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Published on: February 27, 2016
BATF alleviates ox-LDL-induced HCAEC injury by regulating SIRT1 expression in coronary heart disease
Bei Tian1, Jingyu Ji1, Can Jin2
1Nursing Department, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China.
Insights
B cell activating transcription factor (BATF) protects against oxidized low-density lipoprotein (ox-LDL) induced injury in coronary heart disease. It works by regulating Sirtuin 1 (SIRT1), offering potential new therapeutic strategies for this condition.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Gene Regulation
Background:
- Coronary heart disease (CHD) is a major health issue influenced by genetics and environment.
- Oxidized low-density lipoprotein (ox-LDL) plays a key role in CHD development.
- Understanding the roles of B cell activating transcription factor (BATF) and Sirtuin 1 (SIRT1) is crucial for CHD research.
Purpose of the Study:
- To investigate the combined effect of BATF and SIRT1 on ox-LDL-induced cell injury.
- To explore the potential of BATF and SIRT1 as therapeutic targets for CHD.
Main Methods:
- Bioinformatics analysis of the GSE42148 dataset to identify key genes.
- In vitro experiments using human coronary artery endothelial cells (HCAEC) to assess BATF's protective effects.
- Investigating the synergistic interaction between BATF and SIRT1 in response to ox-LDL.
Main Results:
- BATF expression was found to be significantly lower in CHD samples.
- BATF demonstrated a protective effect against ox-LDL-induced HCAEC injury.
- BATF was identified as a key regulator of SIRT1 expression following ox-LDL exposure, and their combined action mitigated apoptosis and cellular damage.
Conclusions:
- BATF shows promise as a protective factor against ox-LDL-induced HCAEC injury, potentially via SIRT1 regulation.
- These findings offer new insights into CHD pathogenesis and potential therapeutic interventions.
Background:
Coronary heart disease (CHD) represents a significant global health concern, arising from an intricate interplay between genetic predisposition and environmental influences, with a pivotal involvement of oxidized low-density lipoprotein (ox-LDL) in the pathophysiology of it. We aimed to elucidate the synergistic dynamics of B cell activating transcription factor (BATF) and Sirtuin 1 (SIRT1) in cell injury caused by ox-LDL, reveal potential therapeutic strategies for CHD.
Methods:
The GSE42148 dataset was used to analyze Differentially expressed genes (DEGs) to construct a gene co-expression network. Then bioinformatics analysis was performed on key modules to select the BATF gene. In vitro experiments were conducted to investigate the protective impact of BATF against human coronary artery endothelial cells (HCAEC) injury induced by ox-LDL. Further investigations probed the synergistic impact of BATF and SIRT1 modulation on cellular apoptosis and damage in the presence of ox-LDL.
Results:
BATF was significantly down-regulated in the CHD sample of the GSE42148 dataset. In vitro assays have proven that BATF alleviates ox-LDL-induced HCAEC injury. Notably, BATF emerged as a pivotal regulator of SIRT1 expression post ox-LDL exposure. Subsequent experiments underscored the interplay between BATF and SIRT1 in mitigating ox-LDL-induced apoptosis and Lactate Dehydrogenase (LDH) activity elevation, highlighting their collaborative role in cellular protection.
Conclusion:
The research findings suggested a prospective protective function of BATF in HCAEC injury induced by ox-LDL, likely through the mediation of SIRT1 regulation. These results could offer fresh perspectives on the etiology of CHD and possible treatment avenues.
