Publications by authors named "Ambra Vestri"

7 Publications

  • Page 1 of 1

Plasmonic Metasurfaces Based on Pyramidal Nanoholes for High-Efficiency SERS Biosensing.

ACS Appl Mater Interfaces 2021 Sep 1;13(36):43715-43725. Epub 2021 Sep 1.

Institute of Applied Sciences and Intelligent Systems "E. Caianiello" CNR, 80078 Pozzuoli, Italy.

An inverted pyramidal metasurface was designed, fabricated, and studied at the nanoscale level for the development of a label-free pathogen detection on a chip platform that merges nanotechnology and surface-enhanced Raman scattering (SERS). Based on the integration and synergy of these ingredients, a virus immunoassay was proposed as a relevant proof of concept for very sensitive detection of hepatitis A virus, for the first time to our best knowledge, in a very small volume (2 μL), without complex signal amplification, allowing to detect a minimal virus concentration of 13 pg/mL. The proposed work aims to develop a high-flux and high-accuracy surface-enhanced Raman spectroscopy (SERS) nanobiosensor for the detection of pathogens to provide an effective method for early and easy water monitoring, which can be fast and convenient.
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http://dx.doi.org/10.1021/acsami.1c12525DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8447193PMC
September 2021

SERS Biosensor Based on Engineered 2D-Aperiodic Nanostructure for In-Situ Detection of Viable Bacterium in Complex Matrix.

Nanomaterials (Basel) 2021 Mar 31;11(4). Epub 2021 Mar 31.

Institute of Applied Sciences and Intelligent Systems "E. Caianiello" of CNR, 80078 Pozzuoli, Italy.

is a foodborne pathogen globally affecting both the economy and healthcare. Surface Enhanced Raman Spectroscopy (SERS) nano-biosensing can be a promising strategy for its detection. We combined high-performance quasi-crystal patterned nanocavities for Raman enhancement with the use of covalently immobilized Tbilisi bacteriophages as high-performing bio-receptors. We coupled our efficient SERS nano-biosensor to a Raman system to develop an on-field phage-based bio-sensing platform capable of monitoring the target bacteria. The developed biosensor allowed us to identify in milk by our portable SERS device. Upon bacterial capture from samples (10 cells), a signal related to the pathogen recognition was observed, proving the concrete applicability of our system for on-site and in-food detection.
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http://dx.doi.org/10.3390/nano11040886DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8067257PMC
March 2021

Involvement of released sphingosine 1-phosphate/sphingosine 1-phosphate receptor axis in skeletal muscle atrophy.

Biochim Biophys Acta Mol Basis Dis 2018 12 1;1864(12):3598-3614. Epub 2018 Sep 1.

Department of Experimental and Clinical Biomedical Sciences "Mario Serio" -Unit of Biochemical Sciences and Molecular Biology, University of Florence, Viale GB Morgagni, 50, Florence, Italy. Electronic address:

Skeletal muscle (SkM) atrophy is caused by several and heterogeneous conditions, such as cancer, neuromuscular disorders and aging. In most types of SkM atrophy overall rates of protein synthesis are suppressed, protein degradation is consistently elevated and atrogenes, such as the ubiquitin ligase Atrogin-1/MAFbx, are up-regulated. The molecular regulators of SkM waste are multiple and only in part known. Sphingolipids represent a class of bioactive molecules capable of modulating the destiny of many cell types, including SkM cells. In particular, we and others have shown that sphingosine 1phosphate (S1P), formed by sphingosine kinase (SphK), is able to act as trophic and morphogenic factor in myoblasts. Here, we report the first evidence that the atrophic phenotype observed in both muscle obtained from mice bearing the C26 adenocarcinoma and C2C12 myotubes treated with dexamethasone was characterized by reduced levels of active phospho-SphK1. The importance of SphK1 activity is also confirmed by the specific pharmacological inhibition of SphK1 able to increase Atrogin-1/MAFbx expression and reduce myotube size and myonuclei number. Furthermore, we found that SkM atrophy was accomplished by significant increase of S1P transporter Spns2 and in changes in the pattern of S1P receptor (S1PRs) subtype expression paralleled by increased Atrogin-1/MAFbx expression, suggesting a role for the released S1P and of specific S1PR-mediated signaling pathways in the control of the ubiquitin ligase. Altogether, these findings provide the first evidence that SphK1/released S1P/S1PR axis acts as a molecular regulator of SkM atrophy, thereby representing a new possible target for therapy in many patho-physiological conditions.
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http://dx.doi.org/10.1016/j.bbadis.2018.08.040DOI Listing
December 2018

Sphingosine 1-Phosphate Receptor 1 Is Required for MMP-2 Function in Bone Marrow Mesenchymal Stromal Cells: Implications for Cytoskeleton Assembly and Proliferation.

Stem Cells Int 2018 11;2018:5034679. Epub 2018 Mar 11.

Unit of Biochemical Sciences and Molecular Biology, Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Florence, 50 Viale GB Morgagni, 50134 Florence, Italy.

Bone marrow-derived mesenchymal stromal cell- (BM-MSC-) based therapy is a promising option for regenerative medicine. An important role in the control of the processes influencing the BM-MSC therapeutic efficacy, namely, extracellular matrix remodelling and proliferation and secretion ability, is played by matrix metalloproteinase- (MMP-) 2. Therefore, the identification of paracrine/autocrine regulators of MMP-2 function may be of great relevance for improving BM-MSC therapeutic potential. We recently reported that BM-MSCs release the bioactive lipid sphingosine 1-phosphate (S1P) and, here, we demonstrated an impairment of MMP-2 expression/release when the S1P receptor subtype S1PR1 is blocked. Notably, active S1PR1/MMP-2 signalling is required for F-actin structure assembly (lamellipodia, microspikes, and stress fibers) and, in turn, cell proliferation. Moreover, in experimental conditions resembling the damaged/regenerating tissue microenvironment (hypoxia), S1P/S1PR1 system is also required for HIF-1 expression and vinculin reduction. Our findings demonstrate for the first time the trophic role of S1P/S1PR1 signalling in maintaining BM-MSCs' ability to modulate MMP-2 function, necessary for cytoskeleton reorganization and cell proliferation in both normoxia and hypoxia. Altogether, these data provide new perspectives for considering S1P/S1PR1 signalling a pharmacological target to preserve BM-MSC properties and to potentiate their beneficial potential in tissue repair.
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http://dx.doi.org/10.1155/2018/5034679DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5866864PMC
March 2018

Sphingosine 1-Phosphate Receptors: Do They Have a Therapeutic Potential in Cardiac Fibrosis?

Front Pharmacol 2017 2;8:296. Epub 2017 Jun 2.

Department of Experimental and Clinical Biomedical Sciences "Mario Serio", Molecular and Applied Biology Research Unit, University of FlorenceFlorence, Italy.

Sphingosine 1-phosphate (S1P) is a bioactive lipid that is characterized by a peculiar mechanism of action. In fact, S1P, which is produced inside the cell, can act as an intracellular mediator, whereas after its export outside the cell, it can act as ligand of specific G-protein coupled receptors, which were initially named endothelial differentiation gene (Edg) and eventually renamed sphingosine 1-phosphate receptors (S1PRs). Among the five S1PR subtypes, S1PR1, S1PR2 and S1PR3 isoforms show broad tissue gene expression, while S1PR4 is primarily expressed in immune system cells, and S1PR5 is expressed in the central nervous system. There is accumulating evidence for the important role of S1P as a mediator of many processes, such as angiogenesis, carcinogenesis and immunity, and, ultimately, fibrosis. After a tissue injury, the imbalance between the production of extracellular matrix (ECM) and its degradation, which occurs due to chronic inflammatory conditions, leads to an accumulation of ECM and, consequential, organ dysfunction. In these pathological conditions, many factors have been described to act as pro- and anti-fibrotic agents, including S1P. This bioactive lipid exhibits both pro- and anti-fibrotic effects, depending on its site of action. In this review, after a brief description of sphingolipid metabolism and signaling, we emphasize the involvement of the S1P/S1PR axis and the downstream signaling pathways in the development of fibrosis. The current knowledge of the therapeutic potential of S1PR subtype modulators in the treatment of the cardiac functions and fibrinogenesis are also examined.
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http://dx.doi.org/10.3389/fphar.2017.00296DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5454082PMC
June 2017

Crosstalk between sphingolipids and vitamin D3: potential role in the nervous system.

Br J Pharmacol 2017 04 24;174(8):605-627. Epub 2017 Feb 24.

Department of Experimental and Clinical Biomedical Sciences 'Mario Serio', Molecular and Applied Biology Research Unit, University of Florence, Florence, Italy.

Sphingolipids are both structural and bioactive compounds. In particular, ceramide and sphingosine 1-phosphate regulate cell fate, inflammation and excitability. 1-α,25-dihydroxyvitamin D3 (1,25(OH) D ) is known to play an important physiological role in growth and differentiation in a variety of cell types, including neural cells, through genomic actions mediated by its specific receptor, and non-genomic effects that result in the activation of specific signalling pathways. 1,25(OH) D and sphingolipids, in particular sphingosine 1-phosphate, share many common effectors, including calcium regulation, growth factors and inflammatory cytokines, but it is still not known whether they can act synergistically. Alterations in the signalling and concentrations of sphingolipids and 1,25(OH) D have been found in neurodegenerative diseases and fingolimod, a structural analogue of sphingosine, has been approved for the treatment of multiple sclerosis. This review, after a brief description of the role of sphingolipids and 1,25(OH) D , will focus on the potential crosstalk between sphingolipids and 1,25(OH) D in neural cells.
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http://dx.doi.org/10.1111/bph.13726DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6398521PMC
April 2017

Surface plasmon resonance based on molecularly imprinted nanoparticles for the picomolar detection of the iron regulating hormone Hepcidin-25.

J Nanobiotechnology 2015 Aug 27;13:51. Epub 2015 Aug 27.

Department of Biotechnology, University of Verona, Strada Le Grazie 15, 37134, Verona, Italy.

Background: Molecularly imprinted polymer (MIP) technique is a powerful mean to produce tailor made synthetic recognition sites. Here precipitation polymerization was exploited to produce a library of MIP nanoparticles (NPs) targeting the N terminus of the hormone Hepcidin-25, whose serum levels correlate with iron dis-metabolisms and doping. Biotinylated MIP NPs were immobilized to NeutrAvidin™ SPR sensor chip. The response of the MIP NP sensor to Hepcidin-25 was studied.

Findings: Morphological analysis showed MIP NPs of 20-50 nm; MIP NP exhibited high affinity and selectivity for the target analyte: low nanomolar Kds for the interaction NP/Hepcidin-25, but none for the NP/non regulative Hepcidin-20. The MIP NP were integrated as recognition element in SPR allowing the detection of Hepcidin-25 in 3 min. Linearity was observed with the logarithm of Hepcidin-25 concentration in the range 7.2-720 pM. LOD was 5 pM. The response for Hepcidin-20 was limited. Hepcidin-25 determination in real serum samples spiked with known analyte concentrations was also attempted.

Conclusion: The integration of MIP NP to SPR allowed the determination of Hepcidin-25 at picomolar concentrations in short times outperforming the actual state of art. Optimization is still needed for real sample measurements in view of future clinical applications.
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http://dx.doi.org/10.1186/s12951-015-0115-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549936PMC
August 2015
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