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Isolation, Culture, and Adipogenic Induction of Stromal Vascular Fraction-derived Preadipocytes from Mouse Periaortic Adipose Tissue
Published on: July 21, 2023
Pattern specification and immune response transcriptional signatures of pericardial and subcutaneous adipose tissue
Frank H Lau1, Rahul C Deo, Gregory Mowrer
1Center for Regenerative Medicine, Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Insights
Pericardial adipose tissue (PCAT) overexpresses inflammatory chemokines, contributing to cardiovascular disease (CVD). Transcriptional analysis reveals depot-specific gene patterns, suggesting distinct functions for PCAT and subcutaneous fat.
Area of Science:
- Cardiovascular Biology
- Adipose Tissue Metabolism
- Molecular Genetics
Background:
- Cardiovascular disease (CVD) is a leading cause of death in the US.
- Pericardial adipose tissue (PCAT) may contribute to CVD by secreting inflammatory factors.
- The specific cellular origins of PCAT-secreted factors remain unclear.
Purpose of the Study:
- To conduct a large-scale transcriptional analysis comparing PCAT and subcutaneous adipose tissue (SAT).
- To identify differentially expressed genes in isolated pericardial adipocytes versus isolated subcutaneous adipocytes.
- To elucidate the distinct functional roles of different adipose tissue depots in CVD pathogenesis.
Main Methods:
- Analysis of 53 microarrays from 19 individuals, comparing PCAT and SAT.
- Gene expression profiling of isolated pericardial adipocytes and subcutaneous adipocytes.
- Unbiased transcriptional analysis to identify differentially expressed genes.
Main Results:
- PCAT and isolated pericardial adipocytes overexpress atherosclerosis-promoting chemokines.
- Both PCAT and isolated adipocytes exhibit depot-specific homeobox gene expression patterns.
- No significant overlap was found in core lipid processing genes between depots.
Conclusions:
- Transcriptional profiles indicate distinct functional roles for PCAT and SAT.
- Overexpression of chemokines in PCAT suggests its pro-inflammatory contribution to CVD.
- Further research into inter-depot adipose tissue differences is warranted.
Abstract:
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in the United States. Recent studies suggest that pericardial adipose tissue (PCAT) secretes inflammatory factors that contribute to the development of CVD. To better characterize the role of PCAT in the pathogenesis of disease, we performed a large-scale unbiased analysis of the transcriptional differences between PCAT and subcutaneous adipose tissue, analysing 53 microarrays across 19 individuals. As it was unknown whether PCAT-secreted factors are produced by adipocytes or cells in the supporting stromal fraction, we also sought to identify differentially expressed genes in isolated pericardial adipocytes vs. isolated subcutaneous adipocytes. Using microarray analysis, we found that: 1) pericardial adipose tissue and isolated pericardial adipocytes both overexpress atherosclerosis-promoting chemokines and 2) pericardial and subcutaneous fat depots, as well as isolated pericardial adipocytes and subcutaneous adipocytes, express specific patterns of homeobox genes. In contrast, a core set of lipid processing genes showed no significant overlap with differentially expressed transcripts. These depot-specific homeobox signatures and transcriptional profiles strongly suggest different functional roles for the pericardial and subcutaneous adipose depots. Further characterization of these inter-depot differences should be a research priority.
