SREBP1 regulates Lgals3 activation in response to cholesterol loading

Li, Jing; Shen, Hongtao; Owens, Gary K.

doi:10.1016/j.omtn.2022.05.028

Cited by 10 publications

(4 citation statements)

References 54 publications

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“… 45 Moreover, Lgals3 and SREBP1 downregulated myocardin‐related transcription factor A expression in VSMCs. 45 In another study, Owsiany et al used a dual lineage tracing model and found that Lgals3 + VSMCs produce monocyte chemoattractant protein 1, a proinflammatory chemokine. 15 Knockout of monocyte chemoattractant protein 1 specifically in Lgals3 + VSMCs resulted in the formation of atherosclerotic lesions with a greater ACTA2 content in the fibrous cap and decreased Lgals3 + cell content, a feature of stable plaque.…”

Section: Vsmc Phenotypes Reported In Atherosclerotic Lesionsmentioning

confidence: 99%

“…Using mouse, rat, and human models of cholesterol‐loading in VSMCs, Li et al found that SREBP1 (sterol regulatory‐element binding protein‐1) and Krüppel‐like factor‐15 induced up‐ and downregulation of Lgals3, respectively, via binding to the Lgals3 gene promoter (albeit at different sites). 45 Likewise, Lgals3 promoted SREBP1 gene expression, producing a feedforward loop upregulated by cholesterol loading. 45 Moreover, Lgals3 and SREBP1 downregulated myocardin‐related transcription factor A expression in VSMCs.…”

Section: Vsmc Phenotypes Reported In Atherosclerotic Lesionsmentioning

confidence: 99%

“… 45 Likewise, Lgals3 promoted SREBP1 gene expression, producing a feedforward loop upregulated by cholesterol loading. 45 Moreover, Lgals3 and SREBP1 downregulated myocardin‐related transcription factor A expression in VSMCs. 45 In another study, Owsiany et al used a dual lineage tracing model and found that Lgals3 + VSMCs produce monocyte chemoattractant protein 1, a proinflammatory chemokine.…”

Section: Vsmc Phenotypes Reported In Atherosclerotic Lesionsmentioning

confidence: 99%

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Phenotypic Switching of Vascular Smooth Muscle Cells in Atherosclerosis

Chen,

McVey,

Shen

et al. 2023

JAHA

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The medial layer of the arterial wall is composed mainly of vascular smooth muscle cells (VSMCs). Under physiological conditions, VSMCs assume a contractile phenotype, and their primary function is to regulate vascular tone. In contrast with terminally differentiated cells, VSMCs possess phenotypic plasticity, capable of transitioning into other cellular phenotypes in response to changes in the vascular environment. Recent research has shown that VSMC phenotypic switching participates in the pathogenesis of atherosclerosis, where the various types of dedifferentiated VSMCs accumulate in the atherosclerotic lesion and participate in the associated vascular remodeling by secreting extracellular matrix proteins and proteases. This review article discusses the 9 VSMC phenotypes that have been reported in atherosclerotic lesions and classifies them into differentiated VSMCs, intermediately dedifferentiated VSMCs, and dedifferentiated VSMCs. It also provides an overview of several methodologies that have been developed for studying VSMC phenotypic switching and discusses their respective advantages and limitations.

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Section: Vsmc Phenotypes Reported In Atherosclerotic Lesionsmentioning

confidence: 99%

Section: Vsmc Phenotypes Reported In Atherosclerotic Lesionsmentioning

confidence: 99%

Section: Vsmc Phenotypes Reported In Atherosclerotic Lesionsmentioning

confidence: 99%

See 1 more Smart Citation

Phenotypic Switching of Vascular Smooth Muscle Cells in Atherosclerosis

Chen,

McVey,

Shen

et al. 2023

JAHA

View full text Add to dashboard Cite

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“…Sterols regulate SREBP by controlling its endoplasmic reticulum (ER)-to-Golgi apparatus transport ( 5 ). SREBPs control lipogenesis and lipid uptake, SREBP1 preferentially regulates the lipogenic process by activating genes involved in fatty acid and triglyceride synthesis ( 6 ), whereas SREBP2 primarily controls cholesterol homeostasis by activating genes required for cholesterol synthesis and uptake ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Overcharged lipid metabolism in mechanisms of antitumor by Tremella fuciformis‑derived polysaccharide

Pan

2022

Int J Oncol

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Tremella fuciformis-derived polysaccharide (TFP) is a natural macromolecular compound that is well known for whitening skin, as well as for its ability to regulate lipids and immunity. However, its mechanism of action is not clear. In the present study, B16 cells treated with TFP were inoculated subcutaneously in the right flank of C57BL/6 mice to explore the effect of TFP on melanoma in vivo. Western blotting, immunohistochemistry, immunofluorescence staining and transcription analysis of tumors were utilized to assess the expression of key molecules in production of melanin, lipid metabolism and immunity. It was found that TFP promoted B16 cell apoptosis and induced G 2 /M cell cycle arrest, which was associated with activation of cell cycle-related pathways. TFP induced the expression of glucose transporter type 4 and CD36, thus resulting in an increase in the uptake of lipids, which markedly suppressed sterol regulatory element-binding transcription factor 1 and phosphorylated-AMP-activated protein kinase expression; increased the number of lipids in the cell membrane, endoplasmic reticulum and nucleus; and induced the RNA expression of molecules related to lipid metabolism, as revealed by RNA-sequencing in vivo. Increased lipid binding, upregulated lipid storage, and elevated triglyceride and lipid catabolism resulted in disruption of cell volume homeostasis and activated innate immune response, thus inhibiting melanoma development and progression. These data revealed a novel molecular mechanism involved in the antitumor effect of TFP via lipid metabolism.

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Loss of Nrf1 rather than Nrf2 leads to inflammatory accumulation of lipids and reactive oxygen species in human hepatoma cells, which is alleviated by 2-bromopalmitate

Deng,

Zheng,

et al. 2024

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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SREBP1 regulates Lgals3 activation in response to cholesterol loading

Cited by 10 publications

References 54 publications

Phenotypic Switching of Vascular Smooth Muscle Cells in Atherosclerosis

Phenotypic Switching of Vascular Smooth Muscle Cells in Atherosclerosis

Overcharged lipid metabolism in mechanisms of antitumor by Tremella fuciformis‑derived polysaccharide

Loss of Nrf1 rather than Nrf2 leads to inflammatory accumulation of lipids and reactive oxygen species in human hepatoma cells, which is alleviated by 2-bromopalmitate

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