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Article ; Online: Disturbed flow impairs MerTK-mediated efferocytosis in aortic endothelial cells during atherosclerosis.

Wu, Jinzi / Liu, Shijie / Banerjee, Oishani / Shi, Hang / Xue, Bingzhong / Ding, Zufeng

2024 Volume 14, Issue 6, Page(s) 2427–2441

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	c-Mer Tyrosine Kinase/metabolism ; c-Mer Tyrosine Kinase/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/physiopathology ; Humans ; Endothelial Cells/metabolism ; Animals ; Aorta/metabolism ; Aorta/pathology ; Mice ; Phagocytosis ; Apoptosis ; Proto-Oncogene Mas ; Male ; Mice, Inbred C57BL ; Diet, High-Fat ; Cells, Cultured ; Efferocytosis
Chemical Substances	c-Mer Tyrosine Kinase (EC 2.7.10.1) ; MERTK protein, human (EC 2.7.10.1) ; MAS1 protein, human ; Proto-Oncogene Mas ; Mertk protein, mouse (EC 2.7.10.1)
Language	English
Publishing date	2024-03-31
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.93036
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Big data analytics for MerTK genomics reveals its double-edged sword functions in human diseases.

Liu, Shijie / Wu, Jinzi / Yang, Daixuan / Xu, Jianliang / Shi, Hang / Xue, Bingzhong / Ding, Zufeng

Redox biology

2024 Volume 70, Page(s) 103061

Abstract: Rationale: MER proto-oncogene tyrosine kinase (MerTK) is a key receptor for the clearance of apoptotic cells (efferocytosis) and plays important roles in redox-related human diseases. We will explore MerTK biology in human cells, tissues, and diseases ... ...

Abstract	Rationale: MER proto-oncogene tyrosine kinase (MerTK) is a key receptor for the clearance of apoptotic cells (efferocytosis) and plays important roles in redox-related human diseases. We will explore MerTK biology in human cells, tissues, and diseases based on big data analytics. Methods: The human RNA-seq and scRNA-seq data about 42,700 samples were from NCBI Gene Expression Omnibus and analyzed by QIAGEN Ingenuity Pathway Analysis (IPA) with about 170,000 crossover analysis. MerTK expression was quantified as Log2 (FPKM + 0.1). Results: We found that, in human cells, MerTK is highly expressed in macrophages, monocytes, progenitor cells, alpha-beta T cells, plasma B cells, myeloid cells, and endothelial cells (ECs). In human tissues, MerTK has higher expression in plaque, blood vessels, heart, liver, sensory system, artificial tissue, bone, adrenal gland, central nervous system (CNS), and connective tissue. Compared to normal conditions, MerTK expression in related tissues is altered in many human diseases, including cardiovascular diseases, cancer, and brain disorders. Interestingly, MerTK expression also shows sex differences in many tissues, indicating that MerTK may have different impact on male and female. Finally, based on our proteomics from primary human aortic ECs, we validated the functions of MerTK in several human diseases, such as cancer, aging, kidney failure and heart failure. Conclusions: Our big data analytics suggest that MerTK may be a promising therapeutic target, but how it should be modulated depends on the disease types and sex differences. For example, MerTK inhibition emerges as a new strategy for cancer therapy due to it counteracts effect on anti-tumor immunity, while MerTK restoration represents a promising treatment for atherosclerosis and myocardial infarction as MerTK is cleaved in these disease conditions.
MeSH term(s)	Female ; Humans ; Male ; Apoptosis/genetics ; c-Mer Tyrosine Kinase/genetics ; Data Science ; Endothelial Cells/metabolism ; Genomics ; Neoplasms/metabolism ; Phagocytosis ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Brain Diseases/metabolism
Chemical Substances	c-Mer Tyrosine Kinase (EC 2.7.10.1) ; Proto-Oncogene Proteins ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; MERTK protein, human (EC 2.7.10.1)
Language	English
Publishing date	2024-02-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2024.103061
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Article ; Online: Chronic Exposure to Low-Molecular-Weight Polycyclic Aromatic Hydrocarbons Promotes Lipid Accumulation and Metabolic Inflammation.

Bright, Asia / Li, Fenfen / Movahed, Miranda / Shi, Hang / Xue, Bingzhong

Biomolecules

2023 Volume 13, Issue 2

Abstract: 2-naphthol is a low-molecular-weight (LMW) polycyclic aromatic hydrocarbon (PAH) and air pollutant associated with childhood obesity. There has been a recent emergence of studies on the consequences of PAHs on human health. Current epidemiological ... ...

Abstract	2-naphthol is a low-molecular-weight (LMW) polycyclic aromatic hydrocarbon (PAH) and air pollutant associated with childhood obesity. There has been a recent emergence of studies on the consequences of PAHs on human health. Current epidemiological reports suggest LMW-PAHs may contribute to obesity incidences in children, yet most studies focus on high-molecular-weight PAHs. This study explores 2-naphthol's impact on obesity and obesity-associated metabolic disorders. To investigate 2-naphthol's effect on lipid metabolism and inflammation, we employed 3T3-L1 and BAT1 cell lines to model white and brown adipocytes, respectively, alongside a murine macrophage cell line (RAW264.7). We found that 2-naphthol increased the expression of key adipogenic and lipogenic genes while decreasing lipolytic gene expression in chronically treated 3T3-L1 and BAT1 adipocytes. In addition, chronic 2-naphthol treatment also suppressed adrenergic-stimulated thermogenic gene expression in BAT1 brown adipocytes. In consistence, an increase in lipid accumulation was demonstrated in BODIPY and Oil Red O-stained adipocytes. Additionally, 3T3-L1 adipocytes and RAW264.7 macrophages chronically exposed to 2-naphthol showed upregulated mRNA expression of major inflammatory cytokines (e.g., tumor necrosis factor α (
MeSH term(s)	Child ; Humans ; Animals ; Mice ; Pediatric Obesity ; Inflammation ; Adipocytes, Brown ; Lipids
Chemical Substances	2-naphthol (P2Z71CIK5H) ; Lipids
Language	English
Publishing date	2023-01-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom13020196
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Article ; Online: Neuronal GHS-R Differentially Modulates Feeding Patterns under Normal and Obesogenic Conditions.

Lee, Jong Han / Xue, Bingzhong / Chen, Zheng / Sun, Yuxiang

Biomolecules

2022 Volume 12, Issue 2

Abstract: The orexigenic hormone ghrelin increases food intake and promotes obesity through its receptor, growth hormone secretagogue receptor (GHS-R). We previously reported two neuron-specific GHS-R knockout mouse lines, namely pan-neuronal deletion by Syn1-cre ... ...

Abstract	The orexigenic hormone ghrelin increases food intake and promotes obesity through its receptor, growth hormone secretagogue receptor (GHS-R). We previously reported two neuron-specific GHS-R knockout mouse lines, namely pan-neuronal deletion by Syn1-cre and hypothalamic deletion by AgRP-cre, exhibiting differential diet-dependent effects on body weight. GHS-R deficiency in neurons elicited less pronounced metabolic effects under regular diet (RD) than high fat diet (HFD). While there was no difference in total food intake of HFD in either mouse line, Syn1-cre; Ghsr
MeSH term(s)	Animals ; Eating ; Feeding Behavior ; Hypothalamus/metabolism ; Mice ; Mice, Inbred C57BL ; Neurons/metabolism ; Receptors, Ghrelin/genetics
Chemical Substances	Receptors, Ghrelin
Language	English
Publishing date	2022-02-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12020293
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Article ; Online: Diverse and Complementary Effects of Ghrelin and Obestatin.

Villarreal, Daniel / Pradhan, Geetali / Zhou, Yu / Xue, Bingzhong / Sun, Yuxiang

Biomolecules

2022 Volume 12, Issue 4

Abstract: Ghrelin and obestatin are two "sibling proteins" encoded by the same preproghrelin gene but possess an array of diverse and complex functions. While there are ample literature documenting ghrelin's functions, the roles of obestatin are less clear and ... ...

Abstract	Ghrelin and obestatin are two "sibling proteins" encoded by the same preproghrelin gene but possess an array of diverse and complex functions. While there are ample literature documenting ghrelin's functions, the roles of obestatin are less clear and controversial. Ghrelin and obestatin have been perceived to be antagonistic initially; however, recent studies challenge this dogma. While they have opposing effects in some systems, they function synergistically in other systems, with many functions remaining debatable. In this review, we discuss their functional relationship under three "C" categories, namely complex, complementary, and contradictory. Their functions in food intake, weight regulation, hydration, gastrointestinal motility, inflammation, and insulin secretion are complex. Their functions in pancreatic beta cells, cardiovascular, muscle, neuroprotection, cancer, and digestive system are complementary. Their functions in white adipose tissue, thermogenesis, and sleep regulation are contradictory. Overall, this review accumulates the multifaceted functions of ghrelin and obestatin under both physiological and pathological conditions, with the intent of contributing to a better understanding of these two important gut hormones.
MeSH term(s)	Adipose Tissue, White/metabolism ; Ghrelin/metabolism ; Insulin Secretion
Chemical Substances	Ghrelin
Language	English
Publishing date	2022-03-29
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom12040517
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Article ; Online: Adipocyte

Li, Fenfen / Wang, Shirong / Cui, Xin / Jing, Jia / Yu, Liqing / Xue, Bingzhong / Shi, Hang

Cells

2022 Volume 11, Issue 2

Abstract: While the main function of white adipose tissue (WAT) is to store surplus of energy as triacylglycerol, that of brown adipose tissue (BAT) is to burn energy as heat. Epigenetic mechanisms participate prominently in both WAT and BAT energy metabolism. We ... ...

Abstract	While the main function of white adipose tissue (WAT) is to store surplus of energy as triacylglycerol, that of brown adipose tissue (BAT) is to burn energy as heat. Epigenetic mechanisms participate prominently in both WAT and BAT energy metabolism. We previously reported that the histone demethylase ubiquitously transcribed tetratricopeptide (
MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue, Brown/metabolism ; Adiposity ; Animals ; Cold Temperature ; Diet, High-Fat ; Fatty Liver/complications ; Fatty Liver/metabolism ; Fatty Liver/pathology ; Feeding Behavior ; Glucose Intolerance/metabolism ; Histone Demethylases/deficiency ; Histone Demethylases/metabolism ; Insulin Resistance ; Metabolic Syndrome/complications ; Metabolic Syndrome/physiopathology ; Mice, Knockout ; Thermogenesis ; Mice
Chemical Substances	Histone Demethylases (EC 1.14.11.-) ; Utx protein, mouse (EC 1.14.11.-)
Language	English
Publishing date	2022-01-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11020181
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Article ; Online: Adipocyte Utx Deficiency Promotes High-Fat Diet-Induced Metabolic Dysfunction in Mice

Fenfen Li / Shirong Wang / Xin Cui / Jia Jing / Liqing Yu / Bingzhong Xue / Hang Shi

Cells, Vol 11, Iss 181, p

2022 Volume 181

Abstract	While the main function of white adipose tissue (WAT) is to store surplus of energy as triacylglycerol, that of brown adipose tissue (BAT) is to burn energy as heat. Epigenetic mechanisms participate prominently in both WAT and BAT energy metabolism. We previously reported that the histone demethylase ubiquitously transcribed tetratricopeptide ( Utx ) is a positive regulator of brown adipocyte thermogenesis. Here, we aimed to investigate whether Utx also regulates WAT metabolism in vivo. We generated a mouse model with Utx deficiency in adipocytes (AUTXKO). AUTXKO animals fed a chow diet had higher body weight, more fat mass and impaired glucose tolerance. AUTXKO mice also exhibited cold intolerance with an impaired brown fat thermogenic program. When challenged with high-fat diet (HFD), AUTXKO mice displayed adipose dysfunction featured by suppressed lipogenic pathways, exacerbated inflammation and fibrosis with less fat storage in adipose tissues and more lipid storage in the liver; as a result, AUTXKO mice showed a disturbance in whole body glucose homeostasis and hepatic steatosis. Our data demonstrate that Utx deficiency in adipocytes limits adipose tissue expansion under HFD challenge and induces metabolic dysfunction via adipose tissue remodeling. We conclude that adipocyte Utx is a key regulator of systemic metabolic homeostasis.
Keywords	epigenetics ; obesity ; adipose tissue ; Utx ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Single ethanol binge causes severe liver injury in mice fed Western diet.

Yeh, Yu-Te / Wu, Xiangdong / Ma, Yinyan / Ying, Zhekang / He, Ling / Xue, Bingzhong / Shi, Hang / Choi, Youngshim / Yu, Liqing

Hepatology communications

2023 Volume 7, Issue 7

Abstract: Background and aims: Alcohol-associated liver disease (ALD) and NAFLD often coexist in Western societies that consume energy-rich and cholesterol-containing Western diets. Increased rates of ALD mortality in young people in these societies are likely ... ...

Abstract	Background and aims: Alcohol-associated liver disease (ALD) and NAFLD often coexist in Western societies that consume energy-rich and cholesterol-containing Western diets. Increased rates of ALD mortality in young people in these societies are likely attributable to binge drinking. It is largely unknown how alcohol binge causes liver damage in the setting of Western diets. Approach and results: In this study, we showed that a single ethanol binge (5 g/kg body weight) induced severe liver injury as shown by marked increases in serum activities of the 2 aminotransferases AST and ALT in C57BL/6J mice that have been fed a Western diet for 3 weeks. The Western diet plus binge ethanol-fed mice also displayed severe lipid droplet deposition and high contents of triglycerides and cholesterol in the liver, which were associated with increased lipogenic and reduced fatty acid oxidative gene expression. These animals had the highest Cxcl1 mRNA expression and myeloperoxidase (MPO)-positive neutrophils in the liver. Their hepatic ROS and lipid peroxidation were the highest, but their hepatic levels of mitochondrial oxidative phosphorylation proteins remained largely unaltered. Hepatic levels of several ER stress markers, including mRNAs for CHOP, ERO1A, ERO1B, BIM, and BIP, as well as Xbp1 splicing and proteins for BIP/GRP78 and IRE-α were also the highest in these animals. Interestingly, Western diet feeding for 3 weeks or ethanol binge dramatically increased hepatic caspase 3 cleavage, and the combination of the 2 did not further increase it. Thus, we successfully established a murine model of acute liver injury by mimicking human diets and binge drinking. Conclusions: This simple Western diet plus single ethanol binge model recapitulates major hepatic phenotypes of ALD, including steatosis and steatohepatitis characterized by neutrophil infiltration, oxidative stress, and ER stress.
MeSH term(s)	Humans ; Animals ; Mice ; Adolescent ; Mice, Inbred C57BL ; Ethanol/toxicity ; Diet, Western/adverse effects ; Binge Drinking/complications ; Liver Diseases, Alcoholic ; Non-alcoholic Fatty Liver Disease/etiology
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2023-06-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1097/HC9.0000000000000174
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Mechanisms for AgRP neuron-mediated regulation of appetitive behaviors in rodents.

Thomas, M Alex / Xue, Bingzhong

Physiology & behavior

2017 Volume 190, Page(s) 34–42

Abstract: The obesity epidemic is a major health and economic burden facing both developed and developing countries worldwide. Interrogation of the central and peripheral mechanisms regulating ingestive behaviors have primarily focused on food intake, and in the ... ...

Abstract	The obesity epidemic is a major health and economic burden facing both developed and developing countries worldwide. Interrogation of the central and peripheral mechanisms regulating ingestive behaviors have primarily focused on food intake, and in the process uncovered a detailed neuroanatomical framework controlling this behavior. However, these studies have largely ignored the behaviors that bring animals, including humans, in contact with food. It is therefore useful to dichotomize ingestive behaviors as appetitive (motivation to find and store food) and consummatory (consumption of food once found), and utilize an animal model that naturally displays these behaviors. Recent advances in genetics have facilitated the identification of several neuronal populations critical for regulating ingestive behaviors in mice, and novel functions of these neurons and neuropeptides in regulating appetitive behaviors in Siberian hamsters, a natural model of food foraging and food hoarding, have been identified. To this end, hypothalamic agouti-related protein/neuropeptide Y expressing neurons (AgRP neurons) have emerged as a critical regulator of ingestive behaviors. Recent studies by Dr. Timothy Bartness and others have identified several discrete mechanisms through which peripheral endocrine signals regulate AgRP neurons to control food foraging, food hoarding, and food intake. We review here recent advances in our understanding of the neuroendocrine control of ingestive behaviors in Siberian hamsters and other laboratory rodents, and identify novel mechanisms through which AgRP neurons mediate appetitive and consummatory behaviors.
MeSH term(s)	Agouti-Related Protein/physiology ; Animals ; Appetite/physiology ; Eating/physiology ; Feeding Behavior/physiology ; Neurons/physiology
Chemical Substances	Agouti-Related Protein
Language	English
Publishing date	2017-10-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3907-x
ISSN	1873-507X ; 0031-9384
ISSN (online)	1873-507X
ISSN	0031-9384
DOI	10.1016/j.physbeh.2017.10.006
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Article: Crosstalk between Gut Sensory Ghrelin Signaling and Adipose Tissue Sympathetic Outflow Regulates Metabolic Homeostasis.

Alex Thomas, M / Cui, Xin / Artinian, Liana R / Cao, Qiang / Jing, Jia / Silva, Felipe C / Wang, Shirong / Zigman, Jeffrey M / Sun, Yuxiang / Shi, Hang / Xue, Bingzhong

bioRxiv : the preprint server for biology

2023

Abstract: The stomach-derived orexigenic hormone ghrelin is a key regulator of energy homeostasis and metabolism in humans. The ghrelin receptor, growth hormone secretagogue receptor 1a (GHSR), is widely expressed in the brain and gastrointestinal vagal sensory ... ...

Abstract	The stomach-derived orexigenic hormone ghrelin is a key regulator of energy homeostasis and metabolism in humans. The ghrelin receptor, growth hormone secretagogue receptor 1a (GHSR), is widely expressed in the brain and gastrointestinal vagal sensory neurons, and neuronal GHSR knockout results in a profoundly beneficial metabolic profile and protects against diet-induced obesity (DIO) and insulin resistance. Here we show that in addition to the well characterized vagal GHSR, GHSR is robustly expressed in gastrointestinal sensory neurons emanating from spinal dorsal root ganglia. Remarkably, sensory neuron GHSR deletion attenuates DIO through increased energy expenditure and sympathetic outflow to adipose tissue independent of food intake. In addition, neuronal viral tract tracing reveals prominent crosstalk between gut non-vagal sensory afferents and adipose sympathetic outflow. Hence, these findings demonstrate a novel gut sensory ghrelin signaling pathway critical for maintaining energy homeostasis.
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.11.25.568689
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