Rhythm changes of clock genes, apoptosis-related genes and atherosclerosis-related genes in apolipoprotein E knockout mice

Xu, Chen; Lü, Chao; Hua, Lingyang; Jin, Huajun; Li, Yin; Chen, SF; Ran, Qian

doi:10.1016/s0828-282x(09)70122-9

Cited by 20 publications

(18 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our studies also showed that mammalian apoptosis-associated genes c-myc and p53 exhibited circadian expression in C57BL/6J mice, but the rhythms lost completely in apoE-/- mice [18]. What changes occurred to the expression of circadian genes?…”

Section: Introductionmentioning

confidence: 76%

Effect of hyperlipidemia on the expression of circadian genes in apolipoprotein E knock-out atherosclerotic mice

et al. 2009

Self Cite

View full text Add to dashboard Cite

BackgroundCircadian patterns of cardiovascular vulnerability were well characterized, with a peak incidence of acute myocardial infarction and stroke secondary to atherosclerosis in the morning, which showed the circadian clock may take part in the pathological process of atherosclerosis induced by hyperlipidemia. Hence, the effect of hyperlipidemia on the expression of circadian genes was investigated in atherosclerotic mouse model.ResultsIn apoE-/-mice on regular chow or high-fat diet, an atherosclerotic mouse model induced by heperlipidemia, we found that the peak concentration of serum lipids was showed four or eight hours later in apoE-/- mice, compared to C57BL/6J mice. During the artificial light period, a reduce in circulating level of serum lipids corresponded with the observed increase of the expression levels of some the transcription factors involved in lipid metabolism, such as PPARα and RXRα. Meanwhile, the expression of circadian genes was changed following with amplitude reduced or the peak mRNA level delayed.ConclusionsOur studies indicated that heperlipidemia altered both the rhythmicity and expression of circadian genes. Diet-induced circadian disruption may affect the process of atherosclerosis and some acute cardiovascular disease.

show abstract

Section: Introductionmentioning

confidence: 76%

Effect of hyperlipidemia on the expression of circadian genes in apolipoprotein E knock-out atherosclerotic mice

et al. 2009

Self Cite

View full text Add to dashboard Cite

show abstract

“…The clock and atherosclerosis-related genes were found differentially expressed in ApoE −/− mice. For example, ApoE −/− mice showed phase delay in the circadian pattern of serum lipid levels11, altered expression of clock12 and atherosclerosis/thrombosis-related genes13.…”

mentioning

confidence: 99%

Degeneration and energy shortage in the suprachiasmatic nucleus underlies the circadian rhythm disturbance in ApoE−/− mice: implications for Alzheimer’s disease

Zhou

Gao

Nie

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Alzheimer’s disease (AD) patients suffer sleep disorders and circadian rhythm disturbances (CRDs). The underlying mechanisms are incompletely understood, and treatments are lacking. In this study, we characterized the locomotor activity, clock gene expression, morphological degeneration and energy metabolism of suprachiasmatic nucleus (SCN), together with retinal light sensing, in ApoE−/− mice, a model for AD. Compared with the control C57BL/6J mice, ApoE−/− mice exhibited disordered circadian locomotor activity under dim light and constant darkness, with impaired re-entrainment to phase change schedules. Decreased retinal melanopsin expression, together with amyloidosis and tau deposition, was evident in ApoE−/− mice. Mitochondrial and synaptic deterioration, altered SIRT1-mediated energy metabolism and clock gene expression were also observed in ApoE−/− SCN. Supplementation with fat or ketone bodies but not glucose, or intraperitoneal administration of nicotinamide, restored the locomotor rhythmicity and circadian expression of SIRT1 and clock genes, as well as reducing neurodegeneration. Taken together, ApoE deficiency induced degeneration and a significant disturbance in the SCN rhythmicity. Decline of retinal light sensing and SCN structural and metabolic deteriorations represented the major pathologies accounting for the CRDs in ApoE−/− mice. Our curative experiments may help develop future therapies to treat the CRDs and sleep disorders in AD patients.

show abstract

“…Isolation of RNA, primers for peroxisome proliferator-activated receptor-␥ (PPAR␥), lipoprotein lipase (LPL), TIE1, and PECAM1, and methods for real-time PCR have been previously described (1) except that an ABI Prism 7300 Sequence Detection System (Applied Biosystems, Foster City, CA) was used for the current study. Primers for murine preadipocyte factor 1 (Pref-1) (30), vascular endothelial growth factor (VEGF) (25), hypoxia-inducible factor-1␣ (HIF-1␣) (19), CD-68 (37), BAX (35), and CHOP (22) were from the literature. Primers for c-MET were forward 5=-GAAT-GTCGTCCTACACGGCC-3= and reverse 5=-CACTACACAGTCAG-GACACTGC-3=.…”

Section: Methodsmentioning

confidence: 99%

Hepatocyte growth factor regulates neovascularization in developing fat pads

White

Acton

Kamocka

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

White HM, Acton AJ, Kamocka MM, Considine RV. Hepatocyte growth factor regulates neovascularization in developing fat pads. Am J Physiol Endocrinol Metab 306: E189 -E196, 2014. First published December 3, 2013 doi:10.1152/ajpendo.00394.2013In this study, we used lentiviral-delivered shRNA to generate a clonal line of 3T3-F442A preadipocytes with stable silencing of hepatocyte growth factor (HGF) expression and examined the long-term consequence of this modification on fat pad development. HGF mRNA expression was reduced 94%, and HGF secretion 79% (P Ͻ 0.01), compared with preadipocytes treated with nontargeting shRNA. Fat pads derived from HGF knockdown preadipocytes were significantly smaller (P Ͻ 0.01) than control pads beginning at 3 days postinjection (0.022 Ϯ 0.003 vs. 0.037 Ϯ 0.004 g), and further decreased in size at day 7 (0.015 Ϯ 0.004 vs. 0.037 Ϯ 0.003 g) and day 14 (0.008 Ϯ 0.002 vs. 0.045 Ϯ 0.007 g). Expression of the endothelial cell genes TIE1 and PECAM1 increased over time in control fat pads (1.6 Ϯ 0.4 vs. 11.4 Ϯ 1.7 relative units at day 3 and 14, respectively; P Ͻ 0.05) but not in HGF knockdown fat pads (1.1 Ϯ 0.5 vs. 5.9 Ϯ 2.2 relative units at day 3 and 14). Contiguous vascular structures were observed in control fat pads but were much less developed in HGF knockdown fat pads. Differentiation of preadipocytes to mature adipocytes was significantly attenuated in HGF knockdown fat pads. Fat pads derived from preadipocytes with knockdown of the HGF receptor c-MET were smaller than control pads at day 3 postinjection (0.034 Ϯ 0.002 vs. 0.049 Ϯ 0.004 g; P Ͻ 0.05), and remained the same size through day 14. c-MET knockdown fat pads developed a robust vasculature, and preadipocytes differentiated to mature adipocytes. Overall these data suggest that preadipocyte-secreted HGF is an important regulator of neovascularization in developing fat pads. neovascularization; 3T3-F442A; TIE-1; PECAM-1; peroxisome proliferator-activated receptor-␥; lipoprotein lipase THERE IS INTENSE INTEREST in understanding the function of the adipose tissue vasculature in health and disease. It is known that angiogenesis is required to support the substantial growth potential of adipose tissue and that angiogenesis plays a critical role in the development of obesity (8,20,31). On the other hand, a number of studies have suggested that in obesity the adipose tissue is hypoxic, either due to rarefaction or insufficient blood flow, and that adipose tissue hypoxia is a root cause of the chronic inflammation characteristic of obesity (28, 31). In related areas of inquiry, studies to understand adipocyteregulated vascular growth are expected to provide novel insight into the mechanisms responsible for the greater risk of cancer in obese subjects (27), and there continues to be an active interest in targeting the adipose tissue vasculature as a means of treating and/or preventing obesity (5, 13, 34).Our laboratory is investigating the role of hepatocyte growth factor (HGF), a potent angiogenic and mitogenic factor, in the regulati...

show abstract

Rhythm changes of clock genes, apoptosis-related genes and atherosclerosis-related genes in apolipoprotein E knockout mice

Cited by 20 publications

References 33 publications

Effect of hyperlipidemia on the expression of circadian genes in apolipoprotein E knock-out atherosclerotic mice

Effect of hyperlipidemia on the expression of circadian genes in apolipoprotein E knock-out atherosclerotic mice

Degeneration and energy shortage in the suprachiasmatic nucleus underlies the circadian rhythm disturbance in ApoE−/− mice: implications for Alzheimer’s disease

Hepatocyte growth factor regulates neovascularization in developing fat pads

Contact Info

Product

Resources

About