Issue
Copyright (c) 2023 Lingling Qi, Guangyao Peng, Wenting Tang, Youyou Li, Jing Yin, Shan Duan, Lihu Xie, Xiaoping Long
![Creative Commons License](http://i.creativecommons.org/l/by-nc-nd/4.0/88x31.png)
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.The mechanism of lung tissue YKL-40 promoting the interstitial transformation of alveolar epithelial cells and its effect on TGF-β1 level in mice with idiopathic pulmonary fibrosis
Corresponding Author(s) : Xiaoping Long
Cellular and Molecular Biology,
Vol. 69 No. 4: Issue 4
Abstract
This study aimed to investigate the mechanism of lung tissue YKL-40 promoting the interstitial transformation of alveolar epithelial cells in mice with idiopathic pulmonary fibrosis and its effect on the level of TGF-β1. For this purpose, Forty SPF SD mice were randomly divided into 4 groups. They were the blank control group (CK group), virus-negative control group (YKL-40-NC group), YKL-40 knockdown group (YKL-40-inhibitor group) and YKL-40 overexpression group (YKL-40-mimics group), respectively. The mRNA expressions of alveolar epithelial cell mesenchymal transformation-related proteins, pulmonary fibrosis-related factors and TGF-β1-related pathway proteins in the above four groups of mice were compared to determine the mechanism of the promotion of alveolar epithelial cell mesenchymal transformation by YKL-40 in the lung tissues of mice with idiopathic pulmonary fibrosis and the effect of YKL-40 on the level of TGF-β1. The results showed that in terms of lung wet/dry weight ratio, the YKL-40-NC group, YKL-40-inhibitor group and YKL-40-mimics group were significantly increased compared with the CK group (P<0.05). About YKL-40 protein expression, compared with the CK group, AOD value and YKL-40 protein expression in the YKL-40-NC group, YKL-40-inhibitor group and YKL-40-mimics group were significantly increased (P<0.05), and compared with YKL-40-NC group, The AOD value and YKL-40 protein expression in YKL-40-inhibitor group were significantly decreased, while the AOD value and YKL-40 protein expression in YKL-40-mimics group were significantly increased (P<0.05), suggesting successful lentivirus transfection. Compared with the CK group, β-catenin and E-cadherin in the alveolar epithelial cells were significantly increased, while Pro-SPC was significantly decreased (P<0.05). The mRNA expression of pulmonary fibrosis-related factors showed that compared with the CK group, the mRNA expression of vimimin and hydroxyproline was significantly increased, while the mRNA expression of E-cadherin was decreased (P<0.05). However, the mRNA expressions of vimimin and hydroxyproline in the YKL-40-inhibitor group were significantly decreased, but the mRNA expression of E-cadherin was significantly increased. Compared with CK group, the protein expressions of TGF-β1, Smad3, Smad7 and α-Sma in the CK group were significantly increased (P<0.05). The protein expressions of TGF-β1, Smad3, Smad7 and α-SMA in the YKL-40-mimics group were significantly increased, but the protein expressions of TGF-β1, Smad3, Smad7 and α-SMA in YKL-40-inhibitor group were significantly decreased (P<0.05). In general, overexpression of YKL-40 can promote the progression of pulmonary fibrosis and the interstitial transformation of alveolar epithelial cells in mice with idiopathic fibrosis.
Keywords
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX