Enhancing the Regenerative Potential of Adipose-Derived Mesenchymal Stem Cells Through TLR4-Mediated Signaling

Abstract

Introduction: Toll-like receptor 4(TLR4) is a receptor that traditionally plays an important role in immunomodulation (regulation of the immune system) and the initiation of proinflammatory responses. TLR4 is used in the body to recognize molecular patterns of pathogens or damaged cells from outside. However, in recent years, it has also become clear that TLR4 can affect the immune system and the function of stem cells, especially mesenchymal stem cells. Therefore, understanding how TLR4 signaling works at the cellular and molecular level and using this knowledge in regenerative medicine could be potentially useful, especially in the treatment of adipose- derived mesenchymal stem cells (ADMSCs). How these cells can use TLR4 signaling when used to increase their regenerative potential and repair tissues is an area of research. background: Toll-like receptor 4 (TLR4) is traditionally recognized for its crucial role in immunomodulation and proinflammatory responses. Recent advancements suggest that TLR4 also significantly influences the biology of mesenchymal stem cells, particularly adipose-derived mesenchymal stem cells (ADMSCs). Aims: This study aims to elucidate the multifaceted role of TLR4-mediated signaling in ADMSCs. objective: To elucidate the multifaceted impact of TLR4-mediated signaling on the cellular and molecular behavior of ADMSCs, and to assess its implications for regenerative medicine. Method: Employing a comprehensive set of assays, including MTT for cell viability, flow cytometry for surface marker expression, and gene expression analysis, we demonstrate that TLR4 activation significantly modulates key aspects of ADMSC biology. Specifically, TLR4 signaling was found to regulate ADMSCs proliferation, surface marker expression, and regenerative capacity in a dose- and time-dependent manner. Furthermore, TLR4 activation conferred cytoprotective effects against Doxorubicin (DOX)-induced cellular apoptosis. method: A comprehensive set of assays was employed, including 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) for assessing cell viability, flow cytometry for quantifying surface marker expression, and gene expression analysis through quantitative polymerase chain reaction (qPCR). Result: These findings suggest that TLR4 signaling could be used to enhance the regenerative abilities of ADMSCs and enable ADMSC-based therapies to be used more effectively for tissue engineering and therapeutic purposes. result: Our data demonstrated that TLR4 activation significantly modulated key aspects of ADMSC biology in a dose- and time-dependent manner. Specifically, TLR4 signaling regulated mesenchymal stem cell proliferation, surface marker expression, and regenerative capacity. Additionally, TLR4 activation conferred cytoprotective effects against Doxorubicin-induced cellular apoptosis. Conclusion: However, it is important to note that research in this area needs more details and clinical studies.