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SIRT3-mediated inhibition of fOS through histone H3 deacetylation prevents cardiac fibrosis and inflammation

Signal Transduction and Targeted Therapy 2020年第1期5卷 2322-2331页

作者： Xavier Palomer MSilvia Román-Azcona Javier Pizarro-Delgado Ana Planavila francesc Villarroya Brenda Valenzuela-Alcaraz Fátima Crispi Álvaro Sepúlveda-Martínez Irene Miguel-Escalada Jorge ferrer Jfrancisco Nistal Raquel García Mercy MDavidson Emma Barroso Manuel Vázquez-Carrera Department of Pharmacology Toxicology and Therapeutic ChemistryIBUB(Institut de Biomedicina de la Universitat de Barcelona)Research Institute-Pediatric Research InstituteHospital Sant Joan de Déuand CIBER de Diabetes y Enfermedades Metabólicas Asociadas(CIBERDEM)Faculty of Pharmacy and Food SciencesUniversity of BarcelonaBarcelonaSpain Department of Biochemistry and Molecular Biomedicine IBUB and CIBER Fisiopatología de la Obesidad y Nutrición(CIBEROBN)Faculty of BiologyUniversity of BarcelonaBarcelonaSpain aBCNatal-Barcelona Center for Maternal–fetal and Neonatal Medicine(Hospital Clínic and Hospital Sant Joan de Deu) Institut d’Investigacions Biomèdiques August Pi i SunyerUniversitat de Barcelonaand Center for Biomedical Research on Rare Diseases(CIBER-ER)BarcelonaSpain Genomic Programming of Betacells Laboratory Institut d’Investigacions August Pi i Sunyer(IDIBAPS)and CIBERDEMBarcelonaSpain Section of Epigenomics and Disease Department of Medicineand National Institute for Health Research(NIHR)Imperial Biomedical Research CentreImperial College LondonLondonUK Servicio de Cirugía Cardiovascular Hospital Universitario Marqués de ValdecillaDepartamento de Ciencias Médicas y QuirúrgicasFacultad de MedicinaUniversidad de CantabriaInstituto de Investigación Marqués de Valdecilla(IDIVAL)Centro de Investigación Biomédica en Red Cardiovascular(CIBERCV)Instituto de Salud Carlos IIISantanderSpain Departamento de fisiología y farmacología Facultad de MedicinaUniversidad de CantabriaInstituto de Investigación Marqués de Valdecilla(IDIVAL)SantanderSpain Department of Radiation Oncology Columbia UniversityNew YorkNYUSA

Sirtuin 3(SIRT3)is a deacetylase that modulates proteins that control metabolism and protects against oxidative stress.Modulation of SIRT3 activity has been proposed as a promising therapeutic target for ameliorating metabolic diseases and associated cardiac disturbances.In this study,we investigated the role of SIRT3 in inflammation and fibrosis in the heart using male mice with constitutive and systemic deletion of SIRT3 and human cardiac AC16 cells.SIRT3 knockout mice showed cardiac fibrosis and inflammation that was characterized by augmented transcriptional activity of AP-1.Consistent with this,SIRT3 overexpression in human and neonatal rat cardiomyocytes partially prevented the inflammatory and profibrotic response induced by TNf-α.Notably,these effects were associated with a decrease in the mRNA and protein levels of fOS and the DNA-binding activity of AP-1.finally,we demonstrated that SIRT3 inhibits fOS transcription through specific histone H3 lysine K27 deacetylation at its promoter.These findings highlight an important function of SIRT3 in mediating the often intricate profibrotic and proinflammatory responses of cardiac cells through the modulation of the fOS/AP-1 pathway.Since fibrosis and inflammation are crucial in the progression of cardiac hypertrophy,heart failure,and diabetic cardiomyopathy,our results point to SIRT3 as a potential target for treating these diseases.

关键词： SIRT3 inflammation cardiac

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Novel perspectives for neurodegeneration prevention: effects of bioactive polyphenols

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Neural Regeneration Research 2021年第7期16卷 1411-1412页

作者： Stefania crispi Stefania filosa Institute of Biosciences and Bioresources National Research Councilvia P.CastellinoNaplesItaly Department of Marine Biotechnology Stazione Zoologica Anton DohrnNapoliItaly Istituto di Ricovero e Cura a Carattere Scientifico Neuromed PozzilliItaly

Neurodegenerative diseases are becoming a big challenge for modern society.Neurodegenerative disorders strongly impact on patient and their caregivers.Moreover, since the population is becoming older, these pathologies will deeply influence medical and socio-economic conditions in the next years.Therefore, efforts are needed to find new strategies devoted to define new protocols and identify novel substances able to prevent neurodegeneration or to improve the quality of life of people affected by neurodegenerative diseases(Alzheimer's Disease International, 2019).

关键词： prevention diseases neurodegeneration

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Polyphenols-gut microbiota interplay and brain neuromodulation

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Neural Regeneration Research 2018年第12期13卷 2055-2059页

作者： Stefania filosa francesco Di Meo Stefania crispi Institute of Biosciences and Bioresources National Research Council National Research Council via P. Castellino Naples Italy Istituto di Ricovero e Cura a Carattere Scientifico Neuromed Pozzilli Italy

Increasing evidence suggests that food ingested polyphenols can have beneficial effects in neuronal protection acting against oxidative stress and inflammatory injury. Moreover, polyphenols have been reported to promote cognitive functions. Biotransformation of polyphenols is needed to obtain metabolites active in brain and it occurs through their processing by gut microbiota. Polyphenols metabolites could directly act as neurotransmitters crossing the blood-brain barrier or indirectly by modulating the cerebrovascular system. The microbiota-gut-brain axis is considered a neuroendocrine system that acts bidirectionally and plays an important role in stress responses. The metabolites produced by microbiota metabolism can modulate gut bacterial composition and brain biochemistry acting as neurotransmitters in the central nervous system. Gut microbiota composition can be influenced by dietary ingestion of natural bioactive molecules such as probiotics, prebiotics and polyphenol. Microbiota composition can be altered by dietary changes and gastrointestinal dysfunctions are observed in neurodegenerative diseases. In addition, several pieces of evidence support the idea that alterations in gut microbiota and enteric neuroimmune system could contribute to onset and progression of these age-related disorders. The impact of polyphenols on microbiota composition strengthens the idea that maintaining a healthy microbiome by modulating diet is essential for having a healthy brain across the lifespan. Moreover, it is emerging that they could be used as novel therapeutics to prevent brain from neurodegeneration.

关键词： polyphenols gut-microbiota gut-brain axis metagenomic neurodegeneration neurotransmitters prebiotics probiotics

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自制网枪（下）

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微型计算机 2009年第14期29卷 62-65页

作者： crispi jones

各位同学看到上期的《自制网枪（上）》后，是否已经动手把压力舱和渔网做好了，迫不及待地等待我们的下篇。废物不说了，我们现在就开始制作网枪的其他部分。

关键词：制网压力舱制作网

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胎盘血管生成因子和子宫动脉多普勒检查定性不同类型的先兆子痫和孤立的胎儿宫内生长受限

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世界核心医学期刊文摘（妇产科学分册） 2006年第10期2卷 9-9页

作者： crispi f. Domnguez C. Llurba E. 张新艳 Biochemistry and Molecular Biology Center Hospital Vall d'Hebron Universitat Autònoma de Barcelona Barcelona Spain Dr.

Objective: The purpose of this study was to evaluate possible relationships between placental markers and endothelial dysfunction in preeclampsia and intrauterine growth restriction. Study design: A prospective study was conducted in 76 patients with preeclampsia and 37 patients with intrauterine growth restriction that were classified as early onset( f gestational age) or late onset, and 40 control subjects. Plasma levels of placental growth factor, soluble fms-like tyrosine kinase-1, vascular cell adhesion molecule-1, and uterine artery Doppler indices were measured. Results: In early-onset preeclampsia and intrauterine growth restriction, placental growth factor was lower and soluble fms-like tyrosine kinase-1 and vascular cell adhesion molecule-1 higher than in control subjects, although all changes were more pronounced in preeclampsia. In late onset preeclampsia, those patients with abnormal uterine artery Doppler indices had higher soluble fms-like tyrosine kinase-1 and vascular cell adhesion molecule-1 levels. Conclusion: Biochemical changes in early-onset preeclampsia and intrauterine growth restriction point to a common placental disorder and a state of endothelial dysfunction, which may require interaction with other factors to explain the maternal disease in preeclampsia. Data in late-onset preeclampsia suggest that a proportion of them may occur with minimal placental involvement.

关键词：胎儿宫内生长血管生成因子先兆子痫子宫动脉多普勒检查内皮功能失调生化改变研究设计内皮功

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