Pontages veineux in situ. Indications, technique et résultats. A propos d'une étude prospective de 26 cas consécutifs [In situ venous grafts. Indications, technique and results. Prospective study of 26 consecutive cases].

The in situ saphenous vein bypass has been introduced in our department since 1989. A total of 26 bypasses in 22 patients have been followed prospectively. Indications for revascularisation have been severe arterial insufficiency in 73% of the cases (stage III or IV). With the exception of one postoperative death (myocardial infarction), all the patients have recovered uneventfully, with a regression to stage I. No amputation has been necessary. Morbidity has been 30%, with mainly minor local complications. The primary patency rate is 83% at one year and 78% after 2 and 3 years, whereas the secondary patency rate is 91% at one year, and remains constant thereafter up to 3 years. Considering our results and those from the literature, we believe that the in situ technique is very valuable, especially for below-knee vascular reconstruction. Technical difficulties of the method are analysed.

Recruitment of Matrix Metalloproteinase-9 (MMP-9) to the Fibroblast Cell Surface by Lysyl Hydroxylase 3 (LH3) Triggers Transforming Growth Factor-β (TGF-β) Activation and Fibroblast Differentiation.

Solid tumor growth triggers a wound healing response. Similar to wound healing, fibroblasts in the tumor stroma differentiate into myofibroblasts (also referred to as cancer-associated fibroblasts) primarily, but not exclusively, in response to transforming growth factor-β (TGF-β). Myofibroblasts in turn enhance tumor progression by remodeling the stroma. Among proteases implicated in stroma remodeling, matrix metalloproteinases (MMPs), including MMP-9, play a prominent role. Recent evidence indicates that MMP-9 recruitment to the tumor cell surface enhances tumor growth and invasion. In the present work, we addressed the potential relevance of MMP-9 recruitment to and activity at the surface of fibroblasts. We show that recruitment of MMP-9 to the fibroblast cell surface occurs through its fibronectin-like (FN) domain and that the molecule responsible for the recruitment is lysyl hydroxylase 3 (LH3). Functional assays suggest that both pro- and active MMP-9 trigger α-smooth muscle actin expression in cultured fibroblasts, reflecting myofibroblast differentiation, possibly as a result of TGF-β activation. Moreover, the recombinant FN domain inhibited both MMP-9-induced TGF-β activation and α-smooth muscle actin expression by displacing MMP-9 from the fibroblast cell surface. Together our results uncover LH3 as a new docking receptor of MMP-9 on the fibroblast cell surface and demonstrate that the MMP-9 FN domain is essential for the interaction. They also show that the recombinant FN domain inhibits MMP-9-induced TGF-β activation and fibroblast differentiation, providing a potentially attractive therapeutic reagent toward attenuating tumor progression where MMP-9 activity is strongly implicated.