The phenotypic modulation of smooth muscle cells (SMCs) is closely associated with the development and progression of various SMC diseases. We investigated the molecular mechanism of phenotypic modulation triggered by EGF family ligands using a primary culture system of differentiated SMCs. Among four EGF-receptor (EGFR) family members, the EGFR was solely activated by EGF, heparin-binding EGF (HB-EGF), transforming growth factor alpha (TGF alpha), epiregulin (ER), and betacellulin (BTC), resulting in induction of phenotypic modulation of SMCs. This effect was mediated through the coordinated activation of the extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38MAPK) pathways. These results suggest that EGF family ligand- and EGFR-triggered signaling pathways are critically involved in the phenotypic modulation of SMCs.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1006/bbrc.2001.4385 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Short-term starvation boosts anti-PD-L1 therapy by reshaping tumor-associated macrophages in hepatocellular carcinoma.
Hepatology
January 2025
Hepatic Surgery Centre, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, People's Republic of China.
Background And Aims: Immune checkpoint inhibitors (ICIs) have revolutionized systemic hepatocellular carcinoma (HCC) treatment. Nevertheless, numerous patients are refractory to ICIs therapy. It is currently unknown whether diet therapies such as short-term starvation (STS) combined with ICIs can be used to treat HCC.
View Article and Find Full Text PDFHBV and HBsAg strongly reshape the phenotype, function, and metabolism of DCs according to patients' clinical stage.
Hepatol Commun
February 2025
University Grenoble Alpes, Inserm U 1209, CNRS UMR 5309, Institute for Advanced Biosciences, Grenoble, France.
Background: Hepatitis B is a liver infection caused by HBV. Infected individuals who fail to control the viral infection develop chronic hepatitis B and are at risk of developing life-threatening liver diseases, such as cirrhosis or liver cancer. Dendritic cells (DCs) play important roles in the immune response against HBV but are functionally impaired in patients with chronic hepatitis B.
View Article and Find Full Text PDFVopX, a novel T3SS effector, modulates host actin dynamics.
mBio
January 2025
Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, New York, USA.
Unlabelled: Pathogenic strains cause cholera using different mechanisms. O1 and O139 serogroup strains use the toxin-co-regulated pilus (TCP) and cholera toxin (CT) for intestinal colonization and to promote secretory diarrhea, while non-O1/non-O139 serogroup strains are typically non-toxigenic and use alternate virulence factors to cause a clinically similar disease. An O39 serogroup, TCP/CT-negative strain, named AM-19226, uses a type III secretion system (T3SS) to translocate more than 10 effector proteins into the host cell cytosol.
View Article and Find Full Text PDFLitR and its quorum-sensing regulators modulate biofilm formation by .
J Bacteriol
January 2025
Department of Microbiology and Immunology, Stritch School of Medicine Loyola University Chicago, Chicago, Illinois, USA.
Quorum sensing controls numerous processes ranging from the production of virulence factors to biofilm formation. Biofilms, communities of bacteria that are attached to one another and/or a surface, are common in nature, and when they form, they can produce a quorum of bacteria. One model system to study biofilms is the bacterium , which forms a biofilm that promotes the colonization of its symbiotic host.
View Article and Find Full Text PDFEpigenetic modulation rescues neurodevelopmental deficits in Syngap1 mice.
Aging Cell
January 2025
Molecular Biology and Genetics Unit, Transcription and Disease Laboratory, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru, India.
SYNGAP1 is a Ras GTPase-activating protein that plays a crucial role during brain development and in synaptic plasticity. Sporadic heterozygous mutations in SYNGAP1 affect social and emotional behaviour observed in intellectual disability (ID) and autism spectrum disorder (ASD). Although neurophysiological deficits have been extensively studied, the epigenetic landscape of SYNGAP1 mutation-mediated intellectual disability is unexplored.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!