THE DIFFERENTIAL ADHESION FORCES OF ANTERIOR CRUCIATE AND MEDIAL COLLATERAL LIGAMENT FIBROBLASTS - EFFECTS OF TROPOMODULIN, TALIN, VINCULIN, AND ALPHA-ACTININ
Klp. Sung et al., THE DIFFERENTIAL ADHESION FORCES OF ANTERIOR CRUCIATE AND MEDIAL COLLATERAL LIGAMENT FIBROBLASTS - EFFECTS OF TROPOMODULIN, TALIN, VINCULIN, AND ALPHA-ACTININ, Proceedings of the National Academy of Sciences of the United Statesof America, 93(17), 1996, pp. 9182-9187
We have determined the effects of tropomodulin (Tmod), talin, vinculin
, and cy-actinin on ligament fibroblast adhesion, The anterior cruciat
e ligament (ACL), which lacks a functional healing response, and the m
edial collateral ligament (MCL), a functionally healing ligament, were
selected for this study, The micropipette aspiration technique was us
ed to determine the forces needed to separate ACL and MCL cells from a
fibronectin-coated surface, Delivery of exogenous tropomodulin, an ac
tin-filament capping protein, into MCL fibroblasts significantly incre
ased adhesion, whereas its monoclonal antibody (mAb) significantly dec
reased cell adhesiveness. However, for ACL fibroblasts, Tmod significa
ntly reduced adhesion, whereas its mAb had no effect. mAbs to talin, v
inculin, and alpha-actinin significantly decreased the adhesion of bot
h ACL and MCL cells with increasing concentrations of antibody, and al
so reduced stress fiber formation and cell spreading rate as revealed
by immunofluorescence microscopy. Disruption of actin filament and mic
rotubule assembly with cytochalasin D and colchicine, respectively, al
so significantly reduced adhesion in ACL and MCL cells, In conclusion,
both ACL and MCL fibroblast adhesion depends on cytoskeletal assembly
; however, this dependence differs between ACL and MCL fibroblasts in
many ways, especially in the role of Tmod, These results add yet anoth
er possible factor in explaining the clinical differences in healing b
etween the ACL and the MCL.