ArticlePeerJ2017
c-Kit modifies the inflammatory status of smooth muscle cells.
Article in PeerJ, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- C-Kit Is Essential for Vascular Smooth Muscle Cell Phenotypic Switch In Vitro and In Vivo After Injury.Cells · 2025Article
- Loss of c-Kit in Endothelial Cells Protects against Hindlimb Ischemia.Biomedicines · 2024Article
- Effects of weaning on intestinal longitudinal muscle-myenteric plexus function in piglets.Science China. Life sciences · 2024Article
- Proteomics Analysis of Genetic Liability of Abdominal Aortic Aneurysm Identifies Plasma Neogenin and Kit Ligand: The ARIC Study.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Recent advances of natural and bioengineered extracellular vesicles and their application in vascular regeneration.Regenerative biomaterials · 2022Review
- c-Kit expression in smooth muscle cells reduces atherosclerosis burden in hyperlipidemic mice.Atherosclerosis · 2021Article
- M2 macrophage-derived exosomes promote the c-KIT phenotype of vascular smooth muscle cells during vascular tissue repair after intravascular stent implantation.Theranostics · 2020Article
- c-Kit deficiency impairs nitric oxide signaling in smooth muscle cells.Biochemical and biophysical research communications · 2019Article
- c-Kit suppresses atherosclerosis in hyperlipidemic mice.American journal of physiology. Heart and circulatory physiology · 2019Article
- Identification of Epigenetic Mechanisms Involved in the Anti-Asthmatic Effects ofMolecules (Basel, Switzerland) · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundc-Kit is a receptor tyrosine kinase present in multiple cell types, including vascular smooth muscle cells (SMC). However, little is known about how c-Kit influences SMC biology and vascular pathogenesis.
methodsHigh-throughput microarray assays and
resultsThe microarray analysis revealed elevated NF-κB gene expression secondary to the loss of c-Kit that affects both the canonical and alternative NF-κB pathways. Upon stimulation with an oxidized phospholipid as pro-inflammatory agent, c-Kit deficient SMC displayed enhanced NF-κB transcriptional activity, higher phosphorylated/total p65 ratio, and increased protein expression of NF-κB regulated pro-inflammatory mediators with respect to cells from control mice. The pro-inflammatory phenotype of mutant cells was ameliorated after restoring c-Kit activity using lentiviral transduction. Functional assays further demonstrated that c-Kit suppresses NF-κB activity in SMC in a TGFβ-activated kinase 1 (TAK1) and Nemo-like kinase (NLK) dependent manner. DISCUSSION: Our study suggests a novel mechanism by which c-Kit suppresses NF-κB regulated pathways in SMC to prevent their pro-inflammatory transformation.
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Registered trials
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.