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| 1 | Is autophagy an elective strategy to protect neurons from dysregulated cholesterol metabolism?显示文摘The balance of autophagy, apoptosis and necroptosis is crucial to determine the outcome of the cellular response to cholesterol dysregulation. Cholesterol plays a major role in regulating the properties of cell membranes, especially as regards their fluidity, and the regulation of its biosynthesis influences the shape and functions of these membranes. Whilst dietary cholesterol can easily be distributed to most organs, the central nervous system, whose membranes are particularly rich in cholesterol, mainly relies on de novo synthesis. For this reason, defects in the biosynthesis of cholesterol can variably affect the development of central nervous system. Moreover, defective synthesis of cholesterol and its intermediates may reflect both on structural cell anomalies and on the response to inflammatory stimuli. Examples of such disorders include mevalonate kinase deficiency, and Smith-Lemli-Opitz syndrome, due to deficiency in biosynthetic enzymes, and type C Niemann-Pick syndrome, due to altered cholesterol trafficking across cell compartments. Autophagy, as a crucial pathway dedicated to the degradation of cytosolic proteins and organelles, plays an essential role in the maintenance of homeostasis and in the turnover of the cytoplasmic material especially in the presence of imbalances such as those resulting from alteration of cholesterol metabolism. Manipulating the process of autophagy can offer possible strategies for improving neuronal cell viability and function in these genetic disorders. | Elisa Piscianz Liza Vecchi Brumatti Alberto Tommasini Annalisa Marcuzzi | 2019 | Neural Regeneration Research2019，14，4： | 2 |
| 2 | Selective re- sistance to different glucocorticoids in severe autoim- mune disorders显示文摘 | Drigo I Piscianz E Valencic E | 2010 | Clin Immunol2010，134，3： | 1 |
| 3 | Mevalonate kinase deficiency and neurointlammation: balance between apoptosis and pyroptosis显示文摘 | Tricarico P M Marcuzzi A Piscianz E | 2013 | Int J Mol Sci2013，2614，23： | 1 |
| 4 | The immunosuppressive effect of Wharton’s jelly stromal cells depends on the timing of their licensing and on lymphocyte activation显示文摘 | Erica Valencic Elisa Piscianz Marino Andolina Alessandro Ventura Alberto Tommasini | 2010 | Cytotherapy2010，，2： | 1 |
| 5 | Fate of lymphocytes after withdrawal of tofacitinib treatment显示文摘 | Piscianz E Valencic E Cuzzoni E | 2014 | PLoS One2014，9，1： | 1 |
| 6 | Mevalonate kinase deficiency and neuroinflammation:balanee between apoptosis and pyroptosis显示文摘 | Tricarico PM Mareuzzi A Piscianz E | 2013 | Int J Mol Sci2013，14，23： | 1 |
| 7 | Long Noncoding RNA GAS5: A Novel Marker Involved in Glucocorticoid Response显示文摘 | M. Lucafo S. De Iudicibus A. Di Silvestre M. Pelin L. Candussio S. Martelossi A. Tommasini E. Piscianz A. Ventura G. Decorti | 2015 | Current Molecular Medicine2015，，1： | 1 |
| 8 | Altered pattern of tumor necrosis factor-alpha production in peripheral blood monocytes from Crohn's disease显示文摘AIM To evaluate the inflammatory state in Crohn's disease(CD) patients and correlate it with genetic background and microbial spreading.METHODS By means of flow cytometry, production of tumor necrosis factor-alpha(TNF-α) was measured in peripheral blood monocytes from patients suffering from CD, ulcerative colitis(UC) and in healthy subjects after stimulation of the NOD2 and TLR pathways. CD patients were genotyped for the three most common NOD2 variants(R702W, G908 R and L1007Pfs*2) and basal production of TNF-α was correlated to NOD2 genotype. Also, production of TNF-α was correlated to plasmatic levels of LPS Binding Protein(LBP), soluble(s) CD14 and to the activity state of the disease.RESULTS The patients with CD were characterized by a significantly higher monocyte basal expression of TNF-αcompared with healthy subjects and UC patients, and after stimulation with Pam3CSK4(ligand of TLR2/1) and MDP-L18(ligand of NOD2) this difference was maintained, while other microbial stimuli(LPS, ligand of TLR4 and Poly I:C, ligand of TLR3) induced massive activation in CD monocytes as well as in UC and in healthy control cells. There was no significant difference in the production of TNF- α between patients who carried CD-associated heterozygous or homozygous variants in NOD2 and patients with wild type NOD2 genotype. Although serum LBP levels have been shown to correlate positively with the state of activity of the disease, TNF-α production did not show a clear correlation with either LBP or s CD14 levels in plasma. Moreover, no clear correlation was seen between TNF-α production and activity indices in either CD or UC.CONCLUSION Peripheral monocytes from CD express higher basal and stimulated TNF-α than controls, regardless of NOD2 genotype and without a clear correlation with disease activity. | Claudia Loganes Alessia Pin Samuele Naviglio Martina Girardelli Anna Monica Bianco Stefano Martelossi Alberto Tommasini Elisa Piscianz | 2016 | World Journal of Gastroenterology2016，22，41： | 0 |
| 9 | Hydroxychloroquine modulates immunological pathways activated by RNA:DNA hybrids in Aicardi–Goutières syndrome patients carrying RNASEH2 mutations显示文摘Aicardi–Goutières syndrome(AGS)is a rare genetic disease caused by mutations in nine genes that are all involved in nucleic acid metabolism or sensing.1,2 The three RNASEH2 subunits represent the most frequently mutated genes in AGS patients,1,3 and mutations in RNASEH2 subunits lead to the accumulation of endogenous RNA:DNA hybrids that may trigger an interferon-α-mediated immune response4 through the activation of pattern recognition receptors(PRRs).5 PRRs perform surveillance on extracellular,endosomal,and cytosolic compartments to identify signs of infection:endogenous nucleic acids that are inappropriately cleared may enter and accumulate in the cytoplasm,driving inflammation and autoimmune diseases.6 This accumulation may be the cause of the clinical autoimmune phenotype of AGS patients carrying RNASEH2 mutations.A proven effective cure for AGS has not been discovered,and targeting these two pathways may lead to a treatment that improves patients’immunological symptoms.Hydroxychloroquine(HCQ)interferes with normal antigen processing and presentation and is widely used in the clinical treatment of autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis.7 HCQ is also a well-known inhibitor of autophagy that prevents the degradation of autolysosomes.This drug inhibits acidification and maturation of endosomes and increases the pH in lysosomes,resulting in the inhibition of their main functions,such as downstream cell signaling through TLRs.7 Therefore,the aim of our work was to investigate whether HCQ is able to modulate the abnormal inflammatory response driven by RNA:DNA hybrids. | Jessica Garau Daisy Sproviero Francesca Dragoni Elisa Piscianz Carolina Santonicola Davide Tonduti Stephana Carelli Alessandra Tesser Gian Vincenzo Zuccotti Alberto Tommasini Simona Orcesi Orietta Pansarasa Cristina Cereda | 2021 | Cellular & Molecular Immunology2021，18，6： | 0 |
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