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Insulin like growth factor-1 increases fatty liver preservation in IGL-1 solution

World Journal of Gastroenterology 2010年第45期16卷 5693-5700页

作者： Mohamed Amine Zaouali Susagna Padrissa-Altés Ismail Ben Mosbah Hassen Ben Abdennebi Olivier Boillot Antoni Rimola Dalila Saidane-Mosbahi Joan Roselló-Catafau Experimental Hepatic Ischemia-Reperfusion Unit Institut d'Investigacions Biomèdiques de BarcelonaConsejo Superior de Investigaciones Científicas08036 BarcelonaSpain Unitat de Transplantament de Fetgei Viabilitat del' Empelt Institut d'Investigacions Biomèdiques August Pii Sunyer08036 BarcelonaSpain Laboratory of Human Physiology Faculty of PharmacyUniversity of Monastir5000 MonastirTunisia Unit of Hepatic Transplantation Edouard Herriot Hospital69003 LyonFrance Biomedical Research Center Esther Koplowitz CIBER-ehdInstitute of Health Carlos Ⅲ08036 BarcelonaSpain

AIM: To investigate the benefits of insulin like growth factor-1 (IGF-1) supplementation to serum-free institut georges lopez-1 (IGL-1) solution to protect fatty liver against cold ischemia reperfusion injury. METHODS: Steatotic livers were preserved for 24 h in IGL-1  solution supplemented with or without IGF-1 and then perfused "ex vivo " for 2 h at 37℃. We examined the effects of IGF-1 on hepatic damage and function (transaminases, percentage of sulfobromophthalein clearance in bile and vascular resistance). We also studied other factors associated with the poor tolerance of fatty livers to cold ischemia reperfusion injury such as mitochondrial damage, oxidative stress, nitric oxide, tumor necrosis factor-α (TNF-α) and mitogen-activated protein ***: Steatotic livers preserved in IGL-1 solutionsupplemented with IGF-1 showed lower transaminase levels, increased bile clearance and a reduction in vascular resistance when compared to those preserved in IGL-1solution alone. These benefits are mediated by activation of AKT and constitutive endothelial nitric oxide synthase (eNOS), as well as the inhibition of inflammatory cytokines such as TNF-α. Mitochondrial damage and oxidative stress were also ***: IGL-1  enrichment with IGF-1 increasedfatty liver graft preservation through AKT and eNOS activation, and prevented TNF-α release during normothermic reperfusion.

关键词： AKT Institut georges lopez-1 solution Insulin like growth factor-1 Ischemia reperfusion injury Nitric oxide Oxidative stress Steatotic graft preservation

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Effect of stromal cell-derived factor-1/CXCR4 axis in neural stem cell transplantation for Parkinson’s disease

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Neural Regeneration Research 2020年第1期15卷 112-119页

作者： Jiao-Tian Xu Yuan Qian Wei Wang Xiao-Xiang Chen Yang Li Yu Li Zhi-Yong Yang Xiao-Bin Song Di Lu Xing-Li Deng Department of Neurosurgery First Affiliated Hospital of Kunming Medical UniversityKunmingYunnan ProvinceChina Diagnosis Prenatal Unit Department of ObstetricsFirst Affiliated Hospital of Kunming Medical UniversityKunmingYunnan ProvinceChina The People’s Hospital of Chuxiong Yi Autonomous Prefecture ChuxiongYunnan ProvinceChina Rehabilitation Engineering Research Laboratory Biomedicine Engineering Research CenterKunming Medical UniversityKunmingYunnan ProvinceChina

Previous studies have shown that neural stem cell transplantation has the potential to treat Parkinson’s disease,but its specific mechanism of action is still *** cell-derived factor-1 and its receptor,chemokine receptor 4(CXCR4),are important regulators of cell *** speculated that the CXCR4/stromal cell-derived factor 1 axis may be involved in the therapeutic effect of neural stem cell transplantation in the treatment of Parkinson’s disease.A Parkinson’s disease rat model was injected with 6-hydroxydopamine via the right ascending nigrostriatal dopaminergic pathway,and then treated with 5μL of neural stem cell suspension(1.5×104/L)in the right substantia *** were intraperitoneally injected once daily for 3 days with 1.25 mL/kg of the CXCR4 antagonist AMD3100 to observe changes after neural stem cell ***-like behavior in rats was detected using apomorphine-induced *** staining was used to determine the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the *** quantitative real-time polymerase chain reaction,the mRNA expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra were *** addition,western blot assays were performed to analyze the protein expression of stromal cell-derived factor-1 and *** results demonstrated that neural stem cell transplantation noticeably reduced apomorphine-induced rotation,increased the mRNA and protein expression of stromal cell-derived factor-1 and CXCR4 in the right substantia nigra,and enhanced the immunoreactivity of tyrosine hydroxylase,CXCR4,and stromal cell-derived factor-1 in the *** of AMD3100 inhibited the aforementioned *** findings suggest that the stromal cell-derived factor-1/CXCR4 axis may play a significant role in the therapeutic effect of neural stem cell transplantation in a rat model of Parkinson’s *** study was approved by the Ani

关键词： AMD3100 corpus striatum CXCR4 neural stem cells Parkinson’s disease stromal cell-derived factor-1 substantia nigra

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Mudskipper interleukin-34 modulates the functions of monocytes/macrophages via the colony-stimulating factor-1 receptor 1

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Zoological Research 2020年第2期41卷 123-137页

作者： Hai-Yu Shen Yan Zhou Qian-Jin Zhou Ming-Yun Li Jiong Chen State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products Ningbo UniversityNingboZhejiang 315211China Laboratory of Biochemistry and Molecular Biology School of Marine SciencesNingbo UniversityNingboZhejiang 315832China Key Laboratory of Applied Marine Biotechnology of Ministry of Education Ningbo UniversityNingboZhejiang 315832China

Interleukin-34(IL-34)is a novel cytokine that plays an important role in innate immunity and inflammatory processes by binding to the colonystimulating factor-1 receptor(CSF-1R).However,information on the function of IL-34 in fish remains *** the present study,we identified an IL-34 homolog from mudskippers(Boleophthalmus pectinirostris).In silico analysis showed that the mudskipper IL-34(BpIL-34)was similar to other known IL-34 variants in sequence and structure and was most closely related to an orange-spotted grouper(Epinephelus coioides)***-34 transcripts were constitutively expressed in various tissues,with the highest level of expression found in the *** tarda infection significantly up-regulated the mRNA expression of BpIL-34 in the mudskipper *** recombinant mature BpIL-34 peptide(rBpIL-34)was purified and used to produce anti-rBpIL-34 *** blot analysis combined with PNGase F digestion revealed that native BpIL-34 in monocytes/macrophages(MOs/MФs)was *** vitro,rBpIL-34 treatment enhanced the phagocytotic and bactericidal activity of mudskipper MOs/MФs,as well as the mRNA expression of pro-inflammatory cytokines like tumor necrosis factorα(BpTNF-α)and BpIL-1βin these ***,the knockdown of mudskipper CSF-1R1(BpCSF-1R1),but not mudskipper BpCSF-1R2,significantly inhibited the rBpIL-34-mediated enhanced effect on MO/MФ*** conclusion,our results indicate that mudskipper BpIL-34 modulates the functions of MOs/MФs via BpCSF-1R1.

关键词： Interleukin-34 Mudskipper Monocyte/macrophage function Edwardsiella tarda Colonystimulating factor-1 receptor

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Effects of Bifidobacterium infantis on cytokine-induced neutrophil chemoattractant and insulin-like growth factor-1 in the ileum of rats with endotoxin injury

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World Journal of Gastroenterology 2019年第23期25卷 2924-2934页

作者： Wei Wang Mei Sun Yu-Ling Zheng Liu-Yu Sun Shu-Qiang Qu of Pediatrics The Second Affiliated Hospital of Harbin Medical UniversityHarbin 150086Heilongjiang ProvinceChina Department of Pediatric Gastroenterology Shengjing Hospital of China Medical UniversityShenyang 110004Liaoning ProvinceChina

BACKGROUND The digestive tract is the maximal immunizing tissue in the body, and mucosal integrity and functional status of the gut is very important to maintain a healthy organism. Severe infection is one of the most common causes of gastrointestinal dysfunction, and the pathogenesis is closely related to endotoxemia and intestinal barrier injury. Bifidobacterium is one of the main probiotics in the human body that is involved in digestion, absorption, metabolism, nutrition, and *** plays an important role in maintaining the intestinal mucosal barrier integrity. This study investigated the protective mechanism of Bifidobacterium during ileal injury in *** To investigate the effects of Bifidobacterium on cytokine-induced neutrophil chemoattractant(CINC) and insulin-like growth factor 1(IGF-1) in the ileum of rats with endotoxin *** Preweaning rats were randomly divided into three groups: Control(group C),model(group E) and treatment(group T). Group E was intraperitoneally injected with lipopolysaccharide(LPS) to create an animal model of intestinal *** T was intragastrically administered Bifidobacterium suspension 7 d before LPS. Group C was intraperitoneally injected with normal saline. The rats were killed at 2, 6 or 12 h after LPS or physiological saline injection to collect ilealtissue samples. The expression of ileal CINC mRNA was evaluated by reverse transcription-polymerase chain reaction(RT-PCR), and expression of ileal IGF-1 protein and mRNA was detected by immunohistochemistry and RT-PCR,*** The ileum of rats in Group C did not express CINC mRNA, ileums from Group E expressed high levels, which was then significantly decreased in Group T(F =23.947, P 0.05). There was a high level of IGF-1 brown granules in ileal crypts and epithelial cells in Group C, sparse staining in Group E, and dark, dens

关键词： Bifidobacterium Ileum Cytokine-induced neutrophil chemoattractant Insulin-like growth factor-1 Rats

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Signal transduction pathways mediated by colony stimulating factor-1 receptor

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Chinese Science Bulletin 1998年第12期43卷 969-974页

作者： Luo Shouqing Zheng Dexian Chinese Acad Med Sci Inst Hematol Natl Lab Expt Hematol Peking Union Med Coll Tianjin 300020 Peoples R China

Colony-stimulating factor-1 (CSF-1), which is necessary for cell proliferation and differentiation, regulates both immediate and delayed early responses throughout G1 phase. The binding of CSF-1 to its receptor (CSF-1R) triggers phosphorylation of the receptor and its intrinsic tyrosine kinase. The activated receptor binds directly to cytoplasmic effector proteins, which induce multiple-signal transduction pathways. CSF-1 can induce the c-myc gene expression via Ras and Ets-related proteins. The expression of c-fos/jun family genes is also targeted following the activation of Ras. CSF-1R activates STAT1 and STAT3 to participate in signaling, but JAKs do not appear to contribute to signaling by CSF-1R. CSF-1R activates PI3-kinase, and PI3-kinase can interact with downstream proteins by the MAPKK-related pathway independent of Ras/Raf. PC-PLC can enforce signaling in response to CSF-1. Furthermore, the turnover and dephosphorylation by the phosphatase SHPTP1 of CSF-1R are the major mechanism in the negative regulation of signaling by CSF-1R.

关键词： colony stimulating factor-1 receptor signal transduction phosphorylation.

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Hyperbaric oxygen improves functional recovery of rats after spinal cord injury via activating stromal cell-derived factor-1/CXC chemokine receptor 4 axis and promoting brain-derived neurothrophic factor expression

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Chinese Medical Journal 2019年第6期132卷 699-706页

作者： Xiang-Long Meng Yong Hai Xi-Nuo Zhang Yun-Sheng Wang Xue-Hua Liu Lin-Lin Ma Rong Yue Gang Xu Zhuo Li Orthopedic Department Beijing Chaoyang Hospital Capital Medical University Beijing 100020 China Hyperbaric Oxygen Department Beijing Chaoyang Hospital Capital Medical University Beijing 100020 China Hyperbaric Oxygen Department Xinjiang Uygur Autonomous Region People's Hospital Urumqi Xinjiang 830001 China

Background: Spinal cord injury (SCI) is a worldwide medical concern. This study aimed to elucidate the mechanism underlying protective effect of hyperbaric oxygen (HBO) against SCI-induced neurologic defects in rats via exploring the stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) axis and expression of brain-derived neurotrophic factor (BDNF). Methods: An acute SCI rat model was established in Sprague-Dawley rats using the Allen method. Sixty rats were divided into four groups (w = 15 in each group): sham-operated, SCI, SCI treated with HBO (SCI + HBO), and SCI treated with both HBO and AMD3100 (an antagonist of CXCR4;SCI + HBO + AMD) groups. The rats were treated with HBO twice a day for 3 days and thereafter once a day after the surgery for up to 28 days. Following the surgery, neurologic assessments were performed with the Basso-Bettie-Bresnahan (BBB) scoring system on postoperative day (POD) 7, 14, 21, and 28. Spinal cord tissues were harvested to assess the expression of SDF-1, CXCR4, and BDNF at mRNA and protein levels, using quantitative real-time polymerase chain reaction, Western blot analysis, and histopathologic analysis. Results: HBO treatment recovered SCI-induced descent of BBB scores on POD 14,(1.25±0.75 vs. 1.03 ±0.66, P< 0.05), 21 (5.27± 0.89 vs. 2.56± 1.24, P< 0.05), and 28 (11.35±0.56 vs. 4.23± 1.20, P<0.05) compared with the SCI group. Significant differences were found in the mRNA levels of SDF-1 (mRNA: day 21, SCI + HBO vs. SCI + HBO + AMD, 2.89± 1.60 vs. 1.56±0.98, P<0.05), CXCR4 (mRNA: day 7, SCI + HBO vs. SCI, 2.99± 1.60 vs. 1.31 ±0.98, P<0.05;day 14, SCI + HBO vs. SCI + HBO + AMD, 4.18± 1.60 vs. 0.80±0.34, P<0.05;day 21, SCI + HBO vs. SCI, 2.10±1.01 vs.1.15±0.03, P<0.05), and BDNF (mRNA: day 7, SCI + HBO vs. SCI, 3.04±0.41 vs. 2.75±0.31, P<0.05;day 14, SCI + HBO vs. SCI, 3.88± 1.59 vs. 1.11 ±0.40, P<0.05), indicating the involvement of SDF-1/CXCR4 axis in the protective effect of HBO. Conclusions: HBO might promote t

关键词： Brain-derived neurotrophic factor CXC chemokine receptor 4 Hyperbaric oxygen Neurotrophic Stromal cell-derived factor-1 Spinal cord injury

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Allograft Inflammatory factor-1 in Cardiac Ischemia Re-perfusion Injury: Release of Molecular Markers in an <i>in Vitro</i>Setting

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Open Journal of Organ Transplant Surgery 2013年第1期3卷 5-12页

作者： D. Olga McDaniel Xinchun Zhou Debbie A. Rigney Larry S. McDaniel Giorgio Aru Curtis Tribble Lawrence Creswell Walter H. Merrill Department of Microbiology University of Mississippi Medical Center Jackson USA Department of Pathology University of Mississippi Medical Center Jackson USA Department of Surgery University of Mississippi Medical Center Jackson USA

Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associated with organ rejection. We hypothesized that it is either passively released from injured tissues during organ procurement, or actively secreted by allograft infiltrating cells contributing to allograft dysfunction. We investigated the impact of IRI in an in vitro study of human heart tissue during the process of transplantation. The mRNA expression levels for both isoforms of the AIF-1, I2 and I3 were significantly increased after 30 minutes reperfusion (AIF-1 I2: p 0.01 vs. AIF-1 I3: p 0.005). Expression levels for IL-18 and the TLRs were increased after 30 minutes of reperfusion. Only IL-18 and TLR-2 were statistically significant (IL-18: p 0.0001 vs. TLR-2: p 0.01). The mRNA expression levels for AIF-1 I2 and IL-18 were decreased from the original levels of ischemia after 60 and 90 minutes reperfusion. The TLR-2 and -4 were presented with minimal levels of reduction after 60 minutes. However, mRNA expression levels for all were decreased to the original levels of ischemia after 90 minutes, except for AIF-1 I3, but the difference was not statistically significant. AIF-1 and IL-18 were specifically detected in myocytes and interstitial tissues by immunohistochemistry (IHC) stain after IRI. TLR-4 was non-specific, and TLR2 was minimally expressed. The study discusses the evidence supporting that the AIF-1 may have therapeutic potential for strategies in the control of innate immune responses early on, after transplantation.

关键词： Allograft Inflammatory factor-1 Cardiac Myocytes Innate Immunity Ischemia/Reperfusion Rejection Toll-Like Receptors

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Associations between Placental Insulin-Like Growth factor-1 Gene Expression, DNA Methylation and Intrauterine Growth Restriction

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Health 2020年第3期12卷 270-280页

作者： Xiaojuan Li Baifeng Yu Xueli Wu Jiye Zhang Caihong Jia Zhuo Wang Qiaomiao Zhou Hongtao Zhou Guohui Yi Xinping Chen Shengmiao Fu Hainan Provincial People’s Hospital Central Laboratory Key Laboratory of Cellular and Molecular Genetic Transformation of Hainan Province Medicine Haikou China Department of Pediatrics University of Utah Salt Lake City Utah USA Haikou City Maternal and Child Care Hospital Clinical Laboratory Haikou China Tropical Biological Technology Research Institute Chinese Academy of Tropical Agriculture Science Haikou China Prenatal Diagnosis Center Hainan Medical Center for Women and Children Haikou China Hainan Medical College Haikou China

Intrauterine growth restriction (IUGR) is a common fetal development disorder which has great impact on neonatal health. Insulin-like growth factor-1 (IGF1) has an important role in regulating fetal growth. Whether IGF1 DNA methylation was associated with IUGR has not been studied. Placenta samples from IUGR (n = 27) and normal delivery (n = 29) were collected whereas basic information of mothers and infants were also collected. RT-PCR was performed to examine IGF1 transcriptions and bisulfite sequencing PCR was used for DNA methylation analysis. Gene expression analysis found IUGR had significantly lower IGF1 transcription compared to control group (IUGR: 0.330 ± 0.351;control group: 1.001 ± 0.800, t = 3.995, P IGF1 were all highly methylated and there is no difference on DNA methylation rate between IUGR and control group (IUGR: 75%;control group: 81%;P = 0.09). Interestingly, in both IUGR and control groups, male fetus had significantly higher methylation rate than female fetus (IUGR: male: 87%;female: 74%, P = 0.016;control: male: 82%;female: 69%, P = 0.012). There was no correlation between IGF1gene expression and DNA methylation rate (r = 0.095, P = 0.063). Intrauterine fetal growth restriction placenta had significantly lower IGF1gene expression;however, IGF1 DNA methylation level was similar. A potential fetus gender difference was also found in IGF1 DNA methylation rate.

关键词： Placental Insulin-Like Growth factor-1 IUGR

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Metabolic shift in liver: Correlation between perfusion temperature and hypoxia inducible factor-1α

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World Journal of Gastroenterology 2015年第4期21卷 1108-1116页

作者： Andrea Ferrigno Laura Giuseppina Di Pasqua Alberto Bianchi Plinio Richelmi Mariapia VairettiAndrea Ferrigno Unit of Cellular and Molecular Pharmacology and Toxicology Department of Interna Medicine and TherapeuticsUniversity of PaviaPavia 27100 Italy

AIM: To study at what temperature the oxygen carried by the perfusate meets liver requirements in a model of organ perfusion. METHODS: in this study, we correlated hypoxia induciblefactor(Hi F)-1α expression to the perfusion temperature and the hepatic oxygen uptake in a model of isolated perfused rat liver. Livers from Wistar rats were perfused for 6 h with an oxygenated medium at 10, 20, 30 and 37 ℃. Oxygen uptake was measured by an oxygen probe; lactate dehydrogenase activity, lactate release and glycogen were measured spectrophotometrically; bile flow was gravitationally determined; p H of the perfusate was also evaluated; Hi F-1α m RNA and protein expression were analyzed by real time-polymerase chain reaction and ELi SA, respectively. RESULTS: Livers perfused at 10 and 20 ℃ showed no difference in lactate dehydrogenase release after 6 h of perfusion(0.96 ± 0.23 vs 0.93 ± 0.09 m U/min per g) and had lower hepatic damage as compared to 30 and 37 ℃(5.63 ± 0.76 vs 527.69 ± 45.27 m U/min per g, respectively, P s 1). After 6 h, tissue ATP was significantly higher in livers perfused at 10 and 20 ℃than in livers perfused at 30 and 37 ℃(0.89 ± 0.06 and 1.16 ± 0.05 vs 0.57 ± 0.09 and 0.33 ± 0.08 nmol/mg, respectively, P s 1). No sign of hypoxia was observed at 10 and 20 ℃, as highlighted by low lactate release respect to livers perfused at 30 and 37 ℃(121.4 ± 12.6 and 146.3 ± 7.3 vs 281.8 ± 45.3 and 1094.5 ± 71.7 nmol/m L, respectively, P s 1α m RNA(0.40 ± 0.08 and 0.20 ± 0.03 vs 0.60 ± 0.20 and 1.47 ± 0.30, respectively, P s 16 and 3.65 ± 0.06 vs 4.43 ± 0.41 and 6.44 ± 0.82, respectively, P s 10 and 20 ℃ show no sign of liver injury or anaerobiosis, in contrast to livers perfused at 30 and 37 ℃.

关键词： Anaerobiosis Hypoxia inducible factor-1 α ischemia

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Wortmannin influences hypoxia-inducible factor-1 alpha expression and glycolysis in esophageal carcinoma cells

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World Journal of Gastroenterology 2016年第20期22卷 4868-4880页

作者： Ling Zeng Hai-Yun Zhou Na-Na Tang Wei-Feng Zhang Gui-Jun He Bo Hao Ya-Dong Feng Hong Zhu Department of Gastroenterology The First Affiliated Hospital of Nanjing Medical University

AIM: To investigate the influence of phosphatidylinositol-3-kinase protein kinase B(PI3K/AKT)-HIF-1α signaling pathway on glycolysis in esophageal carcinoma cells under hypoxia. METHODS: Esophageal carcinoma cell lines Eca109 and TE13 were cultured under hypoxia environment, and the protein, m RNA and activity levels of hypoxia inducible factor-1 alpha(HIF-1α), glucose transporter 1, hexokinase-Ⅱ, phosphofructokinase 2 and lactate dehydrogenase-A were determined. Supernatant lactic acid concentrations were also detected. The PI3K/AKT signaling pathway was then inhibited with wortmannin, and the effects of hypoxia on the expression or activities of HIF-1α, associated glycolytic enzymes and lactic acid concentrations were observed. Esophageal carcinoma cells were then transfected with interference plasmid with HIF-1α-targeting si RNA to assess impact of the high expression of HIF-1α on ***: HIF-1α is highly expressed in the esophageal carcinoma cell lines tested, and with decreasing levels of oxygen, the expression of HIF-1α and the associated glycolytic enzymes and the extracellular lactic acid concentration were enhanced in the esophageal carcinoma cell lines Eca109 and TE13. In both normoxia and hypoxic conditions, the level of glycolytic enzymesand the secretion of lactic acid were both reduced by wortmannin. The expression and activities of glycolytic enzymes and the lactic acid concentration in cells were reduced by inhibiting HIF-1α, especially the decreasing level of glycolysis was significant under hypoxic ***: The PI3K/AKT pathway and HIF-1α are both involved in the process of glycolysis in esophageal cancer cells.

关键词： Hypoxia-inducible factor-1 alpha Hypoxia Glycolysis Esophageal neoplasms Cell metabolism

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