Introduction: Human decidua basalis mesenchymal stem cells (DBMSCs) are potential therapeutics for the medication to cure inflammatory diseases, like atherosclerosis. The current study investigates the capacity of DBMSCs to stay alive and function in a harmful inflammatory environment induced by high levels of lipopolysaccharide (LPS).
Methods: DBMSCs were exposed to different levels of LPS, and their viability and functional responses (proliferation, adhesion, and migration) were examined. Furthermore, DBMSCs' expression of 84 genes associated with their functional activities in the presence of LPS was investigated.
Results: Results indicated that LPS had no significant effect on DBMSCs' adhesion, migration, and proliferation (24 h and 72 h) (p > 0.05). However, DBMSCs' proliferation was significantly reduced at 10 µg/mL of LPS at 48 h (p < 0.05). In addition, inflammatory cytokines and receptors related to adhesion, proliferation, migration, and differentiation were significantly overexpressed when DBMSCs were treated with 10 µg/mL of LPS (p < 0.05).
Conclusion: These results indicated that DBMSCs maintained their functional activities (proliferation, adhesion, and migration) in the presence of LPS as there was no variation between the treated DBMSCs and the control group. This study will lay the foundation for future preclinical and clinical studies to confirm the appropriateness of DBMSCs as a potential medication to cure inflammatory diseases, like atherosclerosis.
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http://dx.doi.org/10.2147/SCCAA.S332952 | DOI Listing |
Adv Sci (Weinh)
January 2025
LadHyX, CNRS, Ecole Polytechnique, Institut Polytechnique de Paris, Palaiseau, 91120, France.
Navigating complex extracellular environments requires extensive deformation of cells and their nuclei. Most in vitro systems used to study nuclear deformations impose whole-cell confinement that mimics the physical crowding experienced by cells during 3D migration through tissues. Such systems, however, do not reproduce the types of nuclear deformations expected to occur in cells that line tissues such as endothelial or epithelial cells whose physical confinement stems principally from the topography of their underlying basement membrane.
View Article and Find Full Text PDFIn Vitro Model
December 2024
Univ. Lille, Inserm, CHU Lille, Institut Pasteur Lille, U1167 - RID-AGE - Facteurs de Risque Et Déterminants Moléculaires Des Maladies Liées Au Vieillissement, F-59000 Lille, France.
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View Article and Find Full Text PDFJ Ginseng Res
January 2025
Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Background: The non-saponin (NS) fraction is an important active component of with multifunctional pharmacological activities including neuroprotective, immune regulatory, anti-inflammatory, and antioxidant effects. However, the effects of NSs on multiple sclerosis (MS), a chronic and autoimmune demyelinating disorder, have not yet been demonstrated.
Purpose: and Methods: The goal of the present study was to demonstrate the pharmacological actions of NSs on movement dysfunctions and the related mechanisms of action using an experimental autoimmune encephalomyelitis (EAE) mouse model of MS.
Front Pharmacol
January 2025
Huizhou Hospital, Guangzhou University of Traditional Chinese Medicine, Guangzhou, China.
Background: Adipose-derived stem cell (ADSC) transplantation presents a promising approach for osteoporosis (OP) treatment. However, the therapeutic efficacy of ADSCs is hindered by low post-transplantation survival rates and limited capacities for adhesion, migration, and differentiation. Icariin (ICA), the primary active compound of Epimedium, has been shown to promote cell proliferation and induce osteogenic differentiation; however, its specific effects on ADSC osteogenesis and the mechanisms by which ICA enhances osteoporosis treatment through cell transplantation remain inadequately understood.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Chemistry, Ashoka University, Sonipat, Haryana, India.
Pancreatic Ductal Adenocarcinoma (PDAC) is a devastating disease with poor clinical outcomes, which is mainly because of delayed disease detection, resistance to chemotherapy, and lack of specific targeted therapies. The disease's development involves complex interactions among immunological, genetic, and environmental factors, yet its molecular mechanism remains elusive. A major challenge in understanding PDAC etiology lies in unraveling the genetic profiling that governs the PDAC network.
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