Sökning: onr:"swepub:oai:DiVA.org:umu-67794" >
Human tenocytes are...
Human tenocytes are stimulated to proliferate by acetylcholine through an EGFR signalling pathway
-
- Fong, Gloria (författare)
- Umeå universitet,Anatomi
-
- Backman, Ludvig (författare)
- Umeå universitet,Anatomi,Institutionen för kirurgisk och perioperativ vetenskap
-
- Andersson, Gustav (författare)
- Umeå universitet,Anatomi
-
visa fler...
-
- Scott, Alexander (författare)
- Vancouver Coastal Health and Research Institute
-
- Danielson, Patrik (författare)
- Umeå universitet,Anatomi
-
visa färre...
-
(creator_code:org_t)
- 2012-12-05
- 2013
- Engelska.
-
Ingår i: Cell and Tissue Research. - : Springer-Verlag New York. - 0302-766X .- 1432-0878. ; 351:3, s. 465-475
- Relaterad länk:
-
https://link.springe...
-
visa fler...
-
https://urn.kb.se/re...
-
https://doi.org/10.1...
-
visa färre...
Abstract
Ämnesord
Stäng
- Studies of human patellar and Achilles tendons have shown that primary tendon fibroblasts (tenocytes) not only have the capacity to produce acetylcholine (ACh) but also express muscarinic ACh receptors (mAChRs) through which ACh can exert its effects. In patients with tendinopathy (chronic tendon pain) with tendinosis, the tendon tissue is characterised by hypercellularity and angiogenesis, both of which might be influenced by ACh. In this study, we have tested the hypothesis that ACh increases the proliferation rate of tenocytes through mAChR stimulation and have examined whether this mechanism operates via the extracellular activation of the epidermal growth factor receptor (EGFR), as shown in other fibroblastic cells. By use of primary human tendon cell cultures, we identified cells expressing vimentin, tenomodulin and scleraxis and found that these cells also contained enzymes related to ACh synthesis and release (choline acetyltransferase and vesicular acetylcholine transporter). The cells furthermore expressed mAChRs of several subtypes. Exogenously administered ACh stimulated proliferation and increased the viability of tenocytes in vitro. When the cells were exposed to atropine (an mAChR antagonist) or the EGFR inhibitor AG1478, the proliferative effect of ACh decreased. Western blot revealed increased phosphorylation, after ACh stimulation, for both EGFR and the extracellular-signal-regulated kinases 1 and 2. Given that tenocytes have been shown to produce ACh and express mAChRs, this study provides evidence of a possible autocrine loop that might contribute to the hypercellularity seen in tendinosis tendon tissue.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Kirurgi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Surgery (hsv//eng)
Nyckelord
- Muscarinic acetylcholine receptors
- Tendinopathy
- Tendinosis
- Choline acetyltransferase
- Vesicular acetylcholine transporter
- Atropine
- Non-neuronal acetylcholine
- Human
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
Hitta via bibliotek
Till lärosätets databas