Lack of alpha1,2-fucosylation protects mice from bleomycin-induced lung fibrosis: A quantitative proteomic analysis of bronchoalveolar lavage fluid.

Authors

Chenxi Zhu, Yicheng Jiang, Xinjia Mai, Zhaohui Ji, Gulberdiyev Abdylla, Dapeng Zhou

Published in

Carbohydrate research. Volume 567. Pages 110010. Jun 18, 2026. Epub Jun 18, 2026.

Abstract

The mechanisms responsible for pulmonary fibrosis remain incompletely understood. This study investigated the effect of alpha1,2-fucosylation deficiency on bleomycin-induced pulmonary fibrosis using wild-type C57BL/6J mice and Fut1/Fut2/Sec1 triple-knockout mice deficient in alpha1,2-fucosylation. Mice were treated with bleomycin, and lung tissues and bronchoalveolar lavage fluid (BALF) were collected on Day 7 and Day 14. DFTKO mice showed improved survival and attenuated histological lung injury and collagen deposition compared with WT mice. BALF samples were analyzed by TMT 10-plex quantitative proteomics using 18 individual samples, with three biological replicates per genotype/time-point group. Differentially expressed proteins were prioritized using combined criteria of fold change ≥1.2 or ≤0.83, P < 0.05, and VIP score >1. In WT mice, multiple bronchoalveolar lavage proteins were elevated 7 days after bleomycin treatment, including 1) proteins involved in lipid metabolism, antimicrobial defense and inflammation: BPIFA2 (FC = 25.04, VIP = 1.22, P = 0.01), APOA1(FC = 8.37, VIP = 1.23, P = 0.02), C1QTNF5(FC = 7.72, VIP = 1.20, P = 0.049), SERPINA3N(FC = 6.64, VIP = 1.22 P = 0.4); 2) proteins involved in TGF-beta and extracellular matrix signaling: FST(FC = 14.28, VIP = 1.23, P = 0.02), BGN(FC = 13.58, VIP = 1.20, P = 0.02), TIMP1(FC = 10.72, VIP = 1.21, P = 0.04), VCAN(FC = 9.04, VIP = 1.21 P = 0.00008); 3) Collagens: COL5A1(FC = 9.63, VIP = 1.22 P = 0.01), COL5A2(FC = 7.09, VIP = 1.19 P = 0.03). Several proteins involved in detoxification of reactive oxygen species (ROS) were found to be decreased 7 days after bleomycin treatment: SELENBP1(FC = 0.18, VIP = 1.22, P = 0.02), GLRX5(FC = 0.18, VIP = 1.23, P = 0.02), UQCRC1(FC = 0.17, VIP = 1.23, P = 0.0005). In the Day 7 comparison between DFTKO and WT mice, proteins related to DNA damage repair, genome stability, wound healing, and tissue remodeling were increased in DFTKO mice, including H3C1 (FC = 3.66, VIP = 1.68, P = 0.03), SSBP1(FC = 2.96, VIP = 1.78, P = 0.0004), HMGA1(FC = 2.84, VIP = 1.60, P = 0.01), HDGFL3(FC = 3.97, VIP = 1.66, P = 0.01) and CEACAM1(FC = 2.93, VIP = 1.65, P = 0.006). These data suggest α1,2-fucosylated glycans as potential therapeutic targets for pulmonary fibrosis. Lack of alpha1,2 fucosylated structures attenuates bleomycin-induced lung fibrosis, while exact mechanisms will be focus of our future study.

PMID:
42320172
Bibliographic data and abstract were imported from PubMed on 20 Jun 2026.

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