Chitinase-like protein YKL-40 regulates human bronchial epithelial cells proliferation, apoptosis, and migration through TGF-β1/Smads pathway

Abstract

In order to study the effects of chitinase-like protein YKL-40 on proliferation, apoptosis, and migration of human bronchial epithelial cell line (BEAS-2B), and the underlying mechanisms, we cultured BEAS-2B alone or with different concentrations of YKL-40. thiazolyl blue tetrazolium bromide (MTT) assay was used to examine the cell proliferation. Annexin V-fluorescein isothiocyanate isomer (FITC)/propidium iodide staining and scratch assay were performed to test the cell apoptosis and migration. The concentrations of transforming growth factor-β1 (TGF-β1), Smad3, Smad7, alpha-smooth muscle actin (α-SMA), interleukin-4 (IL-4), IL-6, and IL-8 in the cell culture supernatant were detected by enzyme-linked immunosorbent assay. The messenger RNA and protein levels of YKL-40, TGF-β1, Smad3, Smad7, and α-SMA were detected by reverse transcription polymerase chain reaction and Western blot. BEAS-2B cells cultured with different concentrations of YKL-40 showed significantly higher cell proliferation and migration and inflammatory cytokines compared with that of control group, while the cell apoptosis was significantly lower than that of control group ( p < 0.05). In addition, BEAS-2B cells cultured with YKL-40 had increased TGF-β1, Smad3, Smad7, and α-SMA levels in the supernatant, compared with that of BEAS-2B cells cultured alone ( p < 0.05). Furthermore, LY364947, as TGF-β1/Smads signaling pathway inhibitor, decreased cell proliferation and migration ability and enhanced cell apoptosis of BEAS-2B cells compared with control group ( p < 0.05). However, YKL-40 administration reversed the effect of LY364947 on the biological behavior of BEAS-2B cells. YKL-40 could affect the biological behaviors of BEAS-2B cells, which might be related to the TGF-β1/Smads pathway.

Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing

“…•Epidermal Growth Factor [12] •tBHQ (Nrf2 inducer) [180] •Erythroid E2-related factor 2 (Nrf2) [180] •siRNA-knockdown of epiplakin [181] •IWR-1 (Wnt inhibitor) [182] •Platelet-derived growth factor isoform BB (PDGFBB) [183] •Corneal Mesenchymal stromal cells exomes [184] •VEGF [185] •ATF 2 and ATF 7 [186] •Chitinase-like protein YKL-40 [187] •Tankyrase inhibitor XAV939 via TGF-β [188] •Placental growth factor via hypoxia [189] •Lamin A/C (LMNA) knockdown [190] •neonatal Fc receptor [191] •Myocardin-related transcription factor A (MRTF-A) signaling inhibitor CCG-1423 [192] •miR-363 [182] •PGF [189] Natural Products…”

Bronchoconstriction: a potential missing link in airway remodelling

“…In patients with asthma, increased serum levels of YKL-40 are correlated with disease severity, airway remodelling and decreased pulmonary function [49,50]. YKL-40 has been shown to induce the production of pro-inflammatory cytokines, including IL-8 from cultured HBE cells and BEAS-2B cells [51] and to induce proliferation and migration of BEAS-2B cells [52]. These studies investigating the role of YKL-40 in bronchial epithelial cells used submerged cells.…”

Imaginal disc growth factors areDrosophilaChitinase-like Proteins with roles in morphogenesis and CO2response

“…Chitinase-like proteins (CLPs) are secreted glycoproteins with properties of cytokines and growth factors (GUAN et al 2020;KAWAMURA et al 1999;KZHYSHKOWSKA et al 2016;LU et al 2022). Normally, CLPs aid in inflammatory responses, wound healing, and defense against parasites, but they also have a dark side (DI ROSA et al 2016;MAZUR et al 2021;PINTEAC et al 2021;SUTHERLAND et al 2014).…”