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Depot-specific analysis of human adipose cells and their responses to Bisphenol S

Citation

Atlas, Ella et al. (2020), Depot-specific analysis of human adipose cells and their responses to Bisphenol S, Dryad, Dataset, https://doi.org/10.5061/dryad.brv15dv5z

Abstract

Exposure to endocrine disrupting chemicals (EDCs) is associated with adverse health outcomes including obesity and diabetes.  Obesity, and more specifically visceral obesity, is correlated with metabolic disease.  The adipose tissue is an endocrine organ and a potential target for many environmental pollutants including bisphenols.  The subcutaneous and the omental (visceral) depots are comprised of mature adipocytes and residing progenitors, which may be different between the depots and may be EDCs targets.  Bisphenol A (BPA) is a suspected metabolic disruptor, and is being replaced with structurally similar compounds such as bisphenol S (BPS).  Like BPA, BPS induces adipogenesis in murine and primary human subcutaneous preadipocytes.  However, the effect of BPS on omental preadipocytes is not known.  In this study, we show that human primary progenitors from omental depots have a distinct transcriptomic signature as compared to progenitors derived from donor-matched subcutaneous depots.  Furthermore, we show that BPS increases adipogenesis of both omental and subcutaneous preadipocytes and can mimic the action of glucocorticoids or peroxisome proliferator-activated receptor g (PPARg) agonists.  We also show that BPS treatment, at 0.1 µM and 25 µM, modifies the adipokine profiles of both omental and subcutaneous derived adipocytes, in a depot specific manner.  Taken together our data show distinct gene expression profiles in the omental versus subcutaneous progenitors and similar responses to the BPA analogue, BPS.

Usage Notes

Dataset content overview:

Table S1. Primer sequences used for real-time qPCR analysis.

Table S2. Human donor information used for RNA-seq analysis. 

Table S3. Activated upstream regulators identified by IPA. RNA was collected from 4 donor matched subcutaneous (Sc) and omental (Om) preadipocytes and used for RNA-seq analysis. Genes in Om preadipocytes with significant fold change of ≥ + 1.5 or ≤ −1.5 compared to Sc were uploaded in to IPA for analysis using the adipose tissue as the target organ. The upstream regulators were sorted by predicted activation z-score and the activated upstream regulators are shown. 

Table S4. Inhibited upstream regulators identified by IPA. RNA was collected from 4 donor matched subcutaneous (Sc) and omental (Om) preadipocytes and used for RNA-seq analysis. Genes in Om preadipocytes with significant fold change of ≥ + 1.5 or ≤ −1.5 compared to Sc were uploaded in to IPA for analysis using the adipose tissue as the target organ. The upstream regulators were sorted by predicted activation z-score and the inhibited upstream regulators are shown. 

Figure S2. Human primary subcutaneous (Sc) and omental (Om) preadipocytes were induced to differentiate in the presence of 500μM IBMX, 100nM insulin, and 200 nM rosiglitazone and supplemented with either solvent control (EtOH) or 25 μM BPS. At day 12 of differentiation, total RNA was isolated and the expression levels of the indicated adipogenic markers were quantified by real-time qPCR. Levels were normalized to endogenous ACTB and expressed as fold over solvent control. Results from four separate experiments are graphically represented as mean±S.E.M. *p<0.05 and ***p<0.001 compared to solvent control as assessed by student’s t test.