2. Academic Validation
  3. Fibroblast growth factor 10 attenuates chronic obstructive pulmonary disease by protecting against glycocalyx impairment and endothelial apoptosis

Fibroblast growth factor 10 attenuates chronic obstructive pulmonary disease by protecting against glycocalyx impairment and endothelial apoptosis

  • Respir Res. 2022 Oct 1;23(1):269. doi: 10.1186/s12931-022-02193-5.
Tian Jiang  # 1 2 3,  Weiping Hu  # 4,  Shaoyuan Zhang 1 2 3,  Changhao Ren 1,  Siyun Lin 1,  Zhenyu Zhou 5,  Hao Wu 6,  Jun Yin  # 7 8 9,  Lijie Tan  # 10 11 12
Affiliations

Affiliations

  • 1 Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, No.180 Fenglin Road, Shanghai, 200032, China.
  • 2 Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
  • 3 Key Laboratory of Lung Inflammation and Injury, Shanghai, 200032, China.
  • 4 Department of Critical Care and Respiratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
  • 5 Department of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
  • 6 Department of Clinical Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
  • 7 Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, No.180 Fenglin Road, Shanghai, 200032, China. jun_yin@fudan.edu.cn.
  • 8 Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. jun_yin@fudan.edu.cn.
  • 9 Key Laboratory of Lung Inflammation and Injury, Shanghai, 200032, China. jun_yin@fudan.edu.cn.
  • 10 Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, No.180 Fenglin Road, Shanghai, 200032, China. tan.lijie@zs-hospital.sh.cn.
  • 11 Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, 200032, China. tan.lijie@zs-hospital.sh.cn.
  • 12 Key Laboratory of Lung Inflammation and Injury, Shanghai, 200032, China. tan.lijie@zs-hospital.sh.cn.
  • # Contributed equally.
PMID: 36183124 DOI: 10.1186/s12931-022-02193-5
Abstract

Background: The defects and imbalance in lung repair and structural maintenance contribute to the pathogenesis of chronic obstructive pulmonary diseases (COPD), yet the molecular mechanisms that regulate lung repair process are so far incompletely understood. We hypothesized that cigarette smoking causes glycocalyx impairment and endothelial Apoptosis in COPD, which could be repaired by the stimulation of Fibroblast Growth Factor 10 (FGF10)/FGF receptor 1 (FGFR1) signaling.

Methods: We used immunostaining (immunohistochemical [IHC] and immunofluorescence [IF]) and enzyme-linked immunosorbent assay (ELISA) to detect the levels of glycocalyx components and endothelial Apoptosis in animal models and in patients with COPD. We used the murine emphysema model and in vitro studies to determine the protective and reparative role of FGF10/FGFR1.

Results: Exposure to cigarette smoke caused endothelial glycocalyx impairment and emphysematous changes in murine models and human specimens. Pretreatment of FGF10 attenuated the development of emphysema and the shedding of glycocalyx components induced by CSE in vivo. However, FGF10 did not attenuate the emphysema induced by endothelial-specific killing peptide CGSPGWVRC-GG-D(KLAKLAK)2. Mechanistically, FGF10 alleviated smoke-induced endothelial Apoptosis and glycocalyx repair through FGFR1/ERK/SOX9/HS6ST1 signaling in vitro. FGF10 was shown to repair pulmonary glycocalyx injury and endothelial Apoptosis, and attenuate smoke-induced COPD through FGFR1 signaling.

Conclusions: Our results suggest that FGF10 may serve as a potential therapeutic strategy against COPD via endothelial repair and glycocalyx reconstitution.

Keywords

Chronic obstructive pulmonary diseases (COPD); Endothelial apoptosis; Fibroblast growth factor 10 (FGF10); Fibroblast growth factor receptor 1 (FGFR1); Glycocalyx.

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