“…With respect to crosslinking effects, we have previously demonstrated that the apparently higher capacity of the primary trophoblast type III/betaglycan receptor for TGF-/1 than TGF-/2 was not due to an inherent difference in the crosslinking efficiency to 1251I-TGF-/1 versus 1251I-TGF-/32 (i.e., the type III/betaglycan receptor on control placental mesenchymal cell cultures was labeled to the same extent by 1251I-TGF-/1 and 1251I-TGF-/2 in affinity labeling saturation studies [Mitchell et al, 1992] (Mitchell et al, 1992) and some other cells types (Cheifetz et al, 1990 (Attisano et al, 1992 (MacKay and Danielpour, 1991). In addition, of the four TGF-3 binding components purified recently from porcine uterus (Ichijo et al, 1991) (Mitchell, unpublished observations The activities of TGF-f in extracellular matrix remodeling, growth inhibition, and immunosuppression have led various investigators to examine the roles of TGFf in trophoblast invasiveness (Lala and Graham, 1990;Tamada et al, 1990;Lala, 1991, 1992a,b), trophoblast differentiation (Morrish et al, 1991;, and in the maintenance of pregnancy (Altman et al, 1990;Clark et al, 1990Clark et al, , 1991Lea et al, 1992). A greater understanding of the control of trophoblast invasiveness is important for the treatment of certain conditions of pregnancy, such as the overinvasiveness of choriocarcinoma or the underinvasiveness of preeclampsia, as well as for cancer therapy in general.…”