In agreement with published data, we found that several TUNEL positive cells were present in normal corneas and those that were present in keratoconic corneas were distributed mainly in the anterior stroma. In addition, the estimated frequency of occurrence of TUNEL good cells in the sections of non scarred keratoconic corneas, was statistically significantly less than in the sections of the scarred keratoconic corneas but not better than in the area of the corneas. In approaching the issue of whether apoptosis is causal or even a consequence of the keratoconic condition, these observations tend to suggest that there is no genetic predisposition Letrozole solubility for keratoconic stromal cells to undergo apoptosis and that the condition is not caused by factors that trigger apoptosis. It generally does not nevertheless preclude the possibility that TIMP 3, in the context of tissue repair, is involved in the induction of apoptosis in keratoconic stromal cells. This and the chance that TIMP 1 may prevent TIMP 3 induced apoptosis, was recognized by the location of the apoptotic cells and those and the clear association with scarring formation making TIMP 3 and TIMP 1. As well as watching increased amounts of TIMP 3 providing stromal cells in scarred keratoconic corneas, we also discovered that their soluble TIMP 3 content was significantly higher than in normal or non scarred keratoconic corneas. This study shows that virtually all the TIMP 3 that was secreted from the RAdTIMP 3 attacked stromal cells of normal corneas, kept membrane bound. Mitochondrion Previous reports suggested that the structure of the matrix laid down by the stromal cells of scarred keratoconic corneas in vitro differs to that of stromal cells of non scarred keratoconic corneas. They also indicated that the growth media of stromal cells cultured from scarred keratoconic corneas contain much more TIMP 3 than those derived from normal or non scarred keratoconic corneas and that keratoconic buy Hesperidin corneas contain distinct parts, especially where Bowmans Layer is very thinned, which do not stain with anti TIMP 3 antibody. In view of those findings we hypothesise that throughout the thinning procedure, matrix ligands for TIMP 3 are lost and/or less common in scar tissue formation. We also hypothesise that soluble TIMP 3 acts as a for activated MMPs and hence facilitates the deposition of scarring. At the present time, the concentration of TIMP 3 needed to cause apoptosis is not known. However since under normal conditions this protein has a high affinity for the ECM and can accumulate within the matrix surrounding its secretory cells, it’s likely that local concentrations could be high.