We investigated the mechanisms underlying regulation of contraction with measurements of isometric force and intracellular @entity141 concentration ([ @entity141 ]i) in NIH 3T3 fibroblast reconstituted into fibers with the use of a collagen matrix. Treatment with the major phospholipids, neurotransmitters, and growth factors had little effect on baseline isometric force. However, @entity2872 , a @entity2404 (TxA2) analog, increased force and [ @entity141 ]i; EC50 values were 11.0 and 10.0 nM, respectively. The time courses were similar to those induced by calf serum (CS), and the maximal force was 65% of a CS-mediated contraction. The selective TxA2 receptor antagonist @entity13078 abolished the @entity2872 -induced responses. CS-induced contractions are dependent on an intracellular @entity141 store function; however, the @entity2872 response depended not only on intracellular @entity141 stores, but also on @entity141 influx from the extracellular medium. Inhibition of Rho kinase suppressed @entity2872 - and CS-induced responses; in contrast, inhibition of C kinase ( @entity6164 ) reduced only the @entity2872 response. Moreover, addition of @entity2872 to a CS contracture enhanced force and [ @entity141 ]i responses. These results indicate that @entity2872 -induced responses involve @entity6164 and Rho kinase pathways, in contrast to activation by CS. Thus TxA2 may have a role in not only the initial step of wound repair as an activator of @entity1003 , but also in fibroblast contractility in later stages.

Fibroblast fiber contraction: role of C and Rho kinase in activation by XXXX .

@entity2404 :: ('MESH:D013928', 'Chemical') :: ['thromboxane A2'] @entity2872 :: ('MESH:D019796', 'Chemical') :: ['U-46619'] @entity1003 :: ('MESH:D001778', 'Disease') :: ['blood coagulation'] @entity13078 :: ('MESH:C045749', 'Chemical') :: ['SQ-29548'] @entity6164 :: ('MESH:C566847', 'Disease') :: ['PKC'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca2+']
@entity2404 :: (MESH:D013928,Chemical) :: ['thromboxane A2']
