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187 results on '"Puricelli L"'

1. Large colloidal probes for atomic force microscopy: fabrication and calibration issues

Author

Chighizola, M., Puricelli, L., Bellon, L., and Podestà, A.

Subjects
Physics - Applied Physics, Condensed Matter - Mesoscale and Nanoscale Physics, Physics - Instrumentation and Detectors, Quantitative Biology - Quantitative Methods
Abstract

Atomic force microscopy (AFM) is a powerful tool to investigate interaction forces at the micro and nanoscale. Cantilever stiffness, dimensions and geometry of the tip can be chosen according to the requirements of the specific application, in terms of spatial resolution and force sensitivity. Colloidal probes (CPs), obtained by attaching a spherical particle to a tipless (TL) cantilever, offer several advantages for accurate force measurements: tunable and well-characterisable radius; higher averaging capabilities (at the expense of spatial resolution) and sensitivity to weak interactions; a well-defined interaction geometry (sphere on flat), which allows accurate and reliable data fitting by means of analytical models. The dynamics of standard AFM probes has been widely investigated, and protocols have been developed for the calibration of the cantilever spring constant. Nevertheless the dynamics of CPs, and in particular of large CPs, with radius well above 10 um and mass comparable, or larger, than the cantilever mass, is at present still poorly characterised. Here we describe the fabrication and calibration of (large) CPs. We describe and discuss the peculiar dynamical behaviour of CPs, and present an alternative protocol for the accurate calibration of the spring constant., Comment: 29 pages, 8 figures, 2 tables

Published
2020

7. Standardized Nanomechanical Atomic Force Microscopy Procedure (SNAP) for Measuring Soft and Biological Samples

Author

UCL - SST/LIBST - Louvain Institute of Biomolecular Science and Technology, Schillers, H., Rianna, C., Schäpe, J., Luque, T., Doschke, H., Wälte, M., Uriarte, J.J., Campillo, N., Michanetzis, G.P.A., Bobrowska, J., Dumitru, A.C., Herruzo, E.T., Bovio, S., Parot, P., Galluzzi, M., Podestà, A., Puricelli, L., Scheuring, S., Missirlis, Y., Garcia, R., Odorico, M., Teulon, J.-M., Lafont, F., Lekka, M., Rico, F., Rigato, A., Pellequer, J.-L., Oberleithner, H., Navajas, D., Radmacher, M., UCL - SST/LIBST - Louvain Institute of Biomolecular Science and Technology, Schillers, H., Rianna, C., Schäpe, J., Luque, T., Doschke, H., Wälte, M., Uriarte, J.J., Campillo, N., Michanetzis, G.P.A., Bobrowska, J., Dumitru, A.C., Herruzo, E.T., Bovio, S., Parot, P., Galluzzi, M., Podestà, A., Puricelli, L., Scheuring, S., Missirlis, Y., Garcia, R., Odorico, M., Teulon, J.-M., Lafont, F., Lekka, M., Rico, F., Rigato, A., Pellequer, J.-L., Oberleithner, H., Navajas, D., and Radmacher, M.

Published
2017

8. Skin fibroblasts as a tool for identifying the risk of nephropathy in the type 1 diabetic population

Author

Millioni, R, Puricelli, L, Iori, E, Trevisan, R, Tessari, P, Millioni R, Puricelli L, Iori E, Trevisan R, Tessari P, Millioni, R, Puricelli, L, Iori, E, Trevisan, R, Tessari, P, Millioni R, Puricelli L, Iori E, Trevisan R, and Tessari P

Abstract

Human fibroblasts in culture have been employed as an in vitro system to investigate some pathophysiological mechanisms of diabetes mellitus also associated with the development of diabetic nephropathy. In fact, there is increasing evidence that genetic factors either convey the risk of, or protect from, diabetic nephropathy and that the expression profiles and/or the behaviour of the cultured skin fibroblasts from type 1 diabetic patients could reflect these genetic influences. On the other hand, alterations could be attributable not only to changes in DNA sequence, but also to epigenetic factors. Our aim is to make a critical overview of the studies involving primary cultures of skin fibroblasts as tools to investigate the pathophysiology of diabetic nephropathy performed until now in this area. Cultured skin fibroblasts could be useful not only for the identification of patients at risk of developing diabetic renal disease, but also for a better understanding of the complex multifactorial mechanisms leading to the long-term complications in diabetes.

Published
2012

9. Glycolytic enzyme expression and pyruvate kinase activity in cultured fibroblasts from type 1 diabetic patients with and without nephropathy

Author

Iori, E, Millioni, R, Puricelli, L, Arrigoni, G, Lenzini, L, Trevisan, R, James, P, Rossi, G, Pinna, L, Tessari, P, Iori E, Millioni R, Puricelli L, Arrigoni G, Lenzini L, Trevisan R, James P, Rossi GP, Pinna LA, Tessari P, Iori, E, Millioni, R, Puricelli, L, Arrigoni, G, Lenzini, L, Trevisan, R, James, P, Rossi, G, Pinna, L, Tessari, P, Iori E, Millioni R, Puricelli L, Arrigoni G, Lenzini L, Trevisan R, James P, Rossi GP, Pinna LA, and Tessari P

Abstract

Since type 1 diabetes mellitus (T1DM) patients with nephropathy (DN+) are insulin-resistant, we aimed to identify (new) potential molecular sites involved in the alterations of glucose metabolism in these patients. We examined the expression of glycolytic enzymes in cultured fibroblasts from T1DM(DN+) patients as compared to those from T1DM patients without nephropathy (DN-) and from controls. Pyruvate kinase (PK) activity was also determined. Human skin fibroblasts were grown in normal glucose (6 mM). RNAs and proteins were analyzed, respectively, using cRNA microarray and two-dimensional electrophoresis followed by identification with mass spectrometry. PK activity was measured using a spectrophotometric assay. As compared to controls, increases in the gene expression of hexokinase, phosphoglucomutase, phosphofructokinase, aldolase and triosephosphate isomerase were found in T1DM(DN+) patients, but not in T1DM(DN-) patients. In T1DM(DN+) patients, the protein analysis showed an altered expression of three glycolytic enzymes: triosophosphate isomerase, enolase and PK. In addition, PK activity in fibroblasts from T1DM(DN+) patients was lower than that in T1DM(DN-) and in controls. In conclusion, this study reports novel alterations of enzymes involved in glucose metabolism that may be associated with the pathophysiology of insulin resistance and of renal damage in T1DM(DN+) patients.

Published
2008

19. Heregulin inhibits proliferation via ERKs and phosphatidyl-inositol 3-kinase activation but regulates urokinase plasminogen activator independently of these pathways in metastatic mammary tumor cells

Author

Puricelli, L., Proiettii, C.J., Labriola, L., Salatino, M., Balañá, M.E., Ghiso, J.A., Lupu, R., Pignataro, O.P., Charreau, E.H., De Joffé, E.B.K., and Elizalde, P.V.

Subjects
Time Factors, cell migration, urokinase, animal cell, Mice, Cell Movement, Tumor Cells, Cultured, 1-Phosphatidylinositol 3-Kinase, phosphatidylinositol 3 kinase, Enzyme Inhibitors, Neoplasm Metastasis, Phosphorylation, Heregulin, recombinant heregulin beta1, messenger RNA, neu differentiation factor, breast tumor, article, 2 (2 amino 3 methoxyphenyl)chromone, unclassified drug, wortmannin, female, Phenotype, priority journal, Matrix Metalloproteinase 9, Urinary Plasminogen Activator, Mitogen-Activated Protein Kinases, Dimerization, signal transduction, Cell Division, Receptor, erbB-2, Neuregulin-1, Blotting, Western, Receptor, erbB-3, Mammary Neoplasms, Animal, STAT protein, ERKs, gelatinase B, Ribonucleases, metastasis, Animals, Humans, controlled study, mouse, Flavonoids, nonhuman, Dose-Response Relationship, Drug, ErbB receptors, Metastatic mammary tumors, enzyme activation, tumor cell culture, Precipitin Tests, cell proliferation, epidermal growth factor receptor kinase, Gene Expression Regulation, monoclonal antibody, Receptor, Epidermal Growth Factor, Phosphatidylinositol 3-kinase
Abstract

Heregulin (HRG) and type I receptor tyrosine kinase (RTK) expression was investigated in the highly invasive and metastatic LM3 cell line, our previously described model of metastasis for mammary cancer (Bal de Kier Joffe et al. [1986] Invasion Metastasis 6:302-12; Urtreger et al. [1997] Int J Oncol 11:489-96). Although LM3 cells do not express HRG, they exhibit high levels of ErbB-2 and ErbB-3 as well as moderate expression of ErbB-4. Addition of exogenous HRGβ1 resulted in inhibition of both proliferation and migration of LM3 cells. HRGβ1 was also able to decrease the activity of urokinase-type plasminogen activator (uPA) and matrix metalloproteinase 9 (MMP-9), 2 key enzymes in the invasion and metastatic cascade. HRGβ1 treatment of LM3 cells induced tyrosine phosphorylation of ErbB-2, ErbB-3 and ErbB-4 as well as the formation of ErbB-2/ErbB-3 and ErbB-2/ErbB-4 heterodimers. Assessment of the signaling pathways involved in HRGβ1 action indicated that the addition of HRGβ1 to LM3 cells resulted in activation of phosphatidylinositol 3-kinase (PI-3K) and in strong induction of the association of the p85 subunit of PI-3K with ErbB-3. HRGβ1 also caused the rapid activation of ERKI/ERK2 and Stat3 and Stat5 (signal transducers and activators of transcription [STAT]). This is the first demonstration of the ability of HRGβ1 to activate STATs in mammary tumor cells. Blockage of PI-3K activity with its chemical inhibitor wortmannin, or of MEKI/ERKs activity with PD98059, resulted in suppression of the ability of HRGβ1 to inhibit LM3 cell growth. Notwithstanding the suppression of these 2 signaling pathways, HRGβ1 still proved capable of inhibiting uPA activity. Therefore, our results provide evidence that signaling pathways involved in HRGβ1-induced proliferation appear to be distinct from those involved in HRGβ1 regulation of uPA, a protease that plays a pivotal role in invasion and metastasis. © 2002 Wiley-Liss, Inc. Fil:Puricelli, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Labriola, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Salatino, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Balañá, M.E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pignataro, O.P. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Charreau, E.H. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Elizalde, P.V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.

Published
2002

48. Glypican-3 reexpression regulates apoptosis in murine adenocarcinoma mammary cells modulating PI3K/Akt and p38MAPK signaling pathways.

Author

Buchanan, C., Stigliano, I., Garay-Malpartida, H., Rodrigues Gomes, L., Puricelli, L., Sogayar, M., Bal de Kier Joffé, E., and Peters, M.

Abstract

Glypican-3 (GPC3) is a proteoglycan involved in proliferation and cell survival. Several reports demonstrated that GPC3 is downregulated in some tumors, such as breast cancer. Previously, we determined that GPC3 reexpression in the murine mammary adenocarcinoma LM3 cells induced an impairment of their invasive and metastatic capacities, associated with a decrease of their motility and an increase of their cell death. We demonstrated that GPC3 inhibits canonical Wnt signaling, as well as it activates non canonical pathway. Now, we identified signaling pathways responsible for the pro-apoptotic role of GPC3 in LM3 cells. We found for the first time that GPC3 inhibits the PI3K/Akt anti-apoptotic pathway while it stimulates the p38MAPK stress-activated one. We report a concomitant modulation of CDK inhibitors as well as of pro- and anti-apoptotic molecules. Our results provide new clues regarding the mechanism involved in the modulation induced by GPC3 of mammary tumor cell growth and survival. [ABSTRACT FROM AUTHOR]

Published
2010
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49. Review:Natural Antimalarial Agents (1995-2001).

Author

Caniato, R. and Puricelli, L.

Subjects
*ANTIMALARIALS, *MEDICAL research
Abstract

Shows a comparative compilation of studies reported from 1995 to 2001 in natural compounds with antiplasmodial activity. Description of malaria as one of the diseases which have a few drugs available for treatment; Role of traditional remedies as a source of antimalarial drugs; Trials for the development of new antimalarial medicines.

Published
2003
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