Objective: To explore the main mediated molecules of mucin (MUC) 5AC extracellular secretion stimulated by airway shear stress (SS).
Methods: The 16 human bronchial epithelial (HBE) cells were cultured and randomized divided by Stata software into 5 groups: A. control group; B. SS stimulated group; C. SS stimulated & NSC23766 (a specific inhibitor of Rac-1) incubated group; D. SS stimulated & Cytochalasin D incubated group; E. Cortactin-siRNA (a small interfering RNA of Cortactin) transfected & SS stimulated group. Each group consisted of 6 parallel wells. Triplicate experiments were performed for statistical analysis. Rhythmic rotating device was used to simulate the breathing air flow mediated shear stress. The function of Cortactin was inhibited by Cortactin-siRNA. The relative content of MUC5AC in supernatant was measured by enzyme linked immunosorbent assay (ELISA). The p-Cortactin (phosphorylation Cortactin) relative level, Cortactin relative level and the effect of transfection were measured with Western blotting. And laser confocal microscope was used to observe the polymerization of F-actin.
Results: The transfection of Cortactin-siRNA successfully inhibited the function of Cortactin. The relative content of MUC5AC was (0.210 ± 0.013), (0.631 ± 0.025), (0.473 ± 0.112), (0.330 ± 0.067), (0.272 ± 0.019) in groups A, B, C, D and E, the group B was significantly higher than any other group (P = 0.000, 0.043, 0.000, 0.000). The Cortactin relative level in group B (0.670 ± 0.048) was significantly higher than that in group E (0.132 ± 0.014) (P < 0.01). But as compared with groups A, C, D (0.641 ± 0.016, 0.622 ± 0.012, 0.653 ± 0.027), there was no significance (all P > 0.05). The p-Cortactin relative level in group B (0.582 ± 0.067) was significantly higher than that in groups A, C, E (0.131 ± 0.011, 0.393 ± 0.045, 0.170 ± 0.016) (P = 0.000, 0.021, 0.000). But as compared with group D (0.511 ± 0.029), there was no significance (P = 0.246).
Conclusion: Rac-1, Cortactin and F-actin are the main mediated molecules of airway shear stress-stimulated MUC5AC extracellular secretion.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
HDAC6: Tumor Progression and Beyond.
Curr Cancer Drug Targets
January 2025
Human Genetics Laboratory, Institute of Natural Sciences, Federal University of Alfenas (UNIFAL-MG), Alfenas, 37130-001, MG, Brazil.
Histone Deacetylase 6 (HDAC6) is an intriguing therapeutic target in cancer re-search, distinguished as the only HDAC family member predominantly located in the cyto-plasm. HDAC6 features two catalytic domains and a unique ubiquitin-binding domain, which sets it apart from other HDACs. Beyond its role in histone deacetylation, HDAC6 targets vari-ous nonhistone substrates, such as α-tubulin, cortactin, Heat Shock Protein 90 (HSP90), and Heat Shock Factor 1 (HSF1).
View Article and Find Full Text PDFDisruption of the autism-associated gene leads to transcriptional alterations, synapse overgrowth, and defective network activity in the CA1.
J Neurosci
November 2024
Institute of Neuroscience, CNR, Vedano al Lambro, Italy.
Article Synopsis
- Protocadherins, especially Protocadherin 9 (PCDH9), are important for cell-cell interactions and have been linked to Autism Spectrum Disorder (ASD) and Major Depressive Disorder (MDD).
- Knockout (KO) of PCDH9 in mice leads to abnormal neuronal development, characterized by larger presynaptic terminals and increased excitatory synapse activity in the hippocampus.
- The findings suggest that PCDH9 plays a critical role in regulating excitatory synapse morphology and function, influencing glutamatergic transmission and potentially contributing to neurodevelopmental disorders.
Csk controls leukocyte extravasation via local regulation of Src family kinases and cortactin signaling.
Front Immunol
November 2024
Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
C-terminal Src kinase (Csk) targets Src family kinases (SFKs) and thereby inactivates them. We have previously shown that Csk binds to phosphorylated tyrosine 685 of VE-cadherin, an adhesion molecule of major importance for the regulation of endothelial junctions. This tyrosine residue is an SFK target, and its mutation (VE-cadherin-Y685F) inhibits the induction of vascular permeability in various inflammation models.
View Article and Find Full Text PDFYWHAG promotes colorectal cancer progression by regulating the CTTN-Wnt/β-catenin signaling axis.
Med Oncol
March 2024
Wuxi Cancer Institute, Affiliated Hospital of Jiangnan University, Wuxi, 214062, Jiangsu, China.
Colorectal cancer (CRC) ranks as the third most prevalent cancer type globally. Nevertheless, the fundamental mechanisms driving CRC progression remain ambiguous, and the prognosis for the majority of patients diagnosed at an advanced stage is dismal. YWHA/14-3-3 proteins serve as central nodes in several signaling pathways and are closely related to tumorigenesis and progression.
View Article and Find Full Text PDFCortactin is in a complex with VE-cadherin and is required for endothelial adherens junction stability through Rap1/Rac1 activation.
Sci Rep
January 2024
Chair of Vegetative Anatomy, Faculty of Medicine, Ludwig-Maximilians-University (LMU) Munich, Pettenkoferstraße 11, 80336, Munich, Germany.
Vascular permeability is mediated by Cortactin (Cttn) and regulated by several molecules including cyclic-adenosine-monophosphate, small Rho family GTPases and the actin cytoskeleton. However, it is unclear whether Cttn directly interacts with any of the junctional components or if Cttn intervenes with signaling pathways affecting the intercellular contacts and the cytoskeleton. To address these questions, we employed immortalized microvascular myocardial endothelial cells derived from wild-type and Cttn-knock-out mice.
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!