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Publication : Integrin α1β1 participates in chondrocyte transduction of osmotic stress.

First Author  Jablonski CL Year  2014
Journal  Biochem Biophys Res Commun Volume  445
Issue  1 Pages  184-90
PubMed ID  24495803 Mgi Jnum  J:218579
Mgi Id  MGI:5617933 Doi  10.1016/j.bbrc.2014.01.157
Citation  Jablonski CL, et al. (2014) Integrin alpha1beta1 participates in chondrocyte transduction of osmotic stress. Biochem Biophys Res Commun 445(1):184-90
abstractText  BACKGROUND/PURPOSE: The goal of this study was to determine the role of the collagen binding receptor integrin alpha1beta1 in regulating osmotically induced [Ca(2+)]i transients in chondrocytes. METHOD: The [Ca(2+)]i transient response of chondrocytes to osmotic stress was measured using real-time confocal microscopy. Chondrocytes from wildtype and integrin alpha1-null mice were imaged ex vivo (in the cartilage of intact murine femora) and in vitro (isolated from the matrix, attached to glass coverslips). Immunocytochemistry was performed to detect the presence of the osmosensor, transient receptor potential vanilloid-4 (TRPV4), and the agonist GSK1016790A (GSK101) was used to test for its functionality on chondrocytes from wildtype and integrin alpha1-null mice. RESULTS/INTERPRETATION: Deletion of the integrin alpha1 subunit inhibited the ability of chondrocytes to respond to a hypo-osmotic stress with [Ca(2+)]i transients ex vivo and in vitro. The percentage of chondrocytes responding ex vivo was smaller than in vitro and of the cells that responded, more single [Ca(2+)]i transients were observed ex vivo compared to in vitro. Immunocytochemistry confirmed the presence of TRPV4 on wildtype and integrin alpha1-null chondrocytes, however application of GSK101 revealed that TRPV4 could be activated on wildtype but not integrin alpha1-null chondrocytes. Integrin alpha1beta1 is a key participant in chondrocyte transduction of a hypo-osmotic stress. Furthermore, the mechanism by which integrin alpha1beta1 influences osmotransduction is independent of matrix binding, but likely dependent on the chondrocyte osmosensor TRPV4.
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