Un-transfected rabbit corneal endothelial cells (RCECs) were cultivated, using chitosan blend membrane 4ha (chitosan-hyaluronic acid), 631ha (chitosan-hyaluronic acid) and 631s (chitosan-chondroitine sulfate) as scaffold carriers. Their biocompatibilities were studied in regard to cell adherence, morphological changes, growth status and monolayer forming abilities. The results indicated that RCECs cultivated on 4ha and 631ha carriers tended to be aggregated and even desquamated to some extent in local areas, and even more severely on 631ha carrier. And the RCECs cultivated on 631ha carrier could form almost a monolayer 48h later, and those on 4ha carrier could not. Contrarily, the RCECs cultivated on 631s carrier were evenly distributed and were in good status of growth with a good adherence and fibroblast-like morphology which could form almost a monolayer 48h later. And a complete monolayer was formed and was tightly attached to the 631s carrier 72h later. From the above results, it can be concluded that 631s carrier is most probably an ideal scaffold carrier for RCEC cultivation. 631s carrier may have the potential for use in the development of tissue-engineered rabbit corneal endothelium.
Animals ; Biocompatible Materials ; chemistry ; Cell Adhesion ; Cell Culture Techniques ; Cell Line ; Cells, Cultured ; Chitosan ; chemistry ; Endothelium, Corneal ; cytology ; Hyaluronic Acid ; chemistry ; Membranes, Artificial ; Rabbits ; Tissue Engineering ; methods ; Tissue Scaffolds ; chemistry

OBJECTIVETo study the expression of tenascin in normal and fibrotic rat liver.

METHODSLiver fibrosis induced in rat with CCl(4) were divided into three stages: the stage of hepatic injury (4 weeks), early stage of hepatic fibrosis (8 weeks) and later stage of hepatic fibrosis (12 weeks). Tenascin expression in liver tissue was observed by immunohistochemical method and in situ hybridization using digoxigenin-labelled DNA probe.

RESULTSIn normal rat liver there was a weak staining for tenascin. In both liver injury stage and early stage of hepatic fibrosis, both mRNA signal and immunostaining for tenascin were significantly increased as compared to that in normal liver. In later stage of hepatic fibrosis, mRNA signal and immunostaining for tenascin were decreased compared with that in early stage of hepatic fibrosis. The cellular source of tenascin in liver mainly restricted in mesenchymal cells.

CONCLUSIONSTenascin is a component of the extracellular matrix of liver tissue. Plays a role in early matrix organization during liver fibrogenesis.

Animals ; Carbon Tetrachloride ; Disease Models, Animal ; Extracellular Matrix Proteins ; biosynthesis ; genetics ; Image Processing, Computer-Assisted ; Immunohistochemistry ; In Situ Hybridization ; Liver Cirrhosis ; chemically induced ; metabolism ; Male ; RNA, Messenger ; biosynthesis ; Rats ; Rats, Sprague-Dawley ; Tenascin ; biosynthesis ; genetics