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Differences in tumor necrosis factor (TNF)alpha and TNF receptor-1-mediated intracellular signaling factors in normal, inflamed and scar-formed horse tendons.
Abstract: Tumor necrosis factor (TNF) receptors (TNF-R)-mediated cell survival or apoptosis has been demonstrated in many cells, but little is known about survival or apoptotic signals via TNF-R1 in tendinocytes. In this study, we focused on four signaling factors, TNFalpha, TNF-R1, TNFR-associated factor2 (TRAF2) and caspase-3, in order to elucidate the signaling events in tendinocytes. Samples were obtained from normal, inflamed and scar-formed equine superficial digital flexor tendons. To detect these signaling factors, samples were subjected to immunohistochemistry and Western blot analysis, and some samples were also subjected to reverse transcription-polymerase chain reaction (RT-PCR), PCR-Southern blot analysis and in situ hybridization to detect the expression of TNFalpha mRNA. Distribution of the four factors differed depending on the tendon condition, normal, inflamed or scar-formed. In the normal tendon, large amounts of TRAF2 were found in tendinocytes, but the amounts of TNF-R1 were small. TNFalpha mRNA was expressed most highly in the inflamed tendon. TNF-R1, which was only faintly detected in the normal tendon, was detected at a high level in the inflamed tendon, and the amounts of TRAF2 and caspase-3 also increased. Activated caspase-3 was only detected in the inflamed tendon. TNFalpha mRNA was also expressed in the scar-formed tendon, though it showed weak signals, and the expression levels of TNF-R1, TRAF2 and caspase-3 proteins were very low. Two distinct intracellular signaling pathways of TNFalpha, which lead to cell survival and apoptosis, might be present in tendinocytes mediated through TNF-R1. These results, which reflect the dynamism of TNFalpha, provide important clues for means to prevent tendinopathy.
Publication Date: 2005-11-09 PubMed ID: 16276053DOI: 10.1292/jvms.67.985Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Comparative Study
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
This research explores the changes in intracellular signaling factors in horse tendons under different conditions: normal, inflamed and scar-formed. It particularly focuses on the role of tumor necrosis factor (TNF)alpha and its receptor, TNF receptor-1 (TNF-R1), in cell survival and apoptosis of tendinocytes — the primary cells in tendons.
Objectives of the Research
- The study aimed to understand how TNFalpha and TNF-R1 regulate the survival or apoptosis of tendinocytes, which are the major cells in tendons.
- Four signaling factors involved in this pathway were examined: TNFalpha, TNF-R1, TNF receptor-associated factor 2 (TRAF2), and caspase-3.
Research Methods
- The researchers used different methods to obtain detailed information on the expression and distribution of these signaling factors under varying tendon conditions.
- Techniques used included immunohistochemistry, Western blot analysis, reverse transcription-polymerase chain reaction (RT-PCR), PCR-Southern blot analysis, and in situ hybridization.
Key Findings
- In normal tendons, large amounts of TRAF2 were found, but TNF-R1 was less abundant.
- Inflamed tendons showed the highest expression of TNFalpha mRNA, along with an increase in levels of TNF-R1, TRAF2, and caspase-3.
- Activated caspase-3 was specifically detected in inflamed tendons.
- Although TNFalpha mRNA was present in scar-formed tendons, its signal was weak and the expression levels of TNF-R1, TRAF2 and caspase-3 proteins were very low.
Conclusion and Implications
- The study identified two distinct intracellular signaling pathways leading to either survival or apoptosis of tendinocytes mediated through TNF-R1.
- The differences in the expression and distribution of the key signaling factors under varying tendon conditions provide significant insights into how tendinopathies (tendon disorders) might be prevented.
Cite This Article
APA
Hosaka Y, Kirisawa R, Ueda H, Yamaguchi M, Takehana K.
(2005).
Differences in tumor necrosis factor (TNF)alpha and TNF receptor-1-mediated intracellular signaling factors in normal, inflamed and scar-formed horse tendons.
J Vet Med Sci, 67(10), 985-991.
https://doi.org/10.1292/jvms.67.985 Publication
Researcher Affiliations
- Department of Veterinary Anatomy, School of Veterinary Medicine, Rakuno Gakuen University, Ebetsu, Japan.
MeSH Terms
- Animals
- Blotting, Southern / veterinary
- Blotting, Western / veterinary
- Caspase 3
- Caspases / metabolism
- DNA Primers
- Horse Diseases / metabolism
- Horse Diseases / pathology
- Horses
- Immunohistochemistry / veterinary
- In Situ Hybridization / veterinary
- Inflammation / metabolism
- Inflammation / pathology
- Inflammation / veterinary
- Receptors, Tumor Necrosis Factor, Type I / metabolism
- Reverse Transcriptase Polymerase Chain Reaction / veterinary
- Signal Transduction / physiology
- TNF Receptor-Associated Factor 2 / metabolism
- Tendons / metabolism
- Tendons / pathology
- Tumor Necrosis Factor-alpha / metabolism
Citations
This article has been cited 12 times.- Macedo RS, Teodoro WR, Capellozzi VL, Rosemberg DL, Sposeto RB, de Cesar Netto C, Deland JT, Maffulli N, Ellis SJ, Godoy-Santos AL. Histoarchitecture of the fibrillary matrix of human fetal posterior tibial tendons. Sci Rep 2022 Oct 26;12(1):17922.
- Wang Y, Zhang J, Lin Y, Cheng S, Wang D, Rao M, Jiang Y, Huang X, Chen R, Xie Y, Yin P, Cheng B. A Global Phosphorylation Atlas of Proteins Within Pathological Site of Rotator Cuff Tendinopathy. Front Mol Biosci 2021;8:787008.
- Oreff GL, Fenu M, Vogl C, Ribitsch I, Jenner F. Species variations in tenocytes' response to inflammation require careful selection of animal models for tendon research. Sci Rep 2021 Jun 14;11(1):12451.
- Moqbel SAA, Xu K, Chen Z, Xu L, He Y, Wu Z, Ma C, Ran J, Wu L, Xiong Y. Tectorigenin Alleviates Inflammation, Apoptosis, and Ossification in Rat Tendon-Derived Stem Cells via Modulating NF-Kappa B and MAPK Pathways. Front Cell Dev Biol 2020;8:568894.
- Tang C, Chen Y, Huang J, Zhao K, Chen X, Yin Z, Heng BC, Chen W, Shen W. The roles of inflammatory mediators and immunocytes in tendinopathy. J Orthop Translat 2018 Jul;14:23-33.
- Morita W, Dakin SG, Snelling SJB, Carr AJ. Cytokines in tendon disease: A Systematic Review. Bone Joint Res 2017 Dec;6(12):656-664.
- Millar NL, Murrell GA, McInnes IB. Inflammatory mechanisms in tendinopathy - towards translation. Nat Rev Rheumatol 2017 Jan 25;13(2):110-122.
- Torres-Silva R, Lopes-Martins RA, Bjordal JM, Frigo L, Rahouadj R, Arnold G, Leal-Junior EC, Magdalou J, Pallotta R, Marcos RL. The low level laser therapy (LLLT) operating in 660 nm reduce gene expression of inflammatory mediators in the experimental model of collagenase-induced rat tendinitis. Lasers Med Sci 2015 Sep;30(7):1985-90.
- Rio E, Moseley L, Purdam C, Samiric T, Kidgell D, Pearce AJ, Jaberzadeh S, Cook J. The pain of tendinopathy: physiological or pathophysiological?. Sports Med 2014 Jan;44(1):9-23.
- Pires D, Xavier M, Araújo T, Silva JA Jr, Aimbire F, Albertini R. Low-level laser therapy (LLLT; 780 nm) acts differently on mRNA expression of anti- and pro-inflammatory mediators in an experimental model of collagenase-induced tendinitis in rat. Lasers Med Sci 2011 Jan;26(1):85-94.
- Beaumont RE, Flood C, Guest DJ. Inhibition of interleukin-1 receptor-associated kinase (IRAK)-4 provides partial rescue of interleukin-1 beta induced functional and gene expression changes in equine tenocytes. Mol Biol Rep 2025 Nov 6;53(1):54.
- Elkrewi EZ, Al Abdulqader AA, Khasanov R, Maas-Omlor S, Boettcher M, Wessel LM, Schäfer KH, Tapia-Laliena MÁ. Role of Inflammation and the NF-κB Signaling Pathway in Hirschsprung's Disease. Biomolecules 2024 Aug 12;14(8).
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