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Fu SJ, Xu MT, Wang B, Li BW, Ling H, Li Y, Wang Q, Liu XT, Zhang XY, Li AL, Liu MM. Global trend and future landscape of intestinal microcirculation research from 2000 to 2021: A scientometric study. World J Gastroenterol 2023; 29:1523-1535. [PMID: 36998427 PMCID: PMC10044859 DOI: 10.3748/wjg.v29.i9.1523] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/18/2022] [Revised: 02/01/2023] [Accepted: 02/24/2023] [Indexed: 03/07/2023] Open
Abstract
BACKGROUND The intestinal microcirculation functions in food absorption and metabolic substance exchanges. Accumulating evidence indicates that intestinal microcirculatory dysfunction is a significant source of multiple gastrointestinal diseases. To date, there has not been a scientometric analysis of intestinal microcirculatory research.
AIM To investigate the current status, development trends, and frontiers of intestinal microcirculatory research based on bibliometric analysis.
METHODS VOSviewer and CiteSpace 6.1.R2 were used to identify the overall characteristics and knowledge map of intestinal microcirculatory research based on the core literature published from 2000 to 2021 in the Web of Science database. The characteristics of each article, country of origin, institution, journal, cocitations, and other information were analyzed and visualized.
RESULTS There were 1364 publications enrolled in the bibliometric analysis, exhibiting an upward trend from 2000 to 2021 with increased participation worldwide. The United States and Dalhousie University took the lead among countries and institutions, respectively. Shock was the most prolific journal, and Nature Reviews Microbiology Clinical had the most citations. The topical hotspots and frontiers in intestinal microcirculatory research were centered on the pathological processes of functional impairment of intestinal microvessels, diverse intestinal illnesses, and clinical treatment.
CONCLUSION Our study highlights insights into trends of the published research on the intestinal microcirculation and offers serviceable guidance to researchers by summarizing the prolific areas in intestinal disease research to date.
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Affiliation(s)
- Sun-Jing Fu
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Meng-Ting Xu
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Bing Wang
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Bing-Wei Li
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Hao Ling
- Department of Radiology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha 410004, Hunan Province, China
| | - Yuan Li
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Qin Wang
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Xue-Ting Liu
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Xiao-Yan Zhang
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Ai-Ling Li
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
| | - Ming-Ming Liu
- Institute of Microcirculation, Key Laboratory of Microcirculation, Ministry of Health, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
- Diabetes Research Center, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China
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Hu C, Yan C, Wu Y, Tao E, Guo R, Zhu Z, Chen X, Fang M, Jiang M. Low FODMAP Diet Relieves Visceral Hypersensitivity and Is Associated with Changes in Colonic Microcirculation in Water Avoidance Mice Model. Nutrients 2023; 15:1155. [PMID: 36904154 PMCID: PMC10004816 DOI: 10.3390/nu15051155] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2023] [Revised: 02/20/2023] [Accepted: 02/22/2023] [Indexed: 03/02/2023] Open
Abstract
(1) Background: Irritable bowel syndrome (IBS) is a global public health problem, the pathogenesis of which has not been fully explored. Limiting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) can relieve symptoms in some patients with IBS. Studies have shown that normal microcirculation perfusion is necessary to maintain the primary function of the gastrointestinal system. Here, we hypothesized that IBS pathogenesis might be related to abnormalities in colonic microcirculation. A low-FODMAP diet could alleviate visceral hypersensitivity (VH) by improving colonic microcirculation; (2) Methods: C57BL/6 mice were raised to establish an IBS-like rodent model using water avoidance (WA) stress or SHAM-WA as a control, one hour per day for ten days. The mice in the WA group were administered different levels of the FODMAP diet: 2.1% regular FODMAP (WA-RF), 10% high FODMAP diet (WA-HF), 5% medium FODMAP diet (WA-MF), and 0% low FODMAP diet (WA-LF) for the following 14 days. The body weight and food consumption of the mice were recorded. Visceral sensitivity was measured as colorectal distention (CRD) using the abdominal withdrawal reflex (AWR) score. Colonic microcirculation was assessed using laser speckle contrast imaging (LCSI). Vascular endothelial-derived growth factor (VEGF) was detected using immunofluorescence staining; (3) Results: The threshold values of CRD pressure in the WA-RF, WA-HF, and WA-MF groups were significantly lower than those in the SHAM-WA group. Moreover, we observed that colonic microcirculation perfusion decreased, and the expression of VEGF protein increased in these three groups of mice. Interestingly, a low-FODMAP dietary intervention could reverse this situation. Specifically, a low-FODMAP diet increased colonic microcirculation perfusion, reduced VEGF protein expression in mice, and increased the threshold of VH. There was a significant positive correlation between colonic microcirculation and threshold for VH; (4) Conclusions: These results demonstrate that a low-FODMAP diet can alter VH by affecting colonic microcirculation. Changes in intestinal microcirculation may be related to VEGF expression.
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Affiliation(s)
- Chenmin Hu
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
- Department of Pediatrics, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Hangzhou 310006, China
| | - Chenxi Yan
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
| | - Yuhao Wu
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
| | - Enfu Tao
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
| | - Rui Guo
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
| | - Zhenya Zhu
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
| | - Xiaolong Chen
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
| | - Marong Fang
- Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou 310052, China
- Institute of System Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China
| | - Mizu Jiang
- Endoscopy Center and Gastrointestinal Laboratory, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
- Department of Gastroenterology, Children’s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, National Children’s Regional Medical Center, Hangzhou 310052, China
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Farrugia A, Mori F. Therapeutic solutions of human albumin - The possible effect of process-induced molecular alterations on clinical efficacy and safety. J Pharm Sci 2022; 111:1292-1308. [PMID: 35276228 DOI: 10.1016/j.xphs.2022.03.005] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/04/2021] [Revised: 03/04/2022] [Accepted: 03/04/2022] [Indexed: 12/14/2022]
Abstract
Human albumin solutions were developed as therapeutic during the Second World War to address blood loss due to battlefield injury. This indication was based on the recognition that albumin provided most of the oncotic capacity of human plasma. For the succeeding sixty years, this formed the basis for the use of albumin in traumatology and emergency medicine. In more recent times, the pharmacological properties arising from albumin's complex structure have become a focus of attention by clinical researchers. In particular, albumin, through anti-inflammatory and anti-oxidant properties, has been proposed as an agent for the treatment of sepsis, cirrhosis and other inflammatory states. Some evidence for these indications has accrued from a number of small clinical trials and observational studies. These studies have not been confirmed in other large trials. Together with other investigators, we have shown that the process of plasma fractionation results in alterations in the structure of albumin, including those parts of the molecule involved in anti-oxidant and anti-inflammatory effects. Albumin products from diverse manufacturers show heterogeneity in their ability to address these effects. In this article, we review the historical development of albumin solutions, pointing out the variations in fractionation chemistries which different manufacturers have adopted. We suggest ways by which the manufacturing processes have contributed to variations in the physico-chemical properties of molecule. We review the outcomes of clinical studies assessing the role of albumin in ameliorating conditions such as sepsis and cirrhosis, and we speculate as to the extent which heterogeneity in the products may have contributed to variable clinical outcomes. Finally, we argue for a change in the perception of the plasma product industry and its regulatory overseers. Historically, albumin has been viewed as a generic commodity, with different preparations being interchangeable in their clinical application. We suggest that this implied biosimilarity is not necessarily applicable for different albumin solutions. The use of albumin, in indications other than its historical role as a plasma expander, can only be validated by clinical investigation of each separate albumin product.
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Affiliation(s)
- Albert Farrugia
- Faculty of Health and Medical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley WA 6009, Perth, Australia.
| | - Filippo Mori
- Kedrion S.p.A., Research and Innovation Department, Via di Fondovalle, Loc., Bolognana 55027, Gallicano (LU), Italy
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Bayer F, Ascher S, Kiouptsi K, Kittner JM, Stauber RH, Reinhardt C. Colonization with Altered Schaedler Flora Impacts Leukocyte Adhesion in Mesenteric Ischemia-Reperfusion Injury. Microorganisms 2021; 9:1601. [PMID: 34442681 PMCID: PMC8401286 DOI: 10.3390/microorganisms9081601] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/30/2021] [Revised: 07/23/2021] [Accepted: 07/26/2021] [Indexed: 12/12/2022] Open
Abstract
The microbiota impacts mesenteric ischemia-reperfusion injury, aggravating the interaction of leukocytes with endothelial cells in mesenteric venules. The role of defined gut microbiomes in this life-threatening pathology is unknown. To investigate how a defined model microbiome affects the adhesion of leukocytes in mesenteric ischemia-reperfusion, we took advantage of gnotobiotic isolator technology and transferred altered Schaedler flora (ASF) from C3H/HeNTac to germ-free C57BL/6J mice. We were able to detect all eight bacterial taxa of ASF in fecal samples of colonized C57BL/6J mice by PCR. Applying qRT-PCR for quantification of species-specific 16S rDNA sequences of ASF bacteria, we found a major shift in the abundance of ASF 500, which was greater in C57BL/6J mice relative to the C3H/HeNTac founder breeding pair. Using high-speed epifluorescence intravital microscopy to visualize the venules of the small bowel mesentery, we found that gnotobiotic ASF-colonized mice showed reduced leukocyte adherence, both pre- and post-ischemia. Relative to germ-free mice, the counts of adhering leukocytes were increased pre-ischemia but did not significantly increase in ASF-colonized mice in the post-ischemic state. Collectively, our results suggest a protective role of the minimal microbial consortium ASF in mesenteric ischemia-reperfusion injury.
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Affiliation(s)
- Franziska Bayer
- Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany; (F.B.); (S.A.); (K.K.)
| | - Stefanie Ascher
- Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany; (F.B.); (S.A.); (K.K.)
- Department of Chemistry, Biochemistry, Johannes Gutenberg-University Mainz, 55128 Mainz, Germany
| | - Klytaimnistra Kiouptsi
- Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany; (F.B.); (S.A.); (K.K.)
| | - Jens M. Kittner
- Department of Medicine, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany;
- Diakonie Klinikum Neunkirchen, Brunnenstraße 20, 66538 Neunkirchen, Germany
| | - Roland H. Stauber
- Department of Nanobiomedicine/ENT, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany;
| | - Christoph Reinhardt
- Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany; (F.B.); (S.A.); (K.K.)
- German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, 55131 Mainz, Germany
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Scalise AA, Kakogiannos N, Zanardi F, Iannelli F, Giannotta M. The blood-brain and gut-vascular barriers: from the perspective of claudins. Tissue Barriers 2021; 9:1926190. [PMID: 34152937 PMCID: PMC8489939 DOI: 10.1080/21688370.2021.1926190] [Citation(s) in RCA: 41] [Impact Index Per Article: 10.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/08/2023] Open
Abstract
In some organs, such as the brain, endothelial cells form a robust and highly selective blood-to-tissue barrier. However, in other organs, such as the intestine, endothelial cells provide less stringent permeability, to allow rapid exchange of solutes and nutrients where needed. To maintain the structural and functional integrity of the highly dynamic blood–brain and gut–vascular barriers, endothelial cells form highly specialized cell-cell junctions, known as adherens junctions and tight junctions. Claudins are a family of four-membrane-spanning proteins at tight junctions and they have both barrier-forming and pore-forming properties. Tissue-specific expression of claudins has been linked to different diseases that are characterized by barrier impairment. In this review, we summarize the more recent progress in the field of the claudins, with particular attention to their expression and function in the blood–brain barrier and the recently described gut–vascular barrier, under physiological and pathological conditions. Abbreviations: 22q11DS 22q11 deletion syndrome; ACKR1 atypical chemokine receptor 1; AD Alzheimer disease; AQP aquaporin; ATP adenosine triphosphate; Aβ amyloid β; BAC bacterial artificial chromosome; BBB blood-brain barrier; C/EBP-α CCAAT/enhancer-binding protein α; cAMP cyclic adenosine monophosphate (or 3ʹ,5ʹ-cyclic adenosine monophosphate); CD cluster of differentiation; CNS central nervous system; DSRED discosoma red; EAE experimental autoimmune encephalomyelitis; ECV304 immortalized endothelial cell line established from the vein of an apparently normal human umbilical cord; EGFP enhanced green fluorescent protein; ESAM endothelial cell-selective adhesion molecule; GLUT-1 glucose transporter 1; GVB gut-vascular barrier; H2B histone H2B; HAPP human amyloid precursor protein; HEK human embryonic kidney; JACOP junction-associated coiled coil protein; JAM junctional adhesion molecules; LYVE1 lymphatic vessel endothelial hyaluronan receptor 1; MADCAM1 mucosal vascular addressin cell adhesion molecule 1; MAPK mitogen-activated protein kinase; MCAO middle cerebral artery occlusion; MMP metalloprotease; MS multiple sclerosis; MUPP multi-PDZ domain protein; PATJ PALS-1-associated tight junction protein; PDGFR-α platelet-derived growth factor receptor α polypeptide; PDGFR-β platelet-derived growth factor receptor β polypeptide; RHO rho-associated protein kinase; ROCK rho-associated, coiled-coil-containing protein kinase; RT-qPCR real time quantitative polymerase chain reactions; PDGFR-β soluble platelet-derived growth factor receptor, β polypeptide; T24 human urinary bladder carcinoma cells; TG2576 transgenic mice expressing the human amyloid precursor protein; TNF-α tumor necrosis factor α; WTwild-type; ZO zonula occludens.
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Wang X, Liu D. Hemodynamic Influences on Mesenteric Blood Flow in Shock Conditions. Am J Med Sci 2021; 362:243-251. [PMID: 33961846 DOI: 10.1016/j.amjms.2021.04.014] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/26/2020] [Revised: 02/16/2021] [Accepted: 04/26/2021] [Indexed: 01/20/2023]
Abstract
The gastrointestinal (GI) system, is most vulnerable to hypoperfusion among the splanchnic organs. Disturbed perfusion of the mesenteric area may lead to GI dysfunction, cause further injury to the patients and even vital outcomes. However, due to the limitation of detection methods, the hemodynamic influences on mesenteric blood flow in clinical practice are not fully understood. By elucidating the underlying mechanisms, we may be able to recognize disturbed GI perfusion and eventually GI dysfunction at an early phase. Thus, in this review, we will focus on situations where mesenteric blood flow is disturbed due to hemodynamic causes in shock conditions, and the present research status will be discussed. English language articles published before 2020 were identified through a computerized PubMed search using the terms "mesenteric, gastrointestinal, intestinal, splanchnic, blood flow, perfusion" and the cofactors. Relevant publications were retrieved and scanned for additional sources. There were few clinical trials focusing on mesenteric blood flow in shock patients. Most were animal experiments. Based on the best current evidence from these sources, we described the major influences on mesenteric blood flow in the context of physiologic accommodation, disease-related effects and the consequences of medical interventions related to shock conditions. During circulatory shock, sepsis, and medical interventions related to shock treatment, mesenteric blood flow changes and shows different features. We need to carefully consider these issues when making medical decisions, and more work needs to be done on early detection of GI hypoperfusion and its accurate correlation with GI dysfunction.
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Affiliation(s)
- Xinchen Wang
- Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, Dongcheng District, Beijing, China
| | - Dawei Liu
- Department of Critical Care Medicine, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Science, Dongcheng District, Beijing, China.
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7
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Agostini A, Yuchun D, Li B, Kendall DA, Pardon MC. Sex-specific hippocampal metabolic signatures at the onset of systemic inflammation with lipopolysaccharide in the APPswe/PS1dE9 mouse model of Alzheimer's disease. Brain Behav Immun 2020; 83:87-111. [PMID: 31560941 PMCID: PMC6928588 DOI: 10.1016/j.bbi.2019.09.019] [Citation(s) in RCA: 28] [Impact Index Per Article: 5.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/04/2019] [Revised: 09/23/2019] [Accepted: 09/24/2019] [Indexed: 12/27/2022] Open
Abstract
Systemic inflammation enhances the risk and progression of Alzheimer's disease (AD). Lipopolysaccharide (LPS), a potent pro-inflammatory endotoxin produced by the gut, is found in excess levels in AD where it associates with neurological hallmarks of pathology. Sex differences in susceptibility to inflammation and AD progression have been reported, but how this impacts on LPS responses remains under investigated. We previously reported in an APP/PS1 model of AD that systemic LPS administration rapidly altered hippocampal metabolism in males. Here, we used untargeted metabolomics to comprehensively identify hippocampal metabolic processes occurring at onset of systemic inflammation with LPS (100 µg/kg, i.v.) in APP/PS1 mice, at an early pathological stage, and investigated the sexual dimorphism in this response. Four hours after LPS administration, pathways regulating energy metabolism, immune and oxidative stress responses were simultaneously recruited in the hippocampi of 4.5-month-old mice with a more protective response in females despite their pro-inflammatory and pro-oxidant metabolic signature in the absence of immune stimulation. LPS induced comparable behavioural sickness responses in male and female wild-type and APP/PS1 mice and comparable activation of both the serotonin and nicotinamide pathways of tryptophan metabolism in their hippocampi. Elevations in N-methyl-2-pyridone-5-carboxamide, a major toxic metabolite of nicotinamide, correlated with behavioural sickness regardless of sex, as well as with the LPS-induced hypothermia seen in males. Males also exhibited a pro-inflammatory-like downregulation of pyruvate metabolism, exacerbated in APP/PS1 males, and methionine metabolism whereas females showed a greater cytokine response and anti-inflammatory-like downregulation of hippocampal methylglyoxal and methionine metabolism. Metabolic changes were not associated with morphological markers of immune cell activation suggesting that they constitute an early event in the development of LPS-induced neuroinflammation and AD exacerbation. These data suggest that the female hippocampus is more tolerant to acute systemic inflammation.
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Affiliation(s)
- Alessandra Agostini
- School of Life Sciences, Division of Physiology, Pharmacology and Neuroscience, University of Nottingham, Medical School, Queens Medical Centre, Nottingham NG7 2UH, UK
| | - Ding Yuchun
- School of Computer Sciences, University of Nottingham, Jubilee Campus, Wollaton Road, Nottingham NG8 1BB, UK; School of Computing Science, Urban Sciences Building, Newcastle University, 1 Science Square, Science Central, Newcastle upon Tyne NE4 5TG, UK(1)
| | - Bai Li
- School of Computing Science, Urban Sciences Building, Newcastle University, 1 Science Square, Science Central, Newcastle upon Tyne NE4 5TG, UK(1)
| | - David A Kendall
- School of Life Sciences, Division of Physiology, Pharmacology and Neuroscience, University of Nottingham, Medical School, Queens Medical Centre, Nottingham NG7 2UH, UK
| | - Marie-Christine Pardon
- School of Life Sciences, Division of Physiology, Pharmacology and Neuroscience, University of Nottingham, Medical School, Queens Medical Centre, Nottingham NG7 2UH, UK.
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Liu B, Chen J, Zhang S. Emerging role of ubiquitin-specific protease 14 in oncogenesis and development of tumor: Therapeutic implication. Life Sci 2019; 239:116875. [PMID: 31676235 DOI: 10.1016/j.lfs.2019.116875] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/20/2019] [Revised: 09/11/2019] [Accepted: 09/11/2019] [Indexed: 10/25/2022]
Abstract
Ubiquitin (Ub) is a small protein that can be attached to substrate proteins to direct their degradation via the proteasome. Deubiquitinating enzymes (DUBs) reverse this process by removing ubiquitin from its substrate protein. Over the past few decades, ubiquitin-specific protease 14 (USP14), a member of the DUBs, has emerged as an important player in various types of cancers. In this article, we review and summarize biological function of USP14 in tumorigenesis and multiple signaling pathways. To determine its role in cancer, we analyzed USP14 gene expression across a panel of tumors, and discussed that it could serve as a novel bio-marker in several types of cancer. And recent contributions indicated that USP14 has been shown to act as a tumor-promoting gene via the AKT, NF-κB, MAPK pathways etc. Besides, drugs targeting USP14 have shown potential anti-tumor effect and clinical significance. We focus on recent studies that explore the link between USP14 and cancer, and further discuss USP14 as a novel target for cancer therapy.
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Affiliation(s)
- Bing Liu
- College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, Zhejiang Province, China; State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signal Network, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361102, China
| | - Jiangping Chen
- School of International Studies, Zhejiang University, Hangzhou, 310058, Zhejiang Province, China
| | - Song Zhang
- College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, 310058, Zhejiang Province, China.
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Abstract
This review chapter describes the current knowledge about the nature of pericytes in the gut, their interaction with endothelial cells in blood vessels, and their pathophysiological functions in the setting of chronic liver disease. In particular, it focuses on the role of these vascular cell types and related molecular signaling pathways in pathological angiogenesis associated with liver disease and in the establishment of the gut-vascular barrier and the potential implications in liver disease through the gut-liver axis.
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Giridharan VV, Masud F, Petronilho F, Dal-Pizzol F, Barichello T. Infection-Induced Systemic Inflammation Is a Potential Driver of Alzheimer's Disease Progression. Front Aging Neurosci 2019; 11:122. [PMID: 31191296 PMCID: PMC6546917 DOI: 10.3389/fnagi.2019.00122] [Citation(s) in RCA: 53] [Impact Index Per Article: 8.8] [Reference Citation Analysis] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2019] [Accepted: 05/07/2019] [Indexed: 12/18/2022] Open
Affiliation(s)
- Vijayasree V Giridharan
- Department of Psychiatry and Behavioral Sciences, Translational Psychiatry Program, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United States
| | - Faisal Masud
- Department of Anesthesiology, Houston Methodist Hospital, Houston, TX, United States
| | - Fabricia Petronilho
- Health Sciences Unit, Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, University of South Santa Catarina, Tubarão, Brazil
| | - Felipe Dal-Pizzol
- Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciúma, Brazil
| | - Tatiana Barichello
- Department of Psychiatry and Behavioral Sciences, Translational Psychiatry Program, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United States.,Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciúma, Brazil.,Graduate Program in Health Sciences, Laboratory of Neurosciences, Health Sciences Unit, University of Southern Santa Catarina (UNESC), Criciúma, Brazil
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