scholarly journals Noninvasive 40-Hz Light Flicker Rescues Circadian Behavior and Abnormal Lipid Metabolism Induced by Acute Ethanol Exposure via Improving SIRT1 and the Circadian Clock in the Liver-Brain Axis

2020 ◽  
Vol 11 ◽  
Author(s):  
Youli Yao ◽  
Wenjiang Zhang ◽  
Ruibo Ming ◽  
Qiyu Deng ◽  
Along Zuo ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Circadian Clock ◽  
Ethanol Exposure ◽  
Acute Ethanol ◽  
Light Flicker ◽  
Abnormal Lipid Metabolism ◽  
Circadian Behavior ◽  
40 Hz

scholarly journals Non-invasive 40-Hz Light Flicker Ameliorates Alzheimer’s-Associated Rhythm Disorder via Regulating Central Circadian Clock in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Youli Yao ◽  
Ying Ying ◽  
Qiyu Deng ◽  
Wenjiang Zhang ◽  
Huazhang Zhu ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Non Invasive ◽  
Rhythm Disorder ◽  
Light Flicker ◽  
40 Hz

scholarly journals Mirtronic miR-4646-5p promotes gastric cancer metastasis by regulating ABHD16A and metabolite lysophosphatidylserines

2021 ◽  
Author(s):  
Liping Yang ◽  
Yixuan Hou ◽  
Yan-e Du ◽  
Qiao Li ◽  
Fanlin Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Lipid Metabolism ◽  
Gastric Cancer Cell ◽  
Cancer Metastasis ◽  
Host Gene ◽  
Diagnostic Biomarker ◽  
Invasion And Metastasis ◽  
Gastric Cancer Cells ◽  
Tumor Progress ◽  
Abnormal Lipid Metabolism

AbstractThe aberrant classical miRNAs are considered to play significant roles in tumor progression. However, it remains unclear for nonclassical miRNAs, a set of Drosha-independent miRNAs in the process of various biology. Here, we reveal that a nonclassical miR-4646-5p plays a pivotal role in gastric cancer (GC) metastasis. MiR-4646-5p, one of Drosha-independent mirtronic miRNA, is aberrant up-regulated in Drosha-low expressed GC and Drosha-knockdown gastric cancer cells. Mirtronic miR-4646-5p is a specific transcription splicing product of intron 3 of the host gene Abhd16a with the aid of SRSF2. The enhanced miR-4646-5p can stabilize HIF1A by targeting PHD3 to positive feedback regulate Abhd16a and miR-4646-5p itself expressions. ABHD16A, as an emerging phosphatidylserine-specific lipase, involves in lipid metabolism leading to lysophosphatidylserines (lyso-PSs) accumulation, which stimulates RhoA and downstream LIMK/cofilin cascade activity through GPR34/Gi subunit, thus causes metastasis of gastric cancer. In addition, miR-4646-5p/PHD3/HIF1A signaling can also up-regulate RhoA expression and synergistically promote gastric cancer cell invasion and metastasis. Our study provides new insights of nonclassical mirtronic miRNA on tumor progress and may serve as a new diagnostic biomarker for gastric cancer. MiR-4646-5p and its host gene Abhd16a mediated abnormal lipid metabolism may be a new target for clinical treatment of gastric cancer.

Apigenin protects mice against 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced cholestasis

2021 ◽  
Vol 12 (5) ◽  
pp. 2323-2334
Author(s):  
Shihong Zheng ◽  
Peichang Cao ◽  
Zequn Yin ◽  
Xuerui Wang ◽  
Yuanli Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Metabolism ◽  
Liver Fibrosis ◽  
Liver Damage ◽  
Liver Diseases ◽  
Potential Drug ◽  
Abnormal Lipid Metabolism ◽  
And Oxidative Stress

Apigenin prevented the DDC-induced abnormal lipid metabolism, liver damage and liver fibrosis by reducing inflammation and oxidative stress. Apigenin might be a potential drug for the treatment of cholestatic liver diseases.

Differential gene expression and lipid metabolism in fatty liver induced by acute ethanol treatment in mice

2007 ◽  
Vol 223 (3) ◽  
pp. 225-233 ◽  
Author(s):  
Hu-Quan Yin ◽  
Mingoo Kim ◽  
Ju-Han Kim ◽  
Gu Kong ◽  
Kyung-Sun Kang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
Differential Gene Expression ◽  
Ethanol Treatment ◽  
Acute Ethanol ◽  
Differential Gene

scholarly journals Acute ethanol exposure disrupts VEGF receptor cell signaling in endothelial cells

2008 ◽  
Vol 295 (1) ◽  
pp. H174-H184 ◽  
Author(s):  
Katherine A. Radek ◽  
Elizabeth J. Kovacs ◽  
Richard L. Gallo ◽  
Luisa A. DiPietro
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Signaling ◽  
Network Formation ◽  
Ethanol Exposure ◽  
Capillary Network ◽  
Ethanol Metabolism ◽  
Vegf Receptor ◽  
Acute Ethanol

Physiological angiogenesis is regulated by various factors, including signaling through vascular endothelial growth factor (VEGF) receptors. We previously reported that a single dose of ethanol (1.4 g/kg), yielding a blood alcohol concentration of 100 mg/dl, significantly impairs angiogenesis in murine wounds, despite adequate levels of VEGF, suggesting direct effects of ethanol on endothelial cell signaling (40). To examine the mechanism by which ethanol influences angiogenesis in wounds, we employed two different in vitro angiogenesis assays to determine whether acute ethanol exposure (100 mg/dl) would have long-lasting effects on VEGF-induced capillary network formation. Ethanol exposure resulted in reduced VEGF-induced cord formation on collagen and reduced capillary network structure on Matrigel in vitro. In addition, ethanol exposure decreased expression of endothelial VEGF receptor-2, as well as VEGF receptor-2 phosphorylation in vitro. Inhibition of ethanol metabolism by 4-methylpyrazole partially abrogated the effect of ethanol on endothelial cell cord formation. However, mice treated with t-butanol, an alcohol not metabolized by alcohol dehydrogenase, exhibited no change in wound vascularity. These results suggest that products of ethanol metabolism are important factors in the development of ethanol-induced changes in endothelial cell responsiveness to VEGF. In vivo, ethanol exposure caused both decreased angiogenesis and increased hypoxia in wounds. Moreover, in vitro experiments demonstrated a direct effect of ethanol on the response to hypoxia in endothelial cells, as ethanol diminished nuclear hypoxia-inducible factor-1α protein levels. Together, the data establish that acute ethanol exposure significantly impairs angiogenesis and suggest that this effect is mediated by changes in endothelial cell responsiveness to both VEGF and hypoxia.

scholarly journals Circadian Clock Regulation of Hepatic Lipid Metabolism by Modulation of m6A mRNA Methylation

Cell Reports ◽  
2018 ◽  
Vol 25 (7) ◽  
pp. 1816-1828.e4 ◽  
Author(s):  
Xiang Zhong ◽  
Jiayao Yu ◽  
Katya Frazier ◽  
Xiaocheng Weng ◽  
Yi Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Circadian Clock ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid ◽  
Mrna Methylation
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