Serum and glucocorticoid-regulated kinase 1 regulates transforming growth factor β1-connective tissue growth factor pathway in chronic rhinosinusitis

Serum and glucocorticoid-regulated kinase 1 regulates transforming growth factor β1-connective tissue growth factor pathway in chronic rhinosinusitis

Copyright © 2021 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 234(2022) vom: 15. Jan., Seite 108895
1. Verfasser: Lai, Yuting (VerfasserIn)
Weitere Verfasser: Zhang, Peiyuan, Wang, Huan, Hu, Li, Song, Xiaole, Zhang, Jia, Jiang, Wenxiu, Han, Miaomiao, Liu, Quan, Hu, Guohong, Sun, Xicai, Li, Huabin, Wang, Dehui
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2022
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't CTGF Chronic rhinosinusitis SGK1 TGF-β1 Tissue remodeling CCN2 protein, human Immediate-Early Proteins TGFB1 protein, human mehr... Transforming Growth Factor beta1 Connective Tissue Growth Factor 139568-91-5 Protein Serine-Threonine Kinases EC 2.7.11.1 serum-glucocorticoid regulated kinase
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245 1 0 |a Serum and glucocorticoid-regulated kinase 1 regulates transforming growth factor β1-connective tissue growth factor pathway in chronic rhinosinusitis 
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520 |a PURPOSE: Serum/glucocorticoid-regulated kinase 1 (SGK1) has been identified as a crucial regulator in fibrotic disorders. Herein, we explored SGK1 role in tissue remodeling of chronic rhinosinusitis (CRS) 
520 |a METHODS: Lentivirus was employed to generate an SGK1-overexpressing human bronchial epithelial cell (16HBE) line. To screen SGK1 downstream genes, RNA sequencing was performed on SGK1-overexpressing and control cell lines. To determine protein and gene expression levels, immunohistochemistry, western blotting, and quantitative real-time polymerase chain reaction were employed. Correlation analysis was performed using mRNA expression levels of SGK1, transforming growth factor β1 (TGF-β1), and connective tissue growth factor (CTGF) derived from CRS mucosal tissue and GEO database. Gene set enrichment analysis was conducted using gene sets from Molecular Signatures Database. The severity of symptoms in CRS patients was assessed using the 22-Item Sinonasal Outcome Test 
520 |a RESULTS: SGK1 overexpression significantly increased the expression of connective tissue growth factor (CTGF) in 16HBE cells (P < 0.01). Consistently, CTGF protein level was considerably greater in mucosal tissue of CRS without nasal polyps (CRSsNP) than in CRS with nasal polyps (CRSwNP) (P < 0.05) or in control subjects (P < 0.01). TGF-β1 protein level was higher in mucosal tissue of CRSsNP patients than in CRSwNP patients (P < 0.001) or in the control group (P < 0.01). mRNA levels of SGK1 and CTGF (P < 0.05, r = 0.668; P = 0.001, r = 0.630), TGF-β1 and CTGF (P < 0.05, r = 0.560; P < 0.05, r = 0.420), as well as SGK1 and TGF-β1(P < 0.05, r = 0.612; P < 0.05, r = 0.524) were significantly correlated in CRS mucosal tissue and GSE36830 dataset, respectively. TGF-β1-induced upregulated genes were significantly enriched in SGK1 overexpression group. In vitro assays, TGF-β1 promoted SGK1 and CTGF expression in a concentration- and time-dependent manner. Administrating an SGK1 inhibitor, GSK650394, significantly inhibited TGF-β1-induced CTGF expression in 16HBE and dispersed primary nasal polyp cells 
520 |a CONCLUSIONS: TGF-β1 stimulation significantly increases SGK1 and CTGF expression. By regulating TGF-β1-CTGF pathway, SGK1 may participate in tissue remodeling in the pathological mechanism of CRS 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a CTGF 
650 4 |a Chronic rhinosinusitis 
650 4 |a SGK1 
650 4 |a TGF-β1 
650 4 |a Tissue remodeling 
650 7 |a CCN2 protein, human  |2 NLM 
650 7 |a Immediate-Early Proteins  |2 NLM 
650 7 |a TGFB1 protein, human  |2 NLM 
650 7 |a Transforming Growth Factor beta1  |2 NLM 
650 7 |a Connective Tissue Growth Factor  |2 NLM 
650 7 |a 139568-91-5  |2 NLM 
650 7 |a Protein Serine-Threonine Kinases  |2 NLM 
650 7 |a EC 2.7.11.1  |2 NLM 
650 7 |a serum-glucocorticoid regulated kinase  |2 NLM 
650 7 |a EC 2.7.11.1  |2 NLM 
700 1 |a Zhang, Peiyuan  |e verfasserin  |4 aut 
700 1 |a Wang, Huan  |e verfasserin  |4 aut 
700 1 |a Hu, Li  |e verfasserin  |4 aut 
700 1 |a Song, Xiaole  |e verfasserin  |4 aut 
700 1 |a Zhang, Jia  |e verfasserin  |4 aut 
700 1 |a Jiang, Wenxiu  |e verfasserin  |4 aut 
700 1 |a Han, Miaomiao  |e verfasserin  |4 aut 
700 1 |a Liu, Quan  |e verfasserin  |4 aut 
700 1 |a Hu, Guohong  |e verfasserin  |4 aut 
700 1 |a Sun, Xicai  |e verfasserin  |4 aut 
700 1 |a Li, Huabin  |e verfasserin  |4 aut 
700 1 |a Wang, Dehui  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 234(2022) vom: 15. Jan., Seite 108895  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
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