubmed ID
Authors

Christoph Spang, Ludvig J. Backman, Sandrine Le Roux, Jialin Chen, Patrik Danielson

Abstract

A 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. Plantaris 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. Immunoreactions 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. In 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.

Mendeley readers

The data shown below were compiled from readership statistics for 7 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 7 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 2 29%
Student > Bachelor 1 14%
Professor 1 14%
Lecturer 1 14%
Student > Master 1 14%
Other 0 0%
Unknown 1 14%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 1 14%
Nursing and Health Professions 1 14%
Agricultural and Biological Sciences 1 14%
Neuroscience 1 14%
Medicine and Dentistry 1 14%
Other 1 14%
Unknown 1 14%