title: Cell Signaling in Tenocytes: Response to Load and Ligands in Health and Disease.
abstract: Signaling in tenocytes during development, homeostasis and injury involves multiple and redundant pathways. Given that tendons transmit mechanical forces from muscle to bone to effect movement, a key function for tenocytes is the detection of and response to mechanical stimulation. Mechanotransduction involves matrix-integrin-cytoskeleton to nucleus signaling, gap junction intercellular communication, changes in intracellular calcium (Ca(2+)), activation of receptors and their pathways, and responses to biochemical factors such as hormones, growth factors, adenosine triphosphate (ATP) and its derivatives, and neuromodulators. The primary cilium also plays a key role in the detection of mechanical signals. During development, transforming growth factor-β (TGF-β), bone morphogenetic protein (BMP), and hedgehog (Hh) signaling modulate tendon differentiation and formation. The response to injury is complex and varied involving not only inflammatory mediators such as interleukin-1β but also mechanosensing. This chapter reviews the signaling pathways tenocytes use during mechanotransduction, development and in response to injury.
authors.affiliation: Flexcell International Corp., 2730 Tucker St., Suite 200, Burlington, 27215, NC, USA. info@flexcellint.com.
authors.forename: Michelle E
authors.initials: ME
authors.lastname: Wall
authors.affiliation: Department of Reconstructive Sciences, School of Dental Medicine, University of Connecticut Health Center, Farmington, CT, USA.
authors.forename: Nathaniel A
authors.initials: NA
authors.lastname: Dyment
authors.affiliation: Joint Department of Biomedical Engineering, North Carolina State University & University of North Carolina at Chapel Hill, Raleigh, NC, USA.
authors.forename: Josie
authors.initials: J
authors.lastname: Bodle
authors.affiliation: Flexcell International Corp., 2730 Tucker St., Suite 200, Burlington, 27215, NC, USA.
authors.forename: Jon
authors.initials: J
authors.lastname: Volmer
authors.affiliation: Joint Department of Biomedical Engineering, North Carolina State University & University of North Carolina at Chapel Hill, Raleigh, NC, USA.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Loboa
authors.affiliation: Musculoskeletal Research Programme, University of Aberdeen, Foresterhill, Aberdeen, Scotland, UK.
authors.forename: Anna
authors.initials: A
authors.lastname: Cederlund
authors.affiliation: Joint Department of Biomedical Engineering, North Carolina State University & University of North Carolina at Chapel Hill, Raleigh, NC, USA.
authors.forename: Ann M
authors.initials: AM
authors.lastname: Fox
authors.affiliation: Flexcell International Corp., 2730 Tucker St., Suite 200, Burlington, 27215, NC, USA.|Joint Department of Biomedical Engineering, North Carolina State University & University of North Carolina at Chapel Hill, Raleigh, NC, USA.
authors.forename: Albert J
authors.initials: AJ
authors.lastname: Banes
mesh_terms: D000818:Animals; D002450:Cell Communication; D002468:Cell Physiological Phenomena; D004194:Disease; D006801:Humans; D040542:Mechanotransduction, Cellular; D015398:Signal Transduction; D013314:Stress, Mechanical; D013710:Tendons / Q000166:cytology / Q000378:metabolism*; D000070916:Tenocytes / Q000166:cytology / Q000378:metabolism*; D014945:Wound Healing