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p120‐Catenin modulating nuclear factor‐κB activation is partially R ho A / ROCK dependent in scratch injury
Author(s) -
Qin Shenghui,
Qin Lingzhi,
Zhang Chao,
Liu Liwei,
Sun Wenjia,
Li Naping,
Wu Renliang,
Wang Xi
Publication year - 2015
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/wrr.12270
Subject(s) - chemistry , microbiology and biotechnology , scratch , biology , materials science , composite material
p120‐catenin (p120) is known as a cadherin‐associated protein that participates in tumor metastasis and invasion, as well as an anti‐inflammatory mediator. Recently, its anti‐inflammatory role is drawing increasing attention, but the regulatory mechanisms are still unknown. Here, we report that p120 modulated inflammatory responses partially depends on RhoA/ROCK pathway in scratch‐induced injury in human bronchial epithelial cells (BECs). For the first time, we found that p120 was significantly reduced in BECs after scratching, which could induce interleukin‐8 (IL‐8) production through nuclear factor‐κB (NF‐κB) activation accompanied with IκBα phosphorylation. Over‐expression of p120 3A could inhibit NF‐κB activation and IL‐8 mRNA expression and protein synthesis after scratching, while p120 knockdown by small interfering RNA could promote NF‐κB activation and IL‐8 mRNA expression and protein synthesis after scratching. Furthermore, we found that RhoA was the binding partner of p120 in BECs. Although total RhoA and p120‐binded RhoA remained unchanged, the RhoA activity was increased after scratching. Chemical blockade of RhoA/ROCK signaling (Y27632) inhibited scratch‐induced nuclear translocation of NF‐κB p65. Over‐expression of p120 3A attenuated scratch‐induced RhoA activation, whereas silence of p120 significantly elevated scratch‐induced RhoA activation in BCEs. Conclusively, these results indicate an anti‐inflammatory effect of p120 in bronchial epithelial cells through its modulation of NF‐κB signaling depending on RhoA/ROCK pathway.