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Dive into the research topics where Mauro Finicelli is active.

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Featured researches published by Mauro Finicelli.


Molecular Medicine | 2009

Expression Pattern of Stemness-Related Genes in Human Endometrial and Endometriotic Tissues

Amalia Forte; Maria Teresa Schettino; Mauro Finicelli; Marilena Cipollaro; Nicola Colacurci; Luigi Cobellis; Umberto Galderisi

Endometriosis is a chronic disease characterized by the presence of ectopic endometrial tissue outside of the uterus with mixed traits of benign and malignant pathology. In this study we analyzed in endometrial and endometriotic tissues the differential expression of a panel of genes that are involved in preservation of stemness status and consequently considered as markers of stem cell presence. The expression profiles of a panel of 13 genes (SOX2, SOX15, ERAS, SALL4, OCT4, NANOG, UTF1, DPPA2, BMI1, GDF3, ZFP42, KLF4, TCL1) were analyzed by reverse transcription-polymerase chain reaction in human endometriotic (n = 12) and endometrial samples (n = 14). The expression of SALL4 and OCT4 was further analyzed by immunohistochemical methods. Genes UTF1, TCL1, and ZFP42 showed a trend for higher frequency of expression in endometriosis than in endometrium (P< 0.05 for UTF1), whereas GDF3 showed a higher frequency of expression in endometrial samples. Immunohistochemical analysis revealed that SALL4 was expressed in endometriotic samples but not in endometrium samples, despite the expression of the corresponding mRNA in both the sample groups. This study highlights a differential expression of stemness-related genes in ectopic and eutopic endometrium and suggests a possible role of SALL4-positive cells in the pathogenesis of endometriosis.


Journal of Cellular Physiology | 2008

Mesenchymal stem cells effectively reduce surgically induced stenosis in rat carotids

Amalia Forte; Mauro Finicelli; Monica Mattia; Liberato Berrino; Francesco Rossi; Marisa De Feo; Maurizio Cotrufo; Marilena Cipollaro; A. Cascino; Umberto Galderisi

Restenosis following vascular injury remains a pressing clinical problem. Mesenchymal stem cells (MSCs) promise as a main actor of cell‐based therapeutic strategies. The possible therapeutic role of MSCs in vascular stenosis in vivo has been poorly investigated so far. We tested the effectiveness of allogenic bone marrow‐derived MSCs in reduction of stenosis in a model of rat carotid arteriotomy. MSCs were expanded in vitro retaining their proliferative and differentiation potentiality. MSCs were able to differentiate into adipocyte and osteocyte mesenchymal lineage cells, retained specific antigens CD73, CD90, and CD105, expressed smooth muscle alpha‐actin, were mainly in proliferative phase of cell cycle and showed limited senescence. WKY rats were submitted to carotid arteriotomy and to venous administration with 5 × 106 MSCs. MSCs in vivo homed in injured carotids since 3 days after arteriotomy but not in contralateral uninjured carotids. Lumen area in MSC‐treated carotids was 36% greater than in control arteries (P = 0.016) and inward remodeling was limited in MSC‐treated carotids (P = 0.030) 30 days after arteriotomy. MSC treatment affected the expression level of inflammation‐related genes, inducing a decrease of IL‐1β and Mcp‐1 and an increase of TGF‐β in injured carotids at 3 and 7 days after arteriotomy (P < 0.05). Taken together, these results indicate that allogenic MSC administration limits stenosis in injured rat carotids and plays a local immunomodulatory action. J. Cell. Physiol. 217: 789–799, 2008.


Journal of Cellular and Molecular Medicine | 2008

Expression profiles in surgically-induced carotid stenosis: a combined transcriptomic and proteomic investigation.

Amalia Forte; Mauro Finicelli; P. De Luca; Cesare Quarto; Francesco Onorati; Pasquale Santè; Attilio Renzulli; Umberto Galderisi; Liberato Berrino; M. De Feo; Francesco Rossi; Maurizio Cotrufo; A. Cascino; Marilena Cipollaro

Vascular injury aimed at stenosis removal induces local reactions often leading to restenosis. The aim of this study was a concerted transcriptomic‐proteomics analysis of molecular variations in a model of rat carotid arteriotomy, to dissect the molecular pathways triggered by vascular surgical injury and to identify new potential anti‐restenosis targets. RNA and proteins extracted from inbred Wistar Kyoro (WKY) rat carotids harvested 4 hrs, 48 hrs and 7 days after arteriotomy were analysed by Affymetrix rat microarrays and by bidi‐mensional electrophoresis followed by liquid chromatography and tandem mass spectrometry, using as reference the RNA and the proteins extracted from uninjured rat carotids. Results were classified according to their biological function, and the most significant Kyoro Encyclopedia of Genes and Genomes (KEGG) pathways were identified. A total of 1163 mRNAs were differentially regulated in arteriotomy‐injured carotids 4 hrs, 48 hrs and 7 days after injury (P < 0.0001, fold‐change ≥2), while 48 spots exhibited significant changes after carotid arteriotomy (P < 0.05, fold‐change ≥2). Among them, 16 spots were successfully identified and resulted to correspond to a set of 19 proteins. mRNAs were mainly involved in signal transduction, oxidative stress/inflammation and remodelling, including many new potential targets for limitation of surgically induced (re)stenosis (e.g. Arginase I, Kruppel like factors). Proteome analysis confirmed and extended the microrarray data, revealing time‐dependent post‐translational modifications of Hsp27, haptoglobin and contrapsin‐like protease inhibitor 6, and the differential expression of proteins mainly involved in contractility. Transcriptomic and proteomic methods revealed functional categories with different preferences, related to the experimental sensitivity and to mechanisms of regulation. The comparative analysis revealed correlation between transcriptional and translational expression for 47% of identified proteins. Exceptions from this correlation confirm the complementarities of these approaches.


Oncogene | 2017

Deregulation of MicroRNAs mediated control of carnitine cycle in prostate cancer: molecular basis and pathophysiological consequences

Anna Valentino; Anna Calarco; A Di Salle; Mauro Finicelli; Stefania Crispi; Raffaele Adolfo Calogero; Federica Riccardo; A Sciarra; A Gentilucci; U Galderisi; Sabrina Margarucci; Gianfranco Peluso

Cancer cells reprogram their metabolism to maintain both viability and uncontrolled proliferation. Although an interplay between the genetic, epigenetic and metabolic rewiring in cancer is beginning to emerge, it remains unclear how this metabolic plasticity occurs. Here, we report that in prostate cancer cells (PCCs) microRNAs (miRNAs) greatly contribute to deregulation of mitochondrial fatty acid (FA) oxidation via carnitine system modulation. We provide evidence that the downregulation of hsa-miR-124-3p, hsa-miR-129-5p and hsa-miR-378 induced an increase in both expression and activity of CPT1A, CACT and CrAT in malignant prostate cells. Moreover, the analysis of human prostate cancer and prostate control specimens confirmed the aberrant expression of miR-124-3p, miR-129-5p and miR-378 in primary tumors. Forced expression of the miRNAs mentioned above affected tumorigenic properties, such as proliferation, migration and invasion, in PC3 and LNCaP cells regardless of their hormone sensitivity. CPT1A, CACT and CrAT overexpression allow PCCs to be more prone on FA utilization than normal prostate cells, also in the presence of high pyruvate concentration. Finally, the simultaneous increase of CPT1A, CACT and CrAT is fundamental for PCCs to sustain FA oxidation in the presence of heavy lipid load on prostate cancer mitochondria. Indeed, the downregulation of only one of these proteins reduces PCCs metabolic flexibility with the accumulation of FA-intermediate metabolites in the mitochondria. Together, our data implicate carnitine cycle as a primary regulator of adaptive metabolic reprogramming in PCCs and suggest new potential druggable pathways for prevention and treatment of prostate cancer.


Journal of Cellular Physiology | 2016

G-CSF contributes at the healing of tunica media of arteriotomy-injured rat carotids by promoting differentiation of vascular smooth muscle cells.

Barbara Rinaldi; Mauro Finicelli; Maria Donniacuo; Giovanni Di Bernardo; Giulia Gritti; Stefania Del Gaudio; Amalia Forte; Gianfranco Peluso; Marilena Cipollaro; Francesco Rossi; Umberto Galderisi

Restenosis is a complex pathophysiological disease whose causative mechanisms are not fully understood. Previous studies allowed us to demonstrate the efficacy of bone marrow mesenchymal stromal cells (MSCs) transplantation in limiting the pathophysiological remodeling in a model of arteriotomy‐induced (re) stenosis. In the current research we studied the effectiveness of G‐CSF treatment on male rate rats that were subjected carotid arteriotomy in order to evaluate a potentially effective non‐invasive strategy that recapitulates the MSC‐mediated recovery of injured vessels. WKY male rats were subjected carotid arteriotomy and given a nine day treatment (3 days pre‐ to 6 days post‐arteriotomy) with G‐CSF or saline. Carotids were harvested 7 and 30 days following arteriotomy (early‐ and late‐phase, respectively). Although morphometrical analysis did not reveal differences in lumen narrowing between G‐CSF‐ and PBS‐carotids 30 days following arteriotomy, we detected a noticeable conservative effect of G‐CSF treatment on vascular wall morphology. Histological and molecular analysis revealed an increase in cellularity within the tunica media with a concomitant increase of the VSMCs differentiation markers both at early‐ and late‐phases of (re) stenotic response in G‐CSF‐treated carotids (Sm22‐alpha, Myocd, and Smtn). These findings were accompanied by the downregulation of oxidative stress‐related genes in G‐CSF‐injured rats. The effect exerted by G‐CSF in our model of arteriotomy‐induced (re) stenosis seemed support the recovery of the architecture of the tunica media of injured vessels by: (i) inducing VSMCs differentiation; and (ii) limiting the oxidative‐stress response induced by arteriotomy. J. Cell. Physiol. 230: 215–223, 2016.


Clinical Science | 2009

Injury to rat carotid arteries causes time-dependent changes in gene expression in contralateral uninjured arteries

Amalia Forte; Mauro Finicelli; Pasquale De Luca; Ina Nordström; Francesco Onorati; Cesare Quarto; Pasquale Santè; Attilio Renzulli; Umberto Galderisi; Liberato Berrino; Marisa De Feo; Per Hellstrand; Francesco Rossi; Maurizio Cotrufo; A. Cascino; Marilena Cipollaro

Vascular surgery aimed at stenosis removal induces local reactions often leading to restenosis. Although extensive analysis has been focused on pathways activated in injured arteries, little attention has been devoted to associated systemic vascular reactions. The aim of the present study was to analyse changes occurring in contralateral uninjured rat carotid arteries in the acute phase following unilateral injury. WKY (Wistar-Kyoto) rats were subjected to unilateral carotid arteriotomy. Contralateral uninjured carotid arteries were harvested from 4 h to 7 days after injury. Carotid arteries were also harvested from sham-operated rats and uninjured rats. Carotid morphology and morphometry were examined. Affymetrix microarrays were used for differential analysis of gene expression. A subset of data was validated by real-time RT-PCR (reverse transcription-PCR) and verified at the protein level by Western blotting. A total of 1011 genes were differentially regulated in contralateral uninjured carotid arteries from 4 h to 7 days after arteriotomy (P<0.0001; fold change, >or=2) and were classified into 19 gene ontology functional categories. To a lesser extent, mRNA variations also occurred in carotid arteries of sham-operated rats. Among the changes, up-regulation of members of the RAS (renin-angiotensin system) was detected, with possible implications for vasocompensative mechanisms induced by arteriotomy. In particular, a selective increase in the 69 kDa isoform of the N-domain of ACE (angiotensin-converting enzyme), and not the classical somatic 195 kDa isoform, was observed in contralateral uninjured carotid arteries, suggesting that this 69 kDa isoenzyme could influence local AngII (angiotensin II) production. In conclusion, systemic reactions to injury occur in the vasculature, with potential clinical relevance, and suggest that caution is needed in the choice of controls during experimental design in vivo.


Journal of Cellular Physiology | 2018

Metabolic syndrome, Mediterranean diet, and polyphenols: Evidence and perspectives: FINICELLI et al.

Mauro Finicelli; Tiziana Squillaro; Francesca Di Cristo; Anna Di Salle; Mariarosa A. B. Melone; U Galderisi; Gianfranco Peluso

Metabolic syndrome (MetS) is defined as the co‐occurrence of metabolic risk factors that includes insulin resistance, hyperinsulinemia, impaired glucose tolerance, type 2 diabetes mellitus, dyslipidemia, and visceral obesity. The clinical significance of MetS consists of identifying a subgroup of patients sharing a common physiopathological state predisposing to chronic diseases. Clinical and scientific studies pinpoint lifestyle modification as an effective strategy aiming to reduce several features accountable for the risk of MetS onset. Among the healthy dietary patterns, the Mediterranean diet (MedDiet) emerges in terms of beneficial properties associated with longevity. Current evidence highlights the protective effect exerted by MedDiet on the different components of MetS. Interestingly, the effect exerted by polyphenols contained within the representative MedDiet components (i.e., olive oil, red wine, and nuts) seems to be accountable for the beneficial properties associated to this dietary pattern. In this review, we aim to summarize the principal evidence regarding the effectiveness of MedDiet–polyphenols in preventing or delaying the physiopathological components accountable for MetS onset. These findings may provide useful insights concerning the health properties of MedDiet–polyphenols as well as the novel targets destined to a tailored approach to MetS.


Cancer Research | 2015

Abstract P2-06-05: Expression of the pluripotency transcription factor SOX2 in primary breast cancers (BCs): Correlation with clinicopathological features (CPfs) and recurrence

Barbara Pistilli; Giovanni Benedetti; Mauro Finicelli; Tiziana Squillaro; Andrea Marcellusi; Tommasina Biscotti; Alfredo Santinelli; Paola Mariani; Paolo Decembrini; Giancarlo Ciccioli; Luciano Latini; Antonio Giordano; Umberto Galderisi

BACKGROUND SOX2 is one of the pluripotency transcription factors expressed by stem cells, which plays a central role in controlling the expression of genes implicated in embryonic development and stemness manteinance. Key regulators of embryonic stem cell (ESC) identity, such as NANOG, SOX2, OCT4 and GDF3 resulted overexpressed in a variety of solid tumors with a possible role in cancer progression and prognosis. SOX2 expression has mainly been reported in basal-like BC subtype, suggesting a role in conferring a less differentiated phenotype. In our analysis we evaluated a heterogenous group of BC tissues to determine whether the expression of ESC-regulating genes correlated with CPfs and recurrence. METHODS 140 primary invasive BC specimens were collected from 137 female patients who underwent surgery. mRNA expression for SOX2, OCT4, NANOG, GDF3 genes was assessed by RT-PCR. Immunoistochemistry (IHC) was performed for SOX2 with mouse monoclonal antibody (1:50, Y17, Santa Cruz Biotechnology, USA). Correlations with molecular subtypes, menopausal status, grading, ER, PR, ki67 (≤ 20% and > 20%), HER2, T-size and node status were evaluated by Fisher9s exact test and χ2 test. Association of ESC-genes, CPfs and DFS was estimated by univariate and multivariate Cox-regression analysis (p≤ 0.05). Survival analysis (DFS and OS) were calculated by Kaplan-Meier curves and compared by log-rank test. RESULTS In 117 samples assessable by RT-PCR the genes resulted expressed as follows: NANOG=52 (44.5%), SOX2=11 (9.4%), GDF3=9 (7.2%), OCT-4=0. Correlation of mRNA gene expression with CPfs was statistically significant between NANOG and grade 2, GDF3 and node-negative status, SOX2 and higher ki67 (p=0.019, p=0.029, p= 0.035, respectively). Six out of 11 SOX2+ tumors were HER2+ (data not statistically significant); in the remaining 5 samples the fluorescence in situ hybridization was performed but no HER2 amplification was detected. At univariate analysis of DFS, SOX2 expression (HR=2,36; p=0.002), ki67 (HR= 2,19; p=0,028), T-size >1 (HR=2,06; p=2.011), node-status (HR=2,21; p= 0.014); ER/PR(HR=0,58/HR=0,59, p=0.065/p=0.068) resulted statistically significant. At multivariate analysis, SOX2 (HR=2,99; 95% CI 1,41-6,30; p=0.004), node-status (HR=2,44; 95%CI 1,25-4,76; p=0.009) and T-size >1 (HR=1,77; 95% CI=0,99-3,13; p=0.051) were independently associated with increased risk of recurrence. An earlier recurrence was observed in SOX2+ patients (median 34.9 months; 95% CI: 7.5-62.2) than SOX2- patients (median: 60.3 months; 95% CI: 32.6-88.1) (p=0.017); OS resulted shorter in SOX2+ (68.2 months 95%CI: 63.7-151.4 vs 145.3 months 95% CI: 80.5-210.2) albeit not statistically significant (p=0.104). IHC analysis showed a positive score for SOX2 protein expression in all of 11 samples with SOX2 mRNA amplification; SOX2+ protein was not detected in 20 samples randomly selected among the tissues not expressing SOX2 mRNA. CONCLUSIONS Our analysis confirm that ESC-regulating genes correlate with specific CPfs (grading, node-status and ki67). Notably, SOX2 resulted to be an independent prognostic factor, as it was associated with a risk of recurrence increased by 3 times, irrespective of other CPfs. Citation Format: Barbara Pistilli, Giovanni Benedetti, Mauro Finicelli, Tiziana Squillaro, Andrea Marcellusi, Tommasina Biscotti, Alfredo Santinelli, Paola Mariani, Paolo Decembrini, Giancarlo Ciccioli, Luciano Latini, Antonio Giordano, Umberto Galderisi. Expression of the pluripotency transcription factor SOX2 in primary breast cancers (BCs): Correlation with clinicopathological features (CPfs) and recurrence [abstract]. In: Proceedings of the Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2014 Dec 9-13; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2015;75(9 Suppl):Abstract nr P2-06-05.


Clinical Science | 2013

Early cell changes and TGFβ pathway alterations in the aortopathy associated with bicuspid aortic valve stenosis.

Amalia Forte; Alessandro Della Corte; Mario Grossi; Ciro Bancone; Raffaela Provenzano; Mauro Finicelli; Marisa De Feo; Luca Salvatore De Santo; Gianantonio Nappi; Maurizio Cotrufo; Umberto Galderisi; Marilena Cipollaro


Cardiovascular Drugs and Therapy | 2012

Stem Cell Therapy for Arterial Restenosis: Potential Parameters Contributing to the Success of Bone Marrow-Derived Mesenchymal Stromal Cells

Amalia Forte; Barbara Rinaldi; Loredana Sodano; Liberato Berrino; Francesco Rossi; Mauro Finicelli; Mario Grossi; Gilda Cobellis; Chiara Botti; Marisa De Feo; Pasquale Santè; Umberto Galderisi; Marilena Cipollaro

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Umberto Galderisi

Seconda Università degli Studi di Napoli

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Marilena Cipollaro

Seconda Università degli Studi di Napoli

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Amalia Forte

Seconda Università degli Studi di Napoli

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Francesco Rossi

Seconda Università degli Studi di Napoli

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Maurizio Cotrufo

Seconda Università degli Studi di Napoli

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Tiziana Squillaro

Seconda Università degli Studi di Napoli

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Liberato Berrino

Seconda Università degli Studi di Napoli

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Marisa De Feo

Seconda Università degli Studi di Napoli

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Alfredo Santinelli

Marche Polytechnic University

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