Repressive effects of oat extracts on intracellular lipid-droplet formation in adipocytes and a three-dimensional subcutaneous adipose tissue model

Chronic administration of the insulin-sensitising drugs, thiazolidinediones (TZDs), results in low bone mineral density and ‘fatty bones’. This is thought to be due, at least in part, to aberrant differentiation of progenitor mesenchymal stem cells (MSCs) away from osteogenesis towards adipogenesis. This study directly compared the effects of rosiglitazone, pioglitazone, and netoglitazone treatment on osteogenesis and adipogenesis in MSCs derived from subcutaneous (SC) or visceral (PV) white adipose tissue. MSCs were isolated from adipose tissue depots of male Wistar rats and characterised using flow cytometry. The effects of TZD treatment on osteogenic and adipogenic differentiation were assessed histologically (day 14) and by quantitative PCR analysis (Pparγ2(Pparg2),Ap2(Fabp4), Adipsin(Adps),Msx2, Collagen I(Col1a1), andAlp) on days 0, 7, and 10. Uniquely, lipid droplet formation and mineralisation were found to occur concurrently in response to TZD treatment during osteogenesis. Compared with SC MSCs, PV MSCs were more prone to lipid accumulation under controlled osteogenic and adipogenic differentiation conditions. This study demonstrated that the extent of lipid accumulation is dependent on the nature of thePparligand and that SC and PV MSCs respond differently toin vitroTZD treatment, suggesting that metabolic status can contribute to the adverse effects associated with TZD treatment.

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Curcumin Recovers Intracellular Lipid Droplet Formation Through Increasing Perilipin 5 Gene Expression in Activated Hepatic Stellate Cells In Vitro

Current Medical Science ◽

10.1007/s11596-019-2104-5 ◽

2019 ◽

Vol 39 (5) ◽

pp. 766-777 ◽

Cited By ~ 2

Author(s):

Xiao-qun Han ◽

San-qing Xu ◽

Jian-guo Lin

Keyword(s):

Gene Expression ◽

Lipid Droplet ◽

Hepatic Stellate Cells ◽

Stellate Cells ◽

Droplet Formation ◽

Intracellular Lipid ◽

Lipid Droplet Formation ◽

Perilipin 5 ◽

Activated Hepatic Stellate Cells

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Three-Dimensional Cultures of Human Subcutaneous Adipose Tissue-Derived Progenitor Cells Based on RAD16-I Self-Assembling Peptide

Tissue Engineering Part C Methods ◽

10.1089/ten.tec.2015.0270 ◽

2016 ◽

Vol 22 (2) ◽

pp. 113-124 ◽

Cited By ~ 9

Author(s):

Cristina Castells-Sala ◽

Lourdes Recha-Sancho ◽

Aida Llucià-Valldeperas ◽

Carolina Soler-Botija ◽

Antoni Bayes-Genis ◽

...

Keyword(s):

Adipose Tissue ◽

Progenitor Cells ◽

Subcutaneous Adipose Tissue ◽

Three Dimensional ◽

Self Assembling ◽

Subcutaneous Adipose

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Abstract 558: PCPE2 Promotes Adipocyte Maturation via Regulation of SR-BI Activity

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.37.suppl_1.558 ◽

2017 ◽

Vol 37 (suppl_1) ◽

Author(s):

Hao Xu ◽

Sushma Kaul ◽

Elisa Maruko ◽

Kaniz Fatema ◽

Craig A Glastonbury ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Droplet ◽

Critical Role ◽

Hdl Cholesterol ◽

Droplet Formation ◽

Wild Type Cell ◽

Wild Type ◽

Mature Adipocyte ◽

Cellular Mechanisms ◽

Lipid Droplet Formation

Procollagen C-endopeptidase enhancer protein 2 (PCPE2) is an enhancer protein that enhances the cleavage of the C-termini of procollagen by bone morphogenetic protein 1. But the function of PCPE2 is not limited to collagen maturation. Recently our lab reported that PCPE2 increased HDL-associated cholesteryl ester uptake via scavenger receptor class B type 1 (SR-BI), an HDL cholesterol receptor highly expressed in adipose tissue. Interestingly, TwinsUK study in human provided data showing that PCPE2 mRNA is highly correlated with adipose tissue distribution. Further, our lab observed a reduced size of visceral fat pad in PCPE2 deficient mice despite its indifference in body weight compared to the wild type. To study the molecular and cellular mechanisms of how PCPE2 regulates SR-BI function and how it affects adipose tissue formation, we generated PCPE2 knockout (PCPE2 -/- ) cell line from murine preadipocyte 3T3-L1 cell using CRISPR-Cas9 technology. Induction of 3T3-L1 cell to differentiate into mature adipocyte increases the expression of both PCPE2 and SR-BI hand in hand around 3 fold, which parallels the process of lipid droplet formation. Immunofluorescence studies showed that PCPE2 is distributed all over the cell in mature adipocyte, while SR-BI is mostly distributed along the cytoplasmic and lipid droplet membranes, in addition to the perinuclear region. More interestingly, PCPE2 -/- 3T3-L1 cell shows an impairment in lipid droplet formation during the induction of differentiation, with less than 10% of cells generating lipid droplets, and the size of lipid droplet being only about 50% of that in wild type. Although PCPE2 -/- 3T3-L1 cell expresses SR-BI at a higher level compared with wild type cell, nearly 50% of the SR-BI in wild type cell are in homodimer structure while PCPE2 -/- 3T3-L1 cell has almost none SR-BI multimer, indicating that SR-BI in PCPE2 -/- 3T3-L1 cell is inactive. Taken together, we concluded that PCPE2 plays a critical role in keeping SR-BI in active conformation, which, in turn, controls adipocyte maturation. Whether this effect is associated with collagen maturation will be assessed in our future studies.

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Single cell study of adipose tissue mediated lipid droplet formation and biochemical alterations in breast cancer cells

The Analyst ◽

10.1039/c9an00816k ◽

2019 ◽

Vol 144 (18) ◽

pp. 5558-5570 ◽

Cited By ~ 3

Author(s):

Christina Blücher ◽

Carolin Zilberfain ◽

Tom Venus ◽

Nick Spindler ◽

Arne Dietrich ◽

...

Keyword(s):

Breast Cancer ◽

Adipose Tissue ◽

Cancer Cells ◽

Lipid Droplet ◽

Breast Cancer Cells ◽

Neutral Lipids ◽

Droplet Formation ◽

Biochemical Alterations ◽

Lipid Droplet Formation ◽

Staining Methods

Combined staining methods for neutral lipids and confocal Raman microspectroscopy detect increased lipid droplet formation in breast cancer cells influenced by adipose tissue.

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