ArticlePloS one2014
CXCL12 induces connective tissue growth factor expression in human lung fibroblasts through the Rac1/ERK, JNK, and AP-1 pathways.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Molecular Systems Architecture of Fibrotic Lung Microenvironment in Idiopathic Pulmonary Fibrosis.Cells · 2026Pooled it
- Immunosenescence in Idiopathic Pulmonary Fibrosis.Journal of inflammation research · 2026Review
- Interleukin-17A Promotes Airway Remodeling in Chronic Obstructive Pulmonary Disease by Activating C-X-C Motif Chemokine Ligand 12 Secreted by Lung Fibroblasts.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2024Article
- Wound healing effects of Asparagus lucidus Lindl extract through the phosphorylation of ERK1/2.BMC complementary medicine and therapies · 2023Article
- Specific epigenetic regulators serve as potential therapeutic targets in idiopathic pulmonary fibrosis.Heliyon · 2022Review
- Immunoexpression of CXCL12 and CXCR4 in sporadic and Gorlin-Goltz syndrome-related odontogenic keratocysts.Journal of clinical and experimental dentistry · 2022Article
- Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis.Molecules (Basel, Switzerland) · 2022Review
- Uncovering potential genes in colorectal cancer based on integrated and DNA methylation analysis in the gene expression omnibus database.BMC cancer · 2022Article
- Multifaceted Interplay between Hormones, Growth Factors and Hypoxia in the Tumor Microenvironment.Cancers · 2022Review
- Article
- Progress of Statin Therapy in the Treatment of Idiopathic Pulmonary Fibrosis.Oxidative medicine and cellular longevity · 2022Review
- Hypoxia-induced preadipocyte factor 1 expression in human lung fibroblasts through ERK/PEA3/c-Jun pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- VEGFR1-tyrosine kinase signaling in pulmonary fibrosis.Inflammation and regeneration · 2021Review
- Hypoxia and the phenomenon of immune exclusion.Journal of translational medicine · 2021Review
- Cyclam-Modified Polyethyleneimine for Simultaneous TGFβ siRNA Delivery and CXCR4 Inhibition for the Treatment of CClInternational journal of nanomedicine · 2021Article
- [IL-17A activates mouse lung fibroblasts through promoting chemokine CXCL12 secretion].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Article
- Using bioinformatics approach identifies key genes and pathways in idiopathic pulmonary fibrosis.Medicine · 2020Observational
- Revisiting Cell Death Responses in Fibrotic Lung Disease: Crosstalk between Structured and Non-Structured Cells.Diagnostics (Basel, Switzerland) · 2020Review
- The autocrine CXCR4/CXCL12 axis contributes to lung fibrosis through modulation of lung fibroblast activity.Experimental and therapeutic medicine · 2020Article
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CXCL12 (stromal cell-derived factor-1, SDF-1) is a potent chemokine for homing of CXCR4+ fibrocytes to injury sites of lung tissue, which contributes to pulmonary fibrosis. Overexpression of connective tissue growth factor (CTGF) plays a critical role in pulmonary fibrosis. In this study, we investigated the roles of Rac1, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and activator protein-1 (AP-1) in CXCL12-induced CTGF expression in human lung fibroblasts. CXCL12 caused concentration- and time-dependent increases in CTGF expression and CTGF-luciferase activity. CXCL12-induced CTGF expression was inhibited by a CXCR4 antagonist (AMD3100), small interfering RNA of CXCR4 (CXCR4 siRNA), a dominant negative mutant of Rac1 (RacN17), a mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor (PD98059), a JNK inhibitor (SP600125), a p21-activated kinase inhibitor (PAK18), c-Jun siRNA, and an AP-1 inhibitor (curcumin). Treatment of cells with CXCL12 caused activations of Rac1, Rho, ERK, and c-Jun. The CXCL12-induced increase in ERK phosphorylation was inhibited by RacN17. Treatment of cells with PD98059 and SP600125 both inhibited CXCL12-induced c-Jun phosphorylation. CXCL12 caused the recruitment of c-Jun and c-Fos binding to the CTGF promoter. Furthermore, CXCL12 induced an increase in α-smooth muscle actin (α-SMA) expression, a myofibroblastic phenotype, and actin stress fiber formation. CXCL12-induced actin stress fiber formation and α-SMA expression were respectively inhibited by AMD3100 and CTGF siRNA. Taken together, our results suggest that CXCL12, acting through CXCR4, activates the Rac/ERK and JNK signaling pathways, which in turn initiates c-Jun phosphorylation, and recruits c-Jun and c-Fos to the CTGF promoter and ultimately induces CTGF expression in human lung fibroblasts. Moreover, overexpression of CTGF mediates CXCL12-induced α-SMA expression.
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