Hyperlipidaemia impairs the circadian clock and physiological homeostasis of vascular smooth muscle cells via the suppression of Smarcd1

Chen, Siyu; Ding, Yan; Zhao, Zhigang; Wang, Han; Liu, Chang

doi:10.1002/path.4338

Cited by 14 publications

(14 citation statements)

References 46 publications

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“…Intriguing reports regarding the role of SMARCD1 in lipid and cholesterol metabolisms demonstrated that a decrease in the expression of SMARCD1 induced by HFD suppresses fatty acid β-oxidation and induces hepatic steatosis 9 , 21 , while the so-called “Western diet” (high fat and high cholesterol contents) induces SMARCD1 expression, which results in the stimulation of the expression of genes involved in bile acid synthesis, modification, and transport, elevation of plasma cholesterol level, and hyperlipidemia 13 . In other words, fasting and high fat/cholesterol diet both induce SMARCD1, but suppress steatosis and induce hypercholesterolemia/atherosclerosis, respectively.…”

Section: Discussionmentioning

confidence: 97%

SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes

et al. 2017

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Previously, we have identified 16 senescence-associated genes by a subtractive proteomic analysis using presenescent and senescent human fibroblast cells, TIG-1. The aim of this study was to clarify the role of SMARCD1, one of the identified genes, also known as BAF60a, in hepatic senescence. SMARCD1 is a member of the SWI/SNF chromatin remodeling complex family, and regulates the transcription of target genes through the alterations of chromatin structure. We demonstrated that the reduced expression of SMARCD1 triggers cellular senescence and induces the accumulation of lipids, suggesting that SMARCD1 acts as a mediator in these processes. Furthermore, palmitic acid treatment and high-fat diet led to a significant reduction of SMARCD1 expression, and consequently induced cellular senescence and lipid accumulation in HepG2 cells and mouse liver, respectively. The results obtained here suggest that dietary nutrient-associated impaired expression of SMARCD1 triggers cellular senescence and lipid accumulation, indicating a potential application of SMARCD1 in the prevention of lifestyle-related diseases.

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Section: Discussionmentioning

confidence: 97%

SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes

et al. 2017

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“…120 Similarly, hyperglycaemia and hyperlipidemia attenuate the circadian expression of core molecular clock genes in VSMC. 121, 122 …”

Section: Circadian Rhythm In Atherosclerosismentioning

confidence: 99%

Circadian Influence on Metabolism and Inflammation in Atherosclerosis

McAlpine

Świrski

2016

Circulation Research

105

128

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Many aspects of human health and disease display daily rhythmicity. The brain’s suprachiasmic nucleus, which interprets recurring external stimuli, and autonomous molecular networks in peripheral cells together set our biological circadian clock. Disrupted or misaligned circadian rhythms promote multiple pathologies including chronic inflammatory and metabolic diseases like atherosclerosis. Here, we discuss studies suggesting that circadian fluctuations in the vessel wall and in the circulation contribute to atherogenesis. Data from humans and mice indicate that an impaired molecular clock, disturbed sleep and shifting light-dark patterns influence leukocyte and lipid supply in the circulation and alter cellular behavior in atherosclerotic lesions. We propose that a better understanding of both local and systemic circadian rhythms in atherosclerosis will enhance clinical management, treatment and public health policy.

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“…So circadian rhythm disorder of these CCGs in PVSMCs should be attributed to the attenuation expression of clock genes we reported previously. Previous studies have confirmed that the hyperlipidaemia could impair the circadian clock in vivo and in vitro [6, 26]. Especially Chen S et al [6] showed that the free fatty acids (FFAs) could inhibit the clock genes expressions in contractile VSMCs via the suppression of Smarcd1.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have confirmed that the hyperlipidaemia could impair the circadian clock in vivo and in vitro [6, 26]. Especially Chen S et al [6] showed that the free fatty acids (FFAs) could inhibit the clock genes expressions in contractile VSMCs via the suppression of Smarcd1. In this study we revealed that the level of cholesterol, not triglycerides, was significantly elevated in PVSMCs which were most converted to synthetic stages.…”

Section: Discussionmentioning

confidence: 99%

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Intracellular high cholesterol content disorders the clock genes, apoptosis-related genes and fibrinolytic-related genes rhythmic expressions in human plaque-derived vascular smooth muscle cells

Lin

Tang

et al. 2017

Lipids Health Dis

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BackgroundThe clock genes are involved in regulating cardiovascular functions, and their expression disorders would lead to circadian rhythm disruptions of clock-controlled genes (CCGs), resulting in atherosclerotic plaque formation and rupture. Our previous study revealed the rhythmic expression of clock genes were attenuated in human plaque-derived vascular smooth muscle cells (PVSMCs), but failed to detect the downstream CCGs expressions and the underlying molecular mechanism. In this study, we examined the difference of CCGs rhythmic expression between human normal carotid VSMCs (NVSMCs) and PVSMCs. Furthermore, we compared the cholesterol and triglycerides levels between two groups and the link to clock genes and CCGs expressions.MethodsSeven health donors’ normal carotids and 19 carotid plaques yielded viable cultured NVSMCs and PVSMCs. The expression levels of target genes were measured by quantitative real-time PCR and Western-blot. The intracellular cholesterol and triglycerides levels were measured by kits.ResultThe circadian expressions of apoptosis-related genes and fibrinolytic-related genes were disordered. Besides, the cholesterol levels were significant higher in PVSMCs. After treated with cholesterol or oxidized low density lipoprotein (ox-LDL), the expressions of clock genes were inhibited; and the rhythmic expressions of clock genes, apoptosis-related genes and fibrinolytic-related genes were disturbed in NVSMCs, which were similar to PVSMCs.ConclusionThe results suggested that intracellular high cholesterol content of PVSMCs would lead to the disorders of clock genes and CCGs rhythmic expressions. And further studies should be conducted to demonstrate the specific molecular mechanisms involved.

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Hyperlipidaemia impairs the circadian clock and physiological homeostasis of vascular smooth muscle cells via the suppression of Smarcd1

Cited by 14 publications

References 46 publications

SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes

SMARCD1 regulates senescence-associated lipid accumulation in hepatocytes

Circadian Influence on Metabolism and Inflammation in Atherosclerosis

Intracellular high cholesterol content disorders the clock genes, apoptosis-related genes and fibrinolytic-related genes rhythmic expressions in human plaque-derived vascular smooth muscle cells

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