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Dysfunctional calcium homeostasis in aged mice primary tenocytes ő a potential functional link to tendon disorders (863.10)
Author(s) -
Vallejo Julian,
Spence Madoka,
Brotto Leticia,
Brotto Marco,
Abreu Eduardo
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.863.10
Subject(s) - tendon , calcium , calcium metabolism , medicine , homeostasis , dysfunctional family , tendinopathy , neuroscience , physiology , endocrinology , anatomy , biology , clinical psychology
Musculoskeletal diseases (MSKs) afflict more than 1.7 billion people worldwide. In the US, tendon disorders account for a surprising 30‐50% of all sports‐related injuries and close to half of all occupational illnesses. These diseases are further complicated by aging. Tendon disorders are difficult to treat in part because of our poor understanding of tendon physiology and pathophysiology at the cellular and molecular levels. Historically, more attention has been given to other cells of the musculoskeletal unit (bone‐tendon‐muscle) than to tendon cells (i.e., tenocytes), maybe because we lack good functional tests for tenocytes. Calcium plays an important role in tendon physiology and its response to mechanical load, and as a result calcium studies can be a useful tool to evaluate tenocytes. We compared the resting levels of calcium as well as the responses to Ionomycin in young and aged mouse primary tenocytes and found magnitude and the time to the maximal response were reduced in aged tenocytes. We are now conducting systematic studies to dissect the potential mechanisms for these differences. We postulate that dysfunctional calcium homeostasis might be a critical functional link between tenocytes and the organismal manifestation of tendon and MSKs. Grant Funding Source : Supported by Dale & Dorothy Thompson Endowment Fund (MB)