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In situ hybridization studies favouring the occurrence of a local production of BDNF in the human Achilles tendon
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB), Anatomy.
2012 (English)In: Histology and Histopathology, ISSN 0213-3911, E-ISSN 1699-5848, Vol. 27, no 9, 1239-1246 p.Article in journal (Refereed) Published
Abstract [en]

Brain derived neurotrophic factor (BDNF) is a multipotent neurotrophin known for its growth-influencing and apoptosis-modulating functions, as well as for its function to interact with neurotransmitters/neuromodulators. BDNF is reported to be mainly produced in the brain. BDNF can be absorbed into peripheral tissue from the blood stream. Expression of this neurotrophin at the protein level, as well as of the neurotrophin receptor p75, has been previously shown for the principal cells (tenocytes) of the Achilles tendon. However, there is no proof at the mRNA level that BDNF is produced by the tenocytes. As the Achilles tendon tenocytes show "neuronal-like" characteristics, in the form of expressions favouring synthesis of several neuromodulators/neurotransmitters, and as BDNF especially is produced in neurons, it is of interest to confirm this. In the present study, therefore, in situ hybridization for demonstration of BDNF mRNA was performed on biopsies from Achilles tendons of patients with tendinosis and pain-free non-tendinosis individuals. The results showed that the tenocytes of both groups exhibited BDNF mRNA reactions. These observations indeed favour the idea that BDNF is produced by tenocytes in the human Achilles tendon, why Achilles tendon tissue is a tissue in which BDNF can be locally produced. BDNF can have modulatory functions for the tenocytes, including apoptosis-modifying effects via actions on the p75 receptor and interactive effects with neurotransmitters/neuromodulators produced in these cells. This possibility should be further studied for Achilles tendon tissue.

Place, publisher, year, edition, pages
2012. Vol. 27, no 9, 1239-1246 p.
Keyword [en]
Achilles tendon, BDNF, mRNA, In situ hybridization, Tendinopathy
National Category
Cell Biology
Identifiers
URN: urn:nbn:se:umu:diva-57811ISI: 000306521400014OAI: oai:DiVA.org:umu-57811DiVA: diva2:545086
Available from: 2012-08-17 Created: 2012-08-16 Last updated: 2017-12-07Bibliographically approved
In thesis
1. TNF-α and neurotrophins in Achilles tendinosis
Open this publication in new window or tab >>TNF-α and neurotrophins in Achilles tendinosis
2013 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Tenocytes are the principal cells of the human Achilles tendon. In tendinosis, changes in the metabolism and morphology of these cells occur. Neurotrophins are growth factors essential for the development of the nervous system. Tumour necrosis factor alpha (TNF-α) has been found to kill sarcomas but has destructive effects in several major diseases. The two systems have interaction effects and are associated with apoptosis, proliferation, and pain signalling in various diseases. Whether these systems are present in the Achilles tendon and in Achilles tendinosis is unknown. The hypothesis is that the tenocytes produce substances belonging to these systems. In Studies I–III, we show that the potent effects of these substances are also likely to occur in the Achilles tendon. We found tenocyte immunoreactions for the neurotrophins brain-derived neurotrophic factor (BDNF), the nerve growth factor (NGF), the neurotrophin receptor p75, and for TNF-α and both of its receptors, TNFR1 and TNFR2. This occurred in both subjects with painful mid-portion Achilles tendinosis, and in controls. Furthermore, we found mRNA expression for BDNF and TNF-α in tenocytes, which proves that these cells produce these substances. TNFR1 mRNA was also detected for the tenocytes, and TNFR1 immunoreactions were upregulated in tendinosis tendons. This might explain why tenocytes in tendinosis undergo apoptosis more often than in normal tendons. Total physical activity (TPA) level and blood concentration of both soluble TNFR1 and BDNF were measured in Study IV. The results showed that the blood concentration of both factors were similar in subjects with tendinosis and in controls. Nevertheless, the TPA level was related to the blood concentration of sTNFR1 in tendinosis, but not in controls. This relationship should be studied further. The findings of this doctoral thesis show that neurotrophin and TNF-α systems are expressed in the Achilles tendon. We believe that the functions include tissue remodelling, proliferation and apoptosis.

Place, publisher, year, edition, pages
Umeå: Umeå University, 2013. 121 p.
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 1538
Keyword
Achilles tendon, tendinosis, tendinopathy, neurotrophins, TNF-alpha, physical acitivity, apoptosis, proliferation, pain, remodelling
National Category
Basic Medicine
Research subject
Human Anatomy
Identifiers
urn:nbn:se:umu:diva-63660 (URN)978-91-7459-525-3 (ISBN)
Public defence
2013-01-25, Biologihuset, sal BiA201, Umeå universitet, Umeå, 09:00 (Swedish)
Opponent
Supervisors
Available from: 2013-01-04 Created: 2013-01-03 Last updated: 2014-12-18Bibliographically approved

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