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Continuous supply of TGFβ3 via adenoviral vector promotes type I collagen and viability of fibroblasts in alginate hydrogel
Author(s) -
Yao Yongchang,
Zhang Feng,
Zhou Ruijie,
Li Meng,
Wang DongAn
Publication year - 2010
Publication title -
journal of tissue engineering and regenerative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.835
H-Index - 72
eISSN - 1932-7005
pISSN - 1932-6254
DOI - 10.1002/term.263
Subject(s) - smad , transforming growth factor , microbiology and biotechnology , type i collagen , extracellular matrix , chemistry , viral vector , viability assay , small hairpin rna , fibroblast , cell , biology , recombinant dna , gene , in vitro , biochemistry , endocrinology , rna
In recent years, transforming growth factor‐β3 (TGFβ3) has interested more and more researchers with its competence in engineered histogenesis. In the present study we employed recombinant adenoviral vectors to deliver the constitutively active TGF β 3 gene to human dermal fibroblasts, which could maintain the continuous secretion of TGFβ3 from the cells. The expression of type I collagen in the Ad‐TGFβ3 group increased significantly in comparison with other three groups: Neg (cells without treatment of the adenovirus), Ad‐null (cells with treatment of the adenovirus, without the inserted gene) and Ad‐shRNA (cells with treatment of the adenovirus encoding shRNA specific for type I collagen). Additionally, we demonstrated that TGFβ3 enhanced the expression of Smad4 while inhibiting that of MMP‐9, thus promoting the collagen transcription via the Smad signal transduction pathway and restraining collagen degradation by MMP‐9, which contributed to the increasing type I collagen expression level. As type I collagen mediates cell–material interactions by providing anchorage, the viability of encapsulated fibroblasts in Ad‐TGFβ3 group was significantly higher than that in other three groups. Accordingly, this approach forms an effective way to improve the compatibility of non‐adhesive hydrogels containing anchorage‐dependent cells. Copyright © 2010 John Wiley & Sons, Ltd.