Wound repair and proliferation of bronchial epithelial cells regulated by CTNNAL1

Abstract

Adhesion molecules play vital roles in airway hyperresponsiveness (AHR) or airway inflammation. Our previous study indicated that adhesion molecule catenin alpha-like 1 (CTNNAL1) is relevant closely to asthma susceptibility, but its biological function or significance is still unclear. In the present study, we observed the temporal and spatial distribution of CTNNAL1 expression in mouse lung tissue with the OVA-sensitized asthma model and found that the level of CTNNAL1 mRNA showed a prominent negative correlation with pulmonary resistance (R(L)). To study the function of CTNNAL1 in airway, effects of CTNNAL1 on proliferation and wound repair activity of human bronchial epithelial cells (HBEC) was investigated with antisense oligonucleotide (ASO) technique. The results showed that: (1) CTNNAL1 ASO could decelerate the repairing velocity and proliferation of HBEC; (2) CTNNAL1 expression was increased on the edge cells of mechanic wounded area in culture; (3) extracellular matrix component fibronectin (Fn) obviously promoted wound repair activity and proliferation of HBEC, which could be blocked by CTNNAL1 ASO; (4) Western blot showed that Fn could promote FAK phosphorylation, which also be inhibited by CTNNAL1 ASO. In conclusion, the level of CTNNAL1 mRNA expression is highly correlated to airway resistance; CTNNAL1 may contribute to the wound repair and proliferation of HBEC. Furthermore, it may serve to Fn mediated cell-extracellular adhesion and its signal transduction.

α-Catulin Drives Metastasis by Activating ILK and Driving an αvβ3 Integrin Signaling Axis

“…S7). It has been previously shown that a-catulin plays an important role in fibronectin-mediated wound repair and proliferation (41). Thus, after a-catulin induced upregulation of FN1 and integrin a V b 3 expression via the interaction with ILK, FN1 then binds to integrins and activates the a-catulin/ILK complex in a positive feedback loop.…”

The Lbc Rho Guanine Nucleotide Exchange Factor/α-Catulin Axis Functions in Serotonin-induced Vascular Smooth Muscle Cell Mitogenesis and RhoA/ROCK Activation*

“…Moreover, the magnitude of inhibition was comparable with that observed by Lbc siRNA, consistent with ␣-catulin and Lbc cooperation in 5-HT-mediated mitogenesis. ␣-Catulin is distantly related to the cytoskeletal linkers ␣-catenin/vinculin (43,44), and has been linked to epithelial proliferation (45). Its cell biologic function is only partially understood, and whether ␣-catulin has additional roles that influence mitogenesis remains to be determined.…”

Identification of Transcription Factors Regulating CTNNAL1 Expression in Human Bronchial Epithelial Cells

“…In vitro experiments showed that the rate of repair and proliferation of HBEC was slowed down after HBEC was treated with CTNNAL1 ASO, and CTNNAL1 expression was explicitly increased on the cells in wound edges. Those data indicate that CTNNAL1 might be involved in growth regulation and may be beneficial for the recovery of bronchial epithelium damage [8].…”