PubMed · 3310807
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C Durandeau, P M Gendre, P Aumonier. 1987. [Collagen implants].. https://pubmed.ncbi.nlm.nih.gov/3310807/
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During wound repair, fibroblasts accumulate in the injured area until any defect is filled with stratified layers of cells and matrix. Such fibroplasia also occurs in many fibrotic disorders. Transforming growth factor-beta (TGF-beta), a promotor of granulation tissue in vivo and extracellular matrix production in vitro, is expressed during the active fibroplasia of wound healing and fibroproliferative diseases. Under usual tissue culture conditions, normal fibroblasts grow to confluence and then cease proliferation. In this study, culture conditions with TGF-beta 1 have been delineated that promote human fibroblasts to grow in stratified layers mimicking in vivo fibroplasia. When medium supplemented with serum, ascorbate, proline, and TGF-beta was added thrice weekly to normal human dermal fibroblasts, the cells proliferated and stratified up to 16 cell layers thick within the culture dish, producing a tissue-like fibroplasia. TGF-beta stimulated both DNA synthesis as measured by 3H-thymidine uptake and cell proliferation as measured by a Hoechst dye DNA assay in these postconfluent cultures. The stratification was dependent on fibronectin assembly, as demonstrated by anti-fibronectin antibodies which inhibited both basal and TGF-beta-stimulated cell proliferation and stratification. Suppression of collagen matrix assembly in cell layers with beta-amino-proprionitrile (BAPN) did not inhibit basal or TGF-beta stimulated in vitro fibroplasia. BAPN did not interfere with fibronectin matrix assembly as judged by immunofluorescence microscopy. Thus, in concert with serum factors, TGF-beta stimulates postconfluent, fibronectin matrix-dependent, fibroblast growth creating a fibroplasia-like tissue in vitro.
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Microscopic aneurysmal-like structures (ALS) develop spontaneously in the convoluted rat testicular artery and have been previously proposed as a model relevant to cerebral aneurysms. The effect of defects in connective tissue fibres on ALS formation was investigated by microscopy using two approaches: (i) the study of the effect of beta-aminopropionitrile (BAPN), an inhibitor of the cross-linking of elastic and collagen fibres, on the incidence, size and morphology of ALS in spontaneously hypertensive rats (SHR) and their normotensive controls (WKY). The straight spermatic artery was studied for comparison. (ii) The determination of the incidence of spontaneous ALS in Brown Norway (BN) and Long Evans (LE) rats which are highly susceptible (BN) or resistant (LE) to the spontaneous rupture of the arterial internal elastic lamina. (i) BAPN increased the number and size of ALS in SHR and WKY rats and had no effect on the straight spermatic artery and (ii) ALS were more numerous and of greater size in BN than in LE rats. Taken together, these results show that defective connective tissue fibres may favour the formation and induce the enlargement of aneurysmal-like structures. By analogy, these data suggest that a lack of connective tissue fibre integrity may be of importance in cerebral aneurysm formation and development.