The ability of the nonspecific COX-1/2 inhibitor indomethacin, the COX-2-specific inhibitor celecoxib, and the COX-1-specific inhibitor SC-560 to inhibit proliferation was studied in OFs from type I, type II, and non-TED patients by measuring [
3H]thymidine incorporation. Orbital fibroblasts were either untreated or treated for 3 days with 5 ng/mL TGFβ alone or with cotreatment of indomethacin (20 μM), celecoxib (10 μM), or SC-560 (1 μM) on day 1 (
Fig. 7). TGFβ treatment of OFs compared to untreated OFs resulted in an increase in the amount of [
3H]thymidine incorporated by 2.7-fold in type II OFs (
P < 0.001), 1.6-fold in type I OFs, and 1.2-fold in non-TED OFs. The amount of TGFβ-induced [
3H]thymidine incorporated by type II OFs was 1.7-fold higher than by type I OFs (
P < 0.01) and 2.9-fold higher than by non-TED OFs (
P < 0.001). TGFβ-induced [
3H]thymidine incorporation was inhibited by 37% by indomethacin (
P < 0.05), 59% by celecoxib (
P < 0.001), and 31% by SC-560 (
P < 0.05) in type II OFs. The COX inhibitors did not significantly alter TGFβ-induced [
3H]thymidine incorporation in type I or non-TED patients. Similar results were seen in other type I, type II, and non-TED OF strains.