YC-1 induces lipid droplet formation in RAW 264.7 macrophages

Tsui, Leo; Chang, Shwu-Fen; Huang, Hsiang‐Po; Fong, Tsorng Harn; Wang, I‐Jong

doi:10.1186/s12929-016-0218-7

Cited by 8 publications

(3 citation statements)

References 34 publications

(38 reference statements)

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“…YC-1 can also modulate lipolysis, but in a cell-type-specific manner. In RAW 264.7 macrophage cells, YC-1 increased lipid droplet and oxidized LDL foam cell formation through cGMP-dependent protein kinase 129 , whereas in adipocytes, YC-1 induced lipolysis 130 . Another study revealed that YC-1 is a non-competitive inhibitor of p-glycoprotein (multidrug resistance protein 1 (MDR1; also known as ABCB1)) also act via the cGMP-dependent protein kinase ERK 131 .…”

Section: Hif Inhibitors and Therapeutic Effectsmentioning

confidence: 95%

The role of hypoxia-inducible factors in metabolic diseases

2018

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Hypoxia-inducible factors (HIFs), a family of transcription factors activated by hypoxia, consist of three α-subunits (HIF1α, HIF2α and HIF3α) and one β-subunit (HIF1β), which serves as a heterodimerization partner of the HIFα subunits. HIFα subunits are stabilized from constitutive degradation by hypoxia largely through lowering the activity of the oxygen-dependent prolyl hydroxylases that hydroxylate HIFα, leading to their proteolysis. HIF1α and HIF2α are expressed in different tissues and regulate target genes involved in angiogenesis, cell proliferation and inflammation, and their expression is associated with different disease states. HIFs have been widely studied because of their involvement in cancer, and HIF2α-specific inhibitors are being investigated in clinical trials for the treatment of kidney cancer. Although cancer has been the major focus of research on HIF, evidence has emerged that this pathway has a major role in the control of metabolism and influences metabolic diseases such as obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease. Notably increased HIF1α and HIF2α signalling in adipose tissue and small intestine, respectively, promotes metabolic diseases in diet-induced disease models. Inhibition of HIF1α and HIF2α decreases the adverse diet-induced metabolic phenotypes, suggesting that they could be drug targets for the treatment of metabolic diseases.

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Section: Hif Inhibitors and Therapeutic Effectsmentioning

confidence: 95%

The role of hypoxia-inducible factors in metabolic diseases

2018

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“…CoCl 2 -mediated macrophage foam cell formation is similar to that induced by ox-LDL as shown in our previous study. 14 It is reported that hypoxia would contribute markedly to lipid metabolism in atherosclerotic lesions. 21 Hypoxia enhances lipid uptake into RAW 264.7 macrophages and regulates the expression of ox-LDL receptors, which may affect lipid droplet formation in macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…The protocol of oil Red O staining was described in our earlier study. 14 In brief, oil red O powder (Sigma-Aldrich, St. Louis, MO) was dissolved in 2-propanol (Kanto Chemical Corporation, Tokyo, Japan) as 0.5% solution, and then diluted to 0.3% solution with distilled H 2 O. The oil red O solution was filtered through a 0.22 mm filter before use.…”

Section: Oil Red O Stainingmentioning

confidence: 99%

Cobalt Chloride Induces Macrophage Foam Cell Formation: A Chemical Hypoxia Model for Anti-Atherosclerotic Drug Screening

Tsui

Fong

2021

ASSAY and Drug Development Technologies

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Macrophages would engulf circulating oxidized (ox)-lowdensity lipoprotein and form lipid droplet-laden foam cells. Macrophage foam cells are considered an important therapeutic target of atherosclerosis. The aim of the study was to investigate a hypoxic foam cell model for anti-atherosclerotic drug screening using the chemical hypoxia-mimicking agent cobalt chloride (CoCl 2). The oil red O stating results showed that treatment with CoCl 2 could induce lipid accumulation and lead to cell transformation to spindle-shaped and lipid-rich foam cells in RAW 264.7 macrophages. Incubation with 150 lM CoCl 2 for 24 h significantly increased the area of intracellular lipid droplets in macrophages, compared with the control group. Our findings indicate that CoCl 2-triggered macrophage foam cells should be a potential in vitro hypoxia model for atherosclerosis drug discovery.

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