scholarly journals Thiazolidinedione-induced lipid droplet formation during osteogenic differentiation

2014 ◽  
Vol 223 (2) ◽  
pp. 119-132 ◽  
Author(s):  
M van de Vyver ◽  
E Andrag ◽  
I L Cockburn ◽  
W F Ferris
Keyword(s):  
Adipose Tissue ◽  
Lipid Droplet ◽  
Lipid Accumulation ◽  
Adipogenic Differentiation ◽  
Chronic Administration ◽  
Droplet Formation ◽  
Pcr Analysis ◽  
Mineral Density ◽  
Lipid Droplet Formation

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.

scholarly journals Aggregation and fusion of low-density lipoproteins in vivo and in vitro

2013 ◽  
Vol 4 (5) ◽  
pp. 501-518 ◽  
Author(s):  
Mengxiao Lu ◽  
Olga Gursky
Keyword(s):  
Lipid Droplet ◽  
Current Knowledge ◽  
Single Copy ◽  
Droplet Formation ◽  
Low Density Lipoproteins ◽  
Low Density ◽  
Atherosclerotic Lesions ◽  
Lipid Droplet Formation

AbstractLow-density lipoproteins (LDLs, also known as ‘bad cholesterol’) are the major carriers of circulating cholesterol and the main causative risk factor of atherosclerosis. Plasma LDLs are 20- to 25-nm nanoparticles containing a core of cholesterol esters surrounded by a phospholipid monolayer and a single copy of apolipoprotein B (550 kDa). An early sign of atherosclerosis is the accumulation of LDL-derived lipid droplets in the arterial wall. According to the widely accepted ‘response-to-retention hypothesis’, LDL binding to the extracellular matrix proteoglycans in the arterial intima induces hydrolytic and oxidative modifications that promote LDL aggregation and fusion. This enhances LDL uptake by the arterial macrophages and triggers a cascade of pathogenic responses that culminate in the development of atherosclerotic lesions. Hence, LDL aggregation, fusion, and lipid droplet formation are important early steps in atherogenesis. In vitro, a variety of enzymatic and nonenzymatic modifications of LDL can induce these reactions and thereby provide useful models for their detailed analysis. Here, we summarize current knowledge of the in vivo and in vitro modifications of LDLs leading to their aggregation, fusion, and lipid droplet formation; outline the techniques used to study these reactions; and propose a molecular mechanism that underlies these pro-atherogenic processes. Such knowledge is essential in identifying endogenous and exogenous factors that can promote or prevent LDL aggregation and fusion in vivo and to help establish new potential therapeutic targets to decelerate or even block these pathogenic reactions.

scholarly journals Evaluation on the phagocytosis of apoptotic spermatogenic cells by Sertoli cells in vitro through detecting lipid droplet formation by Oil Red O staining

Reproduction ◽  
2006 ◽  
Vol 132 (3) ◽  
pp. 485-492 ◽  
Author(s):  
Huizhen Wang ◽  
Haikun Wang ◽  
Weipeng Xiong ◽  
Yongmei Chen ◽  
Quanhong Ma ◽  
...  
Keyword(s):  
Lipid Droplet ◽  
Sertoli Cells ◽  
Lipid Droplets ◽  
Apoptotic Cell ◽  
Practical Method ◽  
Droplet Formation ◽  
Spermatogenic Cells ◽  
Lipid Droplet Formation ◽  
Oil Red O

During spermatogenesis, more than half of the differentiating spermatogenic cells undergo apoptosis before they mature into spermatozoa. Ultrastructure studies showed that the formation of lipid droplets in Sertoli cells was associated with phagocytosis of residual bodies and apoptotic germ cells by Sertoli cells. Here, a relationship between the phagocytosis of apoptotic spermatogenic cells and lipid droplet formation in Sertoli cells was studiedin vitroby Oil Red O (ORO) staining. The results confirmed that the formation of lipid droplets was a result of phagocytosis of apoptotic spermatogenic cells in Sertoli cells. By comparing phagocytosis of apoptotic spermatogenic cells and thymocytes by Sertoli cells to that by macrophages, we demonstrated that the lipid droplets accumulation in phagocytes depended on phagocytosed apoptotic cell type, but not phagocyte type. However, the size of lipid droplets was related to the type of phagocytes. By this approach, we found that Sertoli cells at different postnatal stages of development had a similar phagocytic ability. These results suggested that the detection of lipid droplets by ORO staining was a practical method to evaluate the phagocytic functions of Sertoli cellsin vitro. This approach could also be considered as anin vitromodel to study the lipid formation, metabolism, and function in Sertoli cells.

scholarly journals In vitro exploration of ACAT contributions to lipid droplet formation during adipogenesis

2018 ◽  
Vol 59 (5) ◽  
pp. 820-829 ◽  
Author(s):  
Yuyan Zhu ◽  
Chih-Yu Chen ◽  
Junjie Li ◽  
Ji-Xin Cheng ◽  
Miran Jang ◽  
...  
Keyword(s):  
Lipid Droplet ◽  
Droplet Formation ◽  
Lipid Droplet Formation

ADRP stimulates lipid accumulation and lipid droplet formation in murine fibroblasts

2002 ◽  
Vol 283 (4) ◽  
pp. E775-E783 ◽  
Author(s):  
Minako Imamura ◽  
Toyoshi Inoguchi ◽  
Shoichiro Ikuyama ◽  
Susumu Taniguchi ◽  
Kunihisa Kobayashi ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Droplet ◽  
Lipid Accumulation ◽  
Lipid Droplets ◽  
Droplet Formation ◽  
Fatty Acid Binding ◽  
Lipogenic Genes ◽  
Lipid Droplet Formation ◽  
Murine Fibroblasts ◽  
Adipose Differentiation

Adipose differentiation-related protein (ADRP) is a lipid droplet-associated protein that is expressed early during adipose differentiation. The present study was undertaken to reveal the role of ADRP in adipose differentiation. In murine fibroblasts infected with green fluorescent protein (GFP)-ADRP fusion protein expression adenovirus vector, confocal microscopic analysis showed the number and size of lipid droplets apparently increased comparing with those of control cells. Overexpressed GFP-ADRP were mainly located at the surface of lipid droplets and appeared to be “ring-shaped.” Triacylglycerol content was also significantly ( P < 0.001) increased in GFP-ADRP-overexpressed cells compared with control cells. ADRP-induced lipid accumulation did not depend on adipocyte-specific gene induction, such as peroxisome proliferator-activated receptor-γ, lipoprotein lipase, or other lipogenic genes, including acyl-CoA synthetase, fatty acid-binding protein, and fatty acid transporter. In conclusion, ADRP stimulated lipid accumulation and lipid droplet formation without induction of other adipocyte-specific genes or other lipogenic genes in murine fibroblasts. The detailed molecular mechanisms of ADRP on lipid accumulation remain to be elucidated.

scholarly journals Decreased PEDF Promotes Hepatic Fatty Acid Uptake and Lipid Droplet Formation in the Pathogenesis of NAFLD

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 270
Author(s):  
Kuang-Tzu Huang ◽  
Kuang-Den Chen ◽  
Li-Wen Hsu ◽  
Chao-Pin Kung ◽  
Shu-Rong Li ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Droplet ◽  
Lipid Accumulation ◽  
Fatty Acid Uptake ◽  
Droplet Formation ◽  
Fatty Acid Transport ◽  
Acid Uptake ◽  
Sequencing Analysis ◽  
Simple Steatosis ◽  
Lipid Droplet Formation

Non-alcoholic fatty liver disease (NAFLD), the leading cause of chronic liver diseases worldwide, ranges from simple steatosis to steatohepatitis, with the risk for progressive fibrosis or even cirrhosis. While simple steatosis is a relatively benign condition, the buildup of toxic lipid metabolites can induce chronic inflammation, ultimately triggering disease progression. Pigment epithelium-derived factor (PEDF) is a secreted, multifunctional glycoprotein with lipid metabolic activities. PEDF promotes lipolysis through binding to adipose triglyceride lipase (ATGL), a key enzyme for triglyceride breakdown. In the current study, we aimed to delineate how changes in PEDF expression affect hepatic lipid accumulation. Our data revealed that hepatic PEDF was downregulated in a mouse NAFLD model. We further showed that decreased PEDF levels in hepatocytes in vitro resulted in elevated fatty acid uptake and lipid droplet formation, with concomitant upregulation of fatty acid transport proteins CD36 and fatty acid binding protein 1 (FABP1). RNA sequencing analysis of PEDF knocked down hepatocytes revealed an alteration in gene expression profile toward lipid accumulation. Additionally, decreased PEDF promotes mobilization of fatty acids, an observation distinct from blocking ATGL activity. Taken together, our data suggest that hepatic PEDF downregulation causes molecular changes that favor triglyceride accumulation, which may further lead to NAFLD progression.

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