2025 Volume 267 Issue 3 Pages 323-336
This study explores the regulatory effects of Heat Shock Protein A1B (HSPA1B) on gene expression related to blood pressure in Human Umbilical Vein Endothelial Cells (HUVECs) and delineates its underlying mechanisms. Given the global prevalence of hypertension as a major risk factor for cardiovascular and cerebrovascular diseases, understanding its molecular underpinnings is crucial. We utilized cloning, cell culture, RNA isolation, cDNA synthesis, PCR amplification, high-throughput sequencing, and alternative splicing analysis to evaluate the impact of HSPA1B overexpression on HUVECs. The findings revealed that HSPA1B overexpression leads to significant changes in gene expression and alternative splicing patterns, implicating various molecular pathways. Notably, genes associated with inflammation, immune response, apoptosis, and endothelial function were upregulated, while others were downregulated. These alterations suggest that HSPA1B may influence endothelial cell responses under stress conditions. This study provides insights into the molecular mechanisms that could contribute to hypertension development and identifies HSPA1B as a potential area for further research in therapeutic strategies to manage this condition.
