These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Differential expressions of lysyl oxidase family in ACL and MCL fibroblasts after mechanical injury.
    Author: Xie J, Huang W, Jiang J, Zhang Y, Xu Y, Xu C, Yang L, Chen PC, Sung KL.
    Journal: Injury; 2013 Jul; 44(7):893-900. PubMed ID: 23010071.
    Abstract:
    Lysyl oxidase (LOX) family has the capacity to catalyse the cross-linking of collagen and elastin, implicating its important fundamental roles in tissue development and injury healing. However, the variations in expression of the LOX family in the normal and injured anterior cruciate ligament (ACL) are not fully known. To better understand the role of LOX family in the self-healing inability mechanism of injured ACL, this study is to measure the LOX family's differential expressions in ACL and medial collateral ligament (MCL) fibroblasts after mechanical injury induced by using an equi-biaxial stretching chamber. The cells received various degrees of mechanical stretch 0% (resting state), 6% (physiological state) and 12% (injurious state), respectively. The gene profile and protein expressions were analysed by semi-quantitative PCR, quantitative real-time PCR and Western blotting. At physiological state, gene expression showed LOX in ACL was 2.6-5.2 folds higher than that in MCL in all culture time periods, LOXL-4 1.2-3.6 folds, but LOXL-3 in MCL showed 1.1-4.8 folds higher than that in ACL. In injurious state, MCL gene expressions were 2.8-29.6 folds higher than ACL in LOX, LOXL-2, LOXL-3 and LOXL-4 at 2, 6 and 12h periods. These differential expression profiles of the LOX family in the two ligament tissues were further used to explain the intrinsic differences between ACL and MCL, and why injured ACL could not be amenable to repair itself, whereas MCL could.
    [Abstract] [Full Text] [Related] [New Search]