In vitro modeling of repetitive motion injury and myofascial release.
OBJECTIVE
In this study we modeled repetitive motion strain (RMS) and myofascial release (MFR) in vitro to investigate possible cellular and molecular mechanisms to potentially explain the immediate clinical outcomes associated with RMS and MFR.


METHODS
Cultured human fibroblasts were strained with 8h RMS, 60s MFR and combined treatment; RMS+MFR. Fibroblasts were immediately sampled upon cessation of strain and evaluated for cell morphology, cytokine secretions, proliferation, apoptosis, and potential changes to intracellular signaling molecules.


RESULTS
RMS-induced fibroblast elongation of lameopodia, cellular decentralization, reduction of cell to cell contact and significant decreases in cell area to perimeter ratios compared to all other experimental groups (p<0.0001). Cellular proliferation indicated no change among any treatment group; however RMS resulted in a significant increase in apoptosis rate (p<0.05) along with increases in death-associated protein kinase (DAPK) and focal adhesion kinase (FAK) phosphorylation by 74% and 58% respectively, when compared to control. These responses were not observed in the MFR and RMS+MFR group. Of the 20 cytokines measured there was a significant increase in GRO secretion in the RMS+MFR group when compared to control and MFR alone.


CONCLUSIONS
Our modeled injury (RMS) appropriately displayed enhanced apoptosis activity and loss of intercellular integrity that is consistent with pro-apoptotic dapk-2 and FAK signaling. Treatment with MFR following RMS resulted in normalization in apoptotic rate and cell morphology both consistent with changes observed in dapk-2. These in vitro studies build upon the cellular evidence base needed to fully explain clinical efficacy of manual manipulative therapies.
Department of Basic Medical Sciences, University of Arizona, College of Medicine, Phoenix, AZ 85004-2157, USA.
Kate R
KR
Meltzer
Thanh V
TV
Cao
Joseph F
JF
Schad
Hollis
H
King
Scott T
ST
Stoll
Paul R
PR
Standley
D000704:Analysis of Variance; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D016022:Case-Control Studies; D049109:Cell Proliferation; D002478:Cells, Cultured; D012090:Cumulative Trauma Disorders / Q000209:etiology* / Q000534:rehabilitation; D016207:Cytokines; D064550:Death-Associated Protein Kinases; D005347:Fibroblasts; D051417:Focal Adhesion Kinase 1; D006801:Humans; D009209:Myofascial Pain Syndromes / Q000534:rehabilitation*
D051017:Apoptosis Regulatory Proteins; D016207:Cytokines; D051417:Focal Adhesion Kinase 1; C496050:PTK2 protein, human; C579104:DAPK2 protein, human; D064550:Death-Associated Protein Kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases