Histone Acetylation Retards the Adipogenic Differentiation of Human Umbilical Cord - Mesenchymal Stem Cells: A Clue for Anti-obesity Approach?

aims: To investigate the epigenetic changes associated with adipogenic differentiation in human umbilical cord blood-derived mesenchymal stem cells (hUCMSCs) using the histone deacetylase inhibitor Trichostatin A (TSA). Introduction:: Obesity represents a significant health and lifestyle issue worldwide. White and brown adipocytes, which originate from resident mesenchymal stem cells (MSCs), are critically involved in the process of adipogenesis. background: Obesity is a major health and lifestyle concern. White and brown adipocytes, derived from resident mesenchymal stem cells (MSCs), play a crucial role in adipogenesis. Understanding the epigenetic regulation of adipogenesis could provide insights into potential obesity interventions. Methodology:: Human umbilical cord-derived mesenchymal stem cells (hUCMSCs) were utilized to investigate epigenetic modifications associated with adipogenic differentiation. Briefly, histone acetylation and/or methylation pattern of hUCMSCs were evaluated with histone deacetylase inhibitor Trichostatin A (TSA) for cell viability, death rate, and adipogenic commitment. objective: To evaluate the effects of TSA on histone acetylation and methylation patterns in hUCMSCs, assessing its impact on cell viability, death rate, and adipogenic differentiation. Results:: Inhibition of histone deacetylation was accompanied by a reduction of the global methylation pattern compared to the baseline levels in untreated cells. These changes decreased cell viability at 36 hrs, while reciprocally increasing the rate of cell death from 24 hrs. Most importantly, TSA-treated cells demonstrated diminished adipogenic differentiation compared to normal cells post-induction. method: hUCMSCs were treated with TSA, and changes in histone acetylation and methylation patterns were analyzed. Cell viability, cell death rate, and adipogenic commitment were assessed to determine the impact of histone deacetylation inhibition. Discussion:: Epigenetic remodeling triggered by inhibition of histone deacetylase led to reduced DNA methylation. The increased cytotoxicity, impairing cell survival due to alteration in chromatin state, reduced adipogenic differentiation potential in TSA-treated cells, promoting disruption of normal lineage commitment pathways. result: TSA treatment led to a regression in the global methylation pattern compared to untreated cells. This resulted in reduced cell viability at 36 hours and increased cell death from 24 hours. TSA-treated cells also exhibited diminished adipogenic differentiation compared to untreated cells post-induction. Conclusion:: Taken together, the results show a possible anti-obesity effect of histone deacetylation inhibitors (HDCAs) in MSCs, resulting in depletion and restriction of their adipogenic differentiation. conclusion: The study suggests that histone deacetylation inhibitors (HDACIs) may have anti-obesity effects by restricting MSC adipogenic differentiation. TSA negatively affected hUCMSCs viability, increased cell death, and limited adipogenic differentiation. Further research is needed to explore small molecules and non-coding RNAs that could modulate epigenetic patterns for non-invasive obesity management. other: NIL