Fig 1: a–f Screening diverse cell types for BAT gene expression markers. a FABP4, b UCP1, c ADIPOQ, d LIPASIN, e CITED1, f MYH3, hES cell-derived clonal embryonic progenitor cell lines were analyzed by Illumina bead array-based gene expression for select adipocyte and BAT gene expression markers in the undifferentiated state and for 5 days in quiescence inducing conditions (Ctrl) or following adipogenic differentiation for 14 days in HyStem-C with BMP4, rosiglitazone, T3, and CL316243 (BMP4, Rosi, T3, CL) (differentiated). (C) Controls include adult BAT and SAT-derived preadipocytes and the clonal progenitor cell line E85 lacking the ability to differentiate into definitive adipocytes. Differentiated cells are identified as having definitive adipocyte markers. Values are shown as relative fluorescence units (RFUs) and represent mean values of two or more biological replicates. (RFU values < 130 considered background signal). (Error bars represent standard deviation)
Fig 2: Relative levels of adipocyte gene expression in diverse differentiation conditions. a FABP4, b UCP1, c ADIPOQ, and d LIPASIN expression in the undifferentiated, 5-day quiescent cell clones and after 14 days of differentiation in HyStem-C with BMP4, rosiglitazone, T3, and CL316243 (BMP4, Rosi, T3, CL), HyStem-C with rosiglitazone, T3, and CL316243 (Rosi, T3, CL), HyStem-C with BMP4, rosiglitazone, T3, FGF21, and CL316243 (B4, Rosi, T, FGF21, CL), or HyStem-C with BMP4, rosiglitazone, T3, CL316243, and cultured at 28 °C. (BMP4, Rosi, T3, CL, 28C). (Error bars represent standard deviation)
Fig 3: Functional and molecular signaling pathway enrichment analysis. A The DAVID databases analysis suggested that most hub genes are involved in the etiology of type 2 diabetes mellitus. ADIPOQ initiates this pathogenic pathway. B–F Oxidative stress, detoxification of reactive oxygen species, cellular response to stress, heart ischemia, hypertension, diabetes, Wnt signaling pathway, apoptosis, and adipocytokine signaling pathway were also highlighted by the KOBAS-i, Wiki Pathway, Reactome, Elsevier pathway collection, and Panther databases. G, H Heart dysfunction and diabetes were identified as pathogenic processes associated with FAM132A, SFRP5, ADIPOQ, TNF, IL-6, C1QTNF1, CAT, SOD1, SOD2, and SOD3 by enrichment of hub genes in the DisGeNET and OMIM databases
Fig 4: Virtual screening of binding affinity between ADIPOQ macromolecules and ligands. A–H Molecular docking affinity between ADIPOQ macromolecules and bioactive compounds derived from propolis as small molecules/ligands were estimated in the search space with dimensions x = 41.3689, y = 52.2768, and z = 50.3145. All bioactive compounds derived from propolis received suitable binding affinity in molecular docking. With the highest affinity score among bioactive compounds' libraries, chrysin binds to the ADIPOQ's active site
Fig 5: Protein–protein network construction and social network analysis. A The heatmap plot of significant genes with differential expression demonstrated the comparison of gene expression of healthy subjects to adult diabetic patients with dyslipidemia considering P.value < 0.001 thresholds. B Construction of the protein–protein interactions network of significant differential expressions involved in adult diabetic dyslipidemia status considering the visualizing parameters of the network. In this network, genes were ranked based on degree and betweenness centrality. The most prominent node indicated a higher degree, and the orange indicated genes with the highest betweenness centrality. IL-6 and ADIPOQ are the master regulatory cut-point genes as druggable candidates for pharmacological approaches and modulating pathogenesis networks in this network
Supplier Page from Abcam for Human Adiponectin ELISA Kit