Background: The atherosclerosis process relates to the dysfunction of different cells in the plaque microenvironment. The vascular smooth muscle cells (VSMCs) play an important role in atherosclerosis. Since the FoxO family is reported to control cell growth, thus the aim of this study was to investigate the effects of Heparin, Betulinic acid, and Ibrutinib on the FoxO1/pFoxO1 axis in vascular smooth muscle cells.
Methods: The VSMCs were cultured in DMEM-F12 medium and, were treated with Heparin (30IU), Betulinic acid (60 μM), and Ibrutinib (2 μM) in the 24 and 48-h periods. The FoxO1 gene expression level was identified using the RT-qPCR technique. The FoxO1 and pFoxO1 protein values were measured by the Western blot technique.
Results: The FoxO1 gene expression levels were reduced significantly in the cellular groups treated with Heparin, Betulinic acid, and Ibrutinib (P < 0.05) in both periods. Moreover, the pFoxO1 and FoxO1 protein values were decreased by Heparin, and Betulinic acid in the VSMCs.
Conclusion: Heparin suppressed the FoxO1/pFoxO1 signaling axis in vascular smooth muscle cells (VSMCs). Furthermore, it modulated the effects of Betulinic acid and Ibrutinib.
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http://dx.doi.org/10.1016/j.bbrep.2025.101954 | DOI Listing |
Circ Res
March 2025
Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, China. (Y.E.L., S.L., Litao Wang, Y.D., L. Wu, H.C., T.Z., J.L., S.X., L.L., J.G., J.R., Y.Z.).
Background: Aortic aneurysm/dissection (AAD) is a life-threatening disease lacking effective pharmacological treatment. Protein ubiquitination plays a pivotal role in cardiovascular diseases. However, the possible contribution of the E3 ubiquitin ligase March2 (membrane-associated RING finger protein 2) to the cause of AAD remains elusive.
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March 2025
Clinic for Radiology, University Hospital Münster, 48149 Münster, Germany.
Endothelin-1 (ET-1) levels are altered in atherosclerosis, while the roles of the endothelin receptors ETR and ETR during the pathogenesis of atherosclerosis remain unclear. Therefore, the focus of this study was to clarify how endothelin receptors are expressed in advanced human atherosclerotic plaques and how this is related to atherosclerotic risk factors. Ex vivo expression analysis was performed by quantitative real-time PCR (qRT-PCR) of 98 atherosclerotic plaques and controls that were obtained from adult patients undergoing vascular surgery.
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February 2025
Provincial Key Laboratory for Developmental Biology and Neurosciences, College of Life Sciences, Fujian Normal University, Fuzhou 350007, China.
AdipoRon is a selective adiponectin receptor agonist that inhibits vascular remodeling by promoting the differentiation of arterial smooth muscle cells (SMCs). Our recent studies have demonstrated that activation of TFEB and its downstream autophagy-lysosomal signaling contribute to adipoRon-induced differentiation of SMCs. The present study was designed to examine whether acid sphingomyelinase (ASM; gene symbol ) is involved in mediating adipoRon-induced activation of TFEB-autophagy signaling and inhibition of proliferation/migration in arterial SMCs.
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February 2025
LR99E10 Human Genetics Laboratory, Faculty of Medicine of Tunis, University of Tunis El Manar, Tunis 1002, Tunisia.
Cellular phenotypic transformation is a key process that occurs during the development and progression of atherosclerosis. Within the arterial wall, endothelial cells, vascular smooth muscle cells, and macrophages undergo phenotypic changes that contribute to the pathogenesis of atherosclerosis. miRNAs have emerged as potential biomarkers for cellular phenotypic changes during atherosclerosis.
View Article and Find Full Text PDFInt J Mol Sci
February 2025
Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC V6T 2B5, Canada.
Diffuse intimal thickening (DIT) is a pre-clinical stage of atherosclerosis characterized by thickened intima. The molecular basis of its susceptibility to atherogenesis is unknown, and mechanistic investigations cannot be performed in commonly used mouse models, in which DIT does not exist. Vascular smooth muscle cells (SMCs) are the predominant cell type that occupies the intima and media of DIT.
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