Silvia Pellerito

University of Florence, Florens, Tuscany, Italy

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Publications (11)44.38 Total impact

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    ABSTRACT: OBJECTIVES: The aim of this study was to evaluate resistin levels in patients with coronary artery disease (CAD) with or without chronic heart failure, in order to define its independent predictor. METHODS: One hundred and seven outpatients with CAD were enrolled in the study and divided into three groups: CAD without left-ventricular systolic dysfunction (group 1); CAD with left-ventricular dysfunction without heart failure symptoms (group 2); CAD with overt heart failure (group 3). Plasma resistin was determined by ELISA. RESULTS: Resistin progressively increased from group 1 (10.7 ± 5.0 ng/ml) to groups 2 (11.8 ± 5.8 ng/ml) and 3 (17.0 ± 6.8 ng/ml), with the difference reaching statistical significance in group 3 versus groups 1 and 2 (P = 0.001). A multivariable model of analysis demonstrated that the best predictor of plasma resistin level was the estimated glomerular filtration rate (P < 0.001), indicating that reduction of kidney function was the main cause of the adipokine increase observed in patients with CAD and overt heart failure. CONCLUSIONS: Our data confirm the rise of resistin plasma levels previously described in patients affected by chronic heart failure; however, in our study, this relationship seemed to be mediated mainly by the level of kidney function, and only partially by the severity of ventricular dysfunction.
    Journal of Cardiovascular Medicine 01/2012; 14(2). DOI:10.2459/JCM.0b013e32834eec93 · 1.41 Impact Factor
  • Pigment Cell & Melanoma Research 04/2009; 22(3):335-8. DOI:10.1111/j.1755-148X.2009.00562.x · 5.64 Impact Factor
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    ABSTRACT: Background: Thoracic impedance (TI) influences the success of external cardioversion (ECV) or defibrillation because current intensity traversing the heart is inversely related to TI. Experimental data suggest that TI decreases after multiple shocks. We undertook a clinical study to determine changes of TI values in patients with atrial fibrillation or flutter requiring ECV.Methods: We enrolled 222 consecutive patients (age 73 ± 11 years; males 67%; body weight 75 ± 13 kg) who underwent ECV between January 2004 and February 2007. Biphasic shocks were delivered through adhesive pads placed in the anteroposterior position. The initial energy was set at 1 J/kg, with progressive increases up to a maximum of 180 J in case of failure. In the last 39 elective patients, plasma concentration of interleukin-6 (IL-6) and tumor necrosis factor (TNF)- were determined before and 6 hours after ECV.Results: Sinus rhythm was restored in 202 patients (91.0%). Of these, 155 (69.8%) required more than one shock (on average, 2.5 ± 1.5 shocks/patient). Final values of energy and peak current intensity were 136 ± 47 J and 50 ± 14 A, respectively. TI decreased significantly by 6.2% from baseline after ≥2 shocks (P < 0.001). The absolute reduction was correlated with baseline TI, number of delivered shocks, and hemoglobin oxygen saturation. IL-6 and TNF- increased with ECV (P < 0.001 and P = 0.014, respectively).Conclusions: TI decreases significantly after multiple shocks, possibly by activation of acute inflammation.
    Pacing and Clinical Electrophysiology 02/2009; 32(3):371 - 377. DOI:10.1111/j.1540-8159.2008.02246.x · 1.25 Impact Factor
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    The Journal of Nutrition Health and Aging 10/2008; 12(8):545-593. DOI:10.1007/BF02983206 · 2.66 Impact Factor
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    ABSTRACT: Melanoma is a highly invasive tumor with elevated mortality rates. Progression and aggressiveness appear related to the achievement of an angiogenic phenotype. Melanoma cells express several angiogenic factors, including fibroblast growth factor (FGF)-1 and FGF-2. The autocrine production and release of FGFs and the subsequent activation of FGF receptors, have a central role in melanoma tumor progression. We demonstrated that FGF-1 is secreted from a human melanoma cell line, A375, under conditions of serum deprivation. The release of FGF-1 is inhibited by the copper chelator ammonium tetrathiomolybdate, suggesting a role of copper in the secretory pathway, and is triggered by activation of phosphatidylinositol 3-kinase (PI3K)/Akt intracellular signaling. Interestingly, overexpression or activation of Akt has been correlated with poor prognosis in melanoma patients. Our data indicate a novel role for Akt in supporting the progression of human melanomas and advocate the need for new treatments targeting PI3K/Akt signaling pathway, to control tumor development and progression.
    Cancer Letters 09/2008; 267(1):67-74. DOI:10.1016/j.canlet.2008.03.001 · 5.02 Impact Factor
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    ABSTRACT: The Notch signaling pathway may play opposing roles in cancer. It can be oncosuppressive or protumoral, depending on the cellular and tissue context. In skin cancer, Notch 1 expression is downregulated, thus supporting the hypothesis of an oncosuppressive role in cutaneous carcinomas. However, as members of the Notch family undergo downregulation upon exposure to UV irradiation, we wondered whether Notch 1 expression in skin carcinomas may be governed by additional factors, including UV exposure. We investigated the expression of Notch 1 and its ligands, Jagged 1, Jagged 2 and Delta-like 1, by immunohistochemistry in a series of premalignant and invasive cutaneous carcinomas, including 4 solar keratoses, 5 Bowen's disease, 5 squamous cell carcinomas on sun-exposed skin, 6 squamous cell carcinomas on sun-protected genital skin and 14 basal cell carcinomas of different histotypes (nodular, superficial type, sclerodermiform/infiltrating and baso-squamous). Expression of Notch 1 was decreased in solar keratoses and invasive squamous cell carcinomas localized on sun-exposed skin. In contrast, marked Notch 1 staining was observed in extragenital Bowen's disease as well as in genital (penile) human papilloma virus-related in situ and invasive squamous cell carcinomas. A diffuse Notch 1 staining was detected in nodular and superficial basal cell carcinomas while sclerodermiform/infiltrating and baso-squamous basal cell carcinomas showed a low to absent Notch 1 expression. Jagged 1, Jagged 2 and Delta-like 1 proteins were expressed in all tissues examined. Present findings show divergent expression of Notch 1 in skin cancer, depending on anatomical site and tumor histotype. Thus, whereas in UV-related squamous cell photocarcinogenesis Notch 1 downregulation could mirror a tumor suppressor function of the receptor, in sun-protected squamous cell carcinomas Notch 1 was upregulated. Furthermore, Notch 1 expression was minimal in basal cell carcinoma subtypes correlated with risk of recurrence (sclerodermiform/infiltrating and baso-squamous) in comparison with nodular and superficial types.
    Modern Pathology 04/2008; 21(3):316-25. DOI:10.1038/modpathol.3801007 · 6.36 Impact Factor
  • C Di Serio, S Pellerito, F Tarantini
    Journal of Pharmacology and Experimental Therapeutics 02/2008; 324(1):404-5; author reply 406-7. DOI:10.1124/jpet.107.131847 · 3.86 Impact Factor
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    ABSTRACT: Thrombin, a key mediator of blood coagulation, exerts a large number of cellular actions via activation of a specific G-protein-coupled receptor, named protease-activated receptor 1 (PAR1). Several studies in experimental animals have demonstrated a therapeutic potential of small molecules with PAR1 antagonistic properties for treatment of diseases such as vascular thrombosis and arterial restenosis. We have studied the biological actions of one highly potent, selective PAR1 antagonist, SCH79797 (N 3-cyclopropyl-7-{[4-(1-methylethyl)phenyl]methyl}-7H-pyrrolo[3,2-f]quinazoline-1,3-diamine), in vitro, and found that this compound was able to interfere with the growth of several human and mouse cell lines, in a concentration-dependent manner. The ED(50) for growth inhibition was 75 nM, 81 nM and 116 nM for NIH 3T3, HEK 293 and A375 cells, respectively. Moreover, in NIH 3T3 cells, SCH79797 inhibited serum-stimulated activation of p44/p42 mitogen-activated protein kinases (MAPK) at low concentrations and induced apoptosis at higher concentrations. However, the antiproliferative and pro-apoptotic effects of SCH79797 are likely not mediated by PAR1 antagonism, as they were also observed in embryonic fibroblasts derived from PAR1 null mice. These data suggest that, in view of the development of PAR1-selective antagonists as therapeutic agents, effects potentially unrelated to PAR1 inhibition should be carefully scrutinized.
    Basic &amp Clinical Pharmacology &amp Toxicology 08/2007; 101(1):63-9. DOI:10.1111/j.1742-7843.2007.00078.x · 2.29 Impact Factor
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    ABSTRACT: Protease-activated receptor (PAR)-1 and PAR-2 are reported to contribute to the fibrotic process in a number of organs, including lung, liver, pancreas, and kidney. The aim of this study was to localize expression and biological activity of PAR-1 and PAR-2 in normal and pathological cutaneous scars. First, we investigated the immunohistochemical expression of PAR-1 and PAR-2 proteins in a series of human normal scars (NS, n = 10), hypertrophic scars (HS, n = 10), and keloids (K, n = 10). Expression of PAR-1 and PAR-2 was observed in all types of scar. Specifically, in HS and K, diffuse PAR-1 and PAR-2 positivity was found in dermal cellular areas composed of myofibroblasts, while no or minor staining was observed in the scattered fibroblasts embedded in abundant extracellular matrix in the context of the more collagenous nodules, irrespective of the type of scar. The hyperplastic epidermis overlying K was also found to be strongly PAR-1 and PAR-2 positive, whilst in most NS and HS the epidermis was faintly to moderately stained. Second, ribonuclease protection assay on paraffin-embedded specimens showed overexpression of PAR-1 and PAR-2 mRNA in K compared to NS and HS. Third, cultured human fibroblasts exposed to TGF-beta1 expressed a myofibroblast phenotype associated with overexpression of PAR-2, while PAR-1 expression was unaffected. Intracellular Ca(2+) mobilization by PAR-2 agonists in myofibroblasts was increased as compared to fibroblasts, whereas the effect of PAR-1 agonists was unchanged. Our in vivo study indicates that PAR-1 and PAR-2 are expressed in cells involved in physiological and pathological scar formation and suggests that in vitro overexpression and exaggerated functional response of PAR-2 may play a role in the function of myofibroblasts in scar evolution from a physiological repair process to a pathological tissue response.
    The Journal of Pathology 08/2007; 212(4):440-9. DOI:10.1002/path.2197 · 7.33 Impact Factor
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    ABSTRACT: The Notch signaling has been implicated in the regulation of self-renewal of adult stem cells and differentiation of precursors along a specific cell lineage, in normal embryonic development and organogenesis. There is also evidence that signaling through Notch receptors regulate cell proliferation and cell survival in several types of cancer, with opposing results depending on tissue context. No data are available in the literature concerning modulation of the expression of Notch receptors, and their ligands, in human cutaneous malignant melanoma. Here, we have investigated, for the first time, the expression of Notch-1, Notch-2, Jagged-1, Jagged-2 and Delta-like 1 proteins, by immunohistochemistry, in a series of benign and malignant human melanocytic lesions: five common melanocytic nevi, five 'dysplastic nevi' and 20 melanomas (five in situ, five T1-T2, five T3-T4 and five metastatic melanomas). We found that the expression of Notch-1 and Notch-2, as well as Notch ligands, was upregulated in 'dysplastic nevi' and melanomas as compared with common melanocytic nevi. These results indicate that the activation of Notch may represent an early event in melanocytic tumor growth and upregulation of Notch signaling may sustain tumor progression.
    Modern Pathology 03/2006; 19(2):246-54. DOI:10.1038/modpathol.3800526 · 6.36 Impact Factor
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    ABSTRACT: 1. Kynurenic (KYNA) and quinolinic (QUIN) acids are neuroactive tryptophan metabolites formed along the kynurenine pathway: the first is considered a non-competitive antagonist and the second an agonist of glutamate receptors of NMDA type. The affinity of these compounds for glutamate receptors is, however, relatively low and does not explain KYNA neuroprotective actions in models of post-ischemic brain damage. 2. We evaluated KYNA effects on the release of fibroblast growth factor (FGF)-1, a potent neurotrophic cytokine. Because KYNA exhibits a neuroprotective profile in vitro and in vivo, we anticipated that it could function as an autocrine/paracrine inducer of FGF-1 release. Studies were performed in several models of FGF-1 secretion (FGF-1 transfected NIH 3T3 cells exposed to heat shock, A375 melanoma cells exposed to serum starvation, growth factor deprived human endothelial cells). To our surprise, KYNA, at low concentration, inhibited FGF-1 release in all cellular models. QUIN, a compound having opposite effects on glutamate receptors, also reduced this release, but its potency was significantly lower than that of KYNA. 3. KYNA and QUIN also displayed a major stimulatory effect on the proliferation rate of mouse microglia and human glioblastoma cells, in vitro. 4. Our data suggest that minor changes of local KYNA concentration may modulate FGF-1 release, cell proliferation, and ultimately tissue damage in different pathological conditions.
    Cellular and Molecular Neurobiology 10/2005; 25(6):981-93. DOI:10.1007/s10571-005-8469-y · 2.20 Impact Factor