ArticleJournal of cellular and molecular medicine2019
FSP1 promotes the biofunctions of adventitial fibroblast through the crosstalk among RAGE, JAK2/STAT3 and Wnt3a/β-catenin signalling pathways.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
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- Mitochondrial dynamics in vascular remodeling and target-organ damage.Frontiers in cardiovascular medicine · 2023Review
- Optimization of skeletal muscle-derived fibroblast isolation and purification without the preplating method.Cell and tissue banking · 2022Article
- Bushen Wenyang Huayu Decoction Targets TLR4/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Chloroquine Potentiates the Anticancer Effect of Pterostilbene on Pancreatic Cancer by Inhibiting Autophagy and Downregulating the RAGE/STAT3 Pathway.Molecules (Basel, Switzerland) · 2021Article
- EPS364, a Novel Deep-Sea Bacterial Exopolysaccharide, Inhibits Liver Cancer Cell Growth and Adhesion.Marine drugs · 2021Article
- Butylphthalide Inhibits Autophagy and Promotes Multiterritory Perforator Flap Survival.Frontiers in pharmacology · 2020Article
- FSP1 promotes the biofunctions of adventitial fibroblast through the crosstalk among RAGE, JAK2/STAT3 and Wnt3a/β-catenin signalling pathways.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
- Erratum issuedCorrigendum.2023
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence indicates that fibroblast-specific protein 1 (FSP1) provides vital effects in cell biofunctions. However, whether FSP1 influences the adventitial fibroblast (AF) and vascular remodelling remains unclear. Therefore, we investigated the potential role and action mechanism of FSP1-mediated AF bioactivity. AFs were cultured and stimulated with FSP1 and siRNA-FSP1 in vitro. Viability assays demonstrated that siRNA-FSP1 counteracted AFs proliferative, migratory and adherent abilities enhanced with FSP1. Flow cytometry revealed that FSP1 increased AFs number in S phase and decreased cellular apoptosis. Contrarily, siRNA-FSP1 displayed the contrary results. RT-PCR, Western blotting and immunocytochemistry showed that FSP1 synchronously up-regulated the expression of molecules in RAGE, JAK2/STAT3 and Wnt3a/β-catenin pathways and induced a proinflammatory cytokine profile characterized by high levels of MCP-1, ICAM-1 and VCAM-1. Conversely, FSP1 knockdown reduced the expression of these molecules and cytokines. The increased number of autophagosomes in FSP1-stimulated group and fewer autophagic corpuscles in siRNA-FSP1 group was observed by transmission electron microscope (TEM). Autophagy-related proteins (LC3B, beclin-1 and Apg7) were higher in FSP1 group than those in other groups. Conversely, the expression of p62 protein was shown an opposite trend of variation. Therefore, these pathways can promote AFs bioactivity, facilitate autophagy and induce the expression of the proinflammatory cytokines. Contrarily, siRNA-FSP1 intercepts the crosstalk of these pathways, suppresses AF functions, restrains autophagy and attenuates the expression of the inflammatory factors. Our findings indicate that crosstalk among RAGE, STAT3/JAK2 and Wnt3a/β-catenin signalling pathways may account for the mechanism of AF functions with the stimulation of FSP1.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.