These observations clearly demonstrate that CatB has a critical role in regulating the expression of collagens III and IV by fibroblasts during chronic activation of TLR2 signaling.
The Regulation of NF-[kappa]B Activation and Oxidative Damage for Decreasing Collagens III and IV by CatB after P.
The mean expression of CatB was significantly increased at 24 and 48 h (Figures 3(c) and 3(d)), while the mean expression of I[kappa]B[alpha] was significantly decreased compared with that of the control group at 24 and 48 h after P.
These observations demonstrate that CatB is involved in the proteolytic degradation of the I[kappa]B[alpha] and oxidative DNA damage during chronic P.
Determination of CatB and Oxidative Damage in Fibroblasts of Inflamed Tissues with Chronic Periodontitis.
The major finding of the present study was clarifying the critical role of CatB in regulating collagen expression by fibroblasts via prolonging TLR2/NF-[kappa]B activation (summarized in Figure 5).
Elevated levels of CatB in fibroblasts are typically observed in many chronic inflammatory diseases, including rheumatoid arthritis as well as periodontitis [32-34].
CatB was recently found to regulate NF-[kappa]B activation .
This is the first report to clarify the novel mechanism of CatB involved in the downregulation of collagens III and IV via chronic activation of TLR2/NF-[kappa]B signaling.
CatB is considered a major lysosomal cysteine protease for the degradation of collagen in soft connective tissues, as it possesses both endopeptidase and exopeptidase activity which differs from other lysosomal cysteine proteases .
CatB regulates the expression of collagens III and IV by fibroblasts via prolonging TLR2/NF-[kappa]B activation and oxidative stress (schematic illustration in Figure 5).
Caption: Figure 1: Expression of CatB and collagens III and IV by BJ fibroblasts after challenge with P.