Role and mechanisms of CHI3L1 in coronary artery lesions in a mouse model of Kawasaki disease-like vasculitis

OBJECTIVES: To explore the role and potential mechanisms of chitinase-3-like protein 1 (CHI3L1) in coronary artery lesions in a mouse model of Kawasaki disease (KD)-like vasculitis.

METHODS: Four-week-old male SPF-grade C57BL/6 mice were randomly divided into a control group and a model group, with 10 mice in each group. The model group mice were intraperitoneally injected with 0.5 mL of lactobacillus casei cell wall extract (LCWE) to establish a mouse model of KD-like vasculitis, while the control group mice were injected with an equal volume of normal saline. The general conditions of the mice were observed on the 3rd, 7th, and 14th day after injection. Changes in coronary artery tissue pathology were observed using hematoxylin-eosin staining. The level of CHI3L1 in mouse serum was measured by enzyme-linked immunosorbent assay. Immunofluorescence staining was used to detect the expression and localization of CHI3L1, von Willebrand factor (vWF), and α-smooth muscle actin (α-SMA) in coronary artery tissue. Western blot analysis was used to detect the expression of CHI3L1, vWF, vascular endothelial cadherin (VE cadherin), Caspase-3, B cell lymphoma-2 (Bcl-2), Bcl-2 associated X protein (Bax), nuclear factor κB (NF-κB), and phosphorylated NF-κB (p-NF-κB) in coronary artery tissue.

RESULTS: The serum level of CHI3L1 in the model group was significantly higher than that in the control group (P<0.05). Compared to the control group, the expression of CHI3L1 in the coronary artery tissue was higher, while the expression of vWF was lower in the model group. The relative expression levels of CHI3L1, Bax, Caspase-3, NF-κB, and p-NF-κB were significantly higher in the model group than in the control group (P<0.05). The relative expression levels of vWF, VE cadherin, and Bcl-2 were lower in the model group than in the control group (P<0.05).

CONCLUSIONS: In the LCWE-induced mouse model of KD-like vasculitis, the expression levels of CHI3L1 in serum and coronary arteries increase, and it may play a role in coronary artery lesions through endothelial cell apoptosis mediated by inflammatory reactions.

Medienart:

E-Artikel

Erscheinungsjahr:

2023

Erschienen:

2023

Enthalten in:

Zur Gesamtaufnahme - volume:25

Enthalten in:

Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics - 25(2023), 12 vom: 15. Dez., Seite 1227-1233

Sprache:

Chinesisch

Weiterer Titel:

CHI3L1在川崎病样血管炎小鼠模型冠状动脉损伤中的作用及机制研究

Beteiligte Personen:

Cao, Yue [VerfasserIn]
Gao, Shuai [VerfasserIn]
Luo, Gang [VerfasserIn]
Zhao, Shui-Yan [VerfasserIn]
Tang, Ya-Qi [VerfasserIn]
DU, Zhan-Hui [VerfasserIn]
Pan, Si-Lin [VerfasserIn]

Links:

Volltext

Themen:

Apoptosis
Bcl-2-Associated X Protein
Cadherins
Caspase 3
Chitinase-3-Like Protein 1
Chitinase-3-like protein 1
Coronary artery lesion
EC 3.4.22.-
English Abstract
Journal Article
Kawasaki disease
Mouse
NF-kappa B
Vasculitis
Von Willebrand Factor

Anmerkungen:

Date Completed 20.12.2023

Date Revised 22.12.2023

published: Print

Citation Status MEDLINE

doi:

10.7499/j.issn.1008-8830.2309080

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM366028367