Silencing of FSTL1 Alleviated LPS-Induced Inflammatory Damage and Oxidative Damage in Human Bronchial Epithelial Cells via BMP4/KLF4 Axis.

Abstract

INTRODUCTION:

Childhood asthma is a common chronic inflammatory lung disease in children, among which airway inflammation is the main driving factor of asthma symptoms. Follistatin-like protein 1 (FSTL1) is involved in multiple inflammatory processes, but its role in airway inflammation has not been fully elucidated.

METHODS:

We used lipopolysaccharide (LPS) to stimulate human primary bronchial epithelial (BEAS-2B) cells to establish an in vitro airway inflammation model. The expression of FSTL1 was detected by qPCR. Cell Counting Kit-8 and Annexin V-PI double staining was used to analyze the viability and apoptosis of BEAS-2B. The content of IL-6, IL-8 and TNF-α was determined by ELISA kit. Western blot was used to detect the protein expression level of the bone morphogenetic protein 4 (BMP4) and KLF4. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and malondialdehyde were measured to assess oxidative stress.

RESULTS:

The mRNA expression of FSTL1 was significantly increased in LPS-treated BEAS-2B cells. Silencing of FSTL1 inhibited the release of IL-6, IL-8, TNF-α, and cell apoptosis as well as enhanced the activities of SOD, CAT, and GSH-Px. Silencing of FSTL1 reversed the inflammatory state of cells by upregulating BMP4 and increasing the expression level of KLF4.

CONCLUSION:

Silencing of FSTL1 reduced LPS-induced BEAS-2B cell damage by regulating the BMP4/KLF4 axis. FSTL1 may be a potential target for the treatment of asthma.

• Authors: Yi Zhang, Liping Yan, Jiao Yang, Xiangni Li
• Journal: International archives of allergy and immunology (Int Arch Allergy Immunol) Vol. 183 Issue 7 Pg. 785-795 ( 2022) ISSN: 1423-0097 [Electronic] Switzerland
• PMID: 35390783 (Publication Type: Journal Article)
• Copyright: © 2022 S. Karger AG, Basel.

Chemical References

• BMP4 protein, human
• Bone Morphogenetic Protein 4
• Follistatin-Related Proteins
• Interleukin-6
• Interleukin-8
• KLF4 protein, human
• Kruppel-Like Factor 4
• Lipopolysaccharides
• Tumor Necrosis Factor-alpha
• FSTL1 protein, human
• Superoxide Dismutase

Topics

• Asthma (genetics, metabolism)
• Bone Morphogenetic Protein 4 (genetics, metabolism)
• Child
• Epithelial Cells (metabolism)
• Follistatin-Related Proteins (genetics, metabolism)
• Gene Silencing
• Humans
• Inflammation (metabolism)
• Interleukin-6 (metabolism)
• Interleukin-8 (metabolism)
• Kruppel-Like Factor 4 (genetics, metabolism)
• Lipopolysaccharides (pharmacology)
• Oxidative Stress
• Superoxide Dismutase
• Tumor Necrosis Factor-alpha (metabolism)