In JoVE (1)
Articles by Olimpia Gamucci in JoVE
الكشف عن جسيمات متناهية الصغر نيون التفاعل مع مجموعات سكانية فرعية خلية المناعة الأولية من قبل التدفق الخلوي Olimpia Gamucci1, Alice Bertero1,2, Maria Ada Malvindi3, Stefania Sabella3, Pier Paolo Pompa3, Barbara Mazzolai1, Giuseppe Bardi1 1Center for Micro-BioRobotics @SSSA, Istituto Italiano di Tecnologia, 2Department of Biology, University of Pisa, 3Center for Biomolecular Nanotechnologies @UniLe, Istituto Italiano di Tecnologia تحليل التفاعل جسيمات متناهية الصغر مع مجموعات سكانية فرعية محددة من الخلايا المناعية بواسطة التدفق الخلوي.
Other articles by Olimpia Gamucci on PubMed
The Obesity and Inflammatory Marker Haptoglobin Attracts Monocytes Via Interaction with Chemokine (C-C Motif) Receptor 2 (CCR2) BMC Biology. 2009 | Pubmed ID: 20017911 Obesity is a chronic low inflammatory state. In the obesity condition the white adipose tissue (WAT) is massively infiltrated with monocytes/macrophages, and the nature of the signals recruiting these inflammatory cells has yet to be fully elucidated. Haptoglobin (Hp) is an inflammatory marker and its expression is induced in the WAT of obese subjects. In an effort to elucidate the biological significance of Hp presence in the WAT and of its upregulation in obesity we formulated the hypothesis that Hp may serve as a macrophage chemoattractant.
Obesity-associated Hepatosteatosis and Impairment of Glucose Homeostasis Are Attenuated by Haptoglobin Deficiency Diabetes. Oct, 2011 | Pubmed ID: 21873550 Haptoglobin (Hp) is upregulated in both inflammation and obesity. The low chronic inflammatory state, caused by massive adipose tissue macrophage (ATM) infiltration found in obesity, and low adiponectin have been implicated in the development of insulin resistance and hepatosteatosis. The aim of this work was to investigate whether and how Hp interferes with the onset of obesity-associated complications.
Haptoglobin Deficiency Determines Changes in Adipocyte Size and Adipogenesis Adipocyte. Jul, 2012 | Pubmed ID: 23700523 Haptoglobin (Hp) is an inflammatory and adiposity marker, its expression during obesity being specifically induced in the white adipose tissue (WAT). We previously reported that when challenged with a high fat diet (HFD) Hp(-/-) mice are partially protected from the onset of insulin resistance and hepatosteatosis. The aim of the present study was to get further insights into Hp function in WAT. To this end, we performed histological and gene expression analysis of the Hp(-/-) WAT, both in standard and obesity conditions, and investigated how Hp deficiency impacts adipogenesis and WAT development. The average size and percentage of very large adipocytes were respectively smaller and reduced in HFD Hp(-/-) mice as compared with HFD WT. The expression of perilipin, HSL and angiogenesis related markers were increased in HFD Hp(-/-) mice. Lean adult Hp(-/-) showed significantly larger adipocytes and lower subcutaneous WAT expression of aP2 and LPL with respect to WT. Hp(-/-) young mice (P30) were characterized by larger adipocyte size and lower expression of adipocyte and adipogenesis markers. Comparison of adipocyte size distribution between young and adult mice revealed attenuated changes in Hp(-/-) mice compared with WT. Mouse embryonic fibroblasts from Hp(-/-) mice were less capable of accumulating triglycerides and exhibited lower expression of PPARγ, aP2, FAS, LPL and Leptin. In conclusion, Hp deficiency tends to blunt the effect of age and diet on the size of adipocytes, which show less susceptibility to develop hypertrophy during obesity and a reduced adipogenic/hyperplastic potential during youth. In addition, Hp deficiency impacts negatively on adipogenesis.