Objective: To explore the impact of Rac1 activation on the proliferation and migration under the stimulation of PDGF-BB (platelet derived growth factor-BB).
Methods: The inhibitory effects of Rac1 inhibitor (NSC23766) and Rac1siRNA on the proliferation and migration of vascular smooth muscle cell under the stimulation of PDGF-BB were measured by CCK8 assay and Transwell chamber. The time characteristics of Rac1 activity and pi-JNK expression under the stimulation of PDGF-BB was detected by GST pulldown assay and Western blot. And the inhibitory effects of NSC23766 and Rac1siRNA on the Rac1 activation and pi-JNK expression were also measured.
Results: Migration and proliferation of vascular smooth muscle cell increased significantly after the stimulation of PDGF-BB (50 µg/L). Migration and proliferation was inhibited significantly after a pretreatment of Rac1siRNA and various concentrations of NSC23766 (25, 50, 100 µg/L). After the stimulation of PDGF-BB, the expression of pi-JNK and Rac1 activity increased over time. Rac1-GTP peaked at 5 minutes and pi-JNK at 15 minute. The expressions of pi-JNK at 15 minutes and Rac1-GTP at 5 minutes were inhibited significantly by Rac1siRNA and NSC23766 in a concentration-dependent manner.
Conclusion: JNK phosphorylation is controlled by Rac1 activation. And Rac1 activation play a pivotal role in the migration and proliferation of aortic smooth muscle cell under the stimulation of PDGF-BB.
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Background: Multiple sclerosis (MS) is a chronic autoimmune disease damaging the central nervous system. Diminished inflammatory disease activity (DA) as people with MS (pwMS) age motivated randomized clinical trials assessing disease-modifying therapy (DMT) discontinuation in older pwMS given the concern for risks outweighing benefits. This study aims to examine whether peripheral production of Myelin Basic Protein (MBP)-driven cytokine responses mediate the aging-associated decline in MS inflammatory DA.
View Article and Find Full Text PDFRespir Res
December 2024
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: Pulmonary hypertension (PH) is a malignant vascular disease characterized by pulmonary arterial remodeling. Neural cell adhesion molecule 1 (NCAM1) is a cell surface glycoprotein that is involved in a variety of diseases, including cardiovascular disease. However, the role of NCAM1 in PH remains underexplored.
View Article and Find Full Text PDFAngiogenesis
December 2024
Department of Pharmaceutical Sciences, Università del Piemonte Orientale, Novara, Italy.
Am J Physiol Lung Cell Mol Physiol
November 2024
Division of Rheumatology, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.
The objective of this study was to assess fibrinogen (FIB) co-modified with citrulline (CIT) and/or malondialdehyde-acetaldehyde (MAA) initiates macrophage-fibroblast interactions leading to extracellular matrix (ECM) deposition that characterizes rheumatoid arthritis-associated interstitial lung disease (RA-ILD). Macrophages (Mϕ) were stimulated with native-FIB, FIB-CIT, FIB-MAA or FIB-MAA-CIT. Supernatants (SN) (Mϕ-SN [U-937-derived] or MϕP-SN [PBMC-derived]) or direct antigens were co-incubated with human lung fibroblasts (HLFs).
View Article and Find Full Text PDFPLoS One
November 2024
Vinmec Hi-Tech Center, Vinmec Healthcare System, Hanoi, Vietnam.
Mesenchymal stem cell (MSC)-derived exosomes (EXs) have emerged as promising therapeutic agents for wound healing. However, the optimal conditions for manufacturing MSC-derived EXs that maximize their wound-healing potential have yet to be established. Hence, we compared the efficacy of five different MSC culture media, including three different serum-free, a platelet-supplemented, and a fetal bovine serum-supplemented media, in exosome manufacturing for wound healing applications.
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