p120-Catenin modulating nuclear factor-κB activation is partially RhoA/ROCKdependent in scratch injury

What is it about?

It is about inflammatory responses in airway wound. In our daily life, we can't avoid to be hurt by some mechanical damage, then our body will repair itself. There are two kinds of repair types, one is completely repair, another is scar repair. To achieve complete repair we should avoid bacterial contamination and inflammation, etc. But we don't know the damage itself also can produce inflammation, this study preliminarily reveals the possible mechanism of the inflammatory responses after mechanical scratch, to help us know more about the body repair mechanism.

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Why is it important?

We think that the most interesting result of this study is that p120 modulated inflammatory response partially depended on RhoA/ROCK pathway in scratching-induced 16HBE 14o-cell injury. The p120 expression is significantly reduced and the RhoA activity is increased by scratching. Activation of RhoA leads to p-IκBα degradation and p65 nuclear translocation, implying a possible effect of p120 on NF-κ B signaling in human bronchial epithelial cells after scratching stimulation. Over-expression of p120 3A inactivate RhoA, while transfection with p120 small interfering RNA (siRNA) significantly elevate RhoA activity. Y27632, a ROCK inhibitor, used to inhibit the RhoA/ROCK signal pathway, can greatly inhibit nuclear translocation of p65. RhoA plays a key role in p120 modulating scratching-induced NF-κ B signaling.

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