0000000000542918

AUTHOR

Roberto Sala

0000-0002-9167-0020

showing 9 related works from this author

SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress.

2005

AbstractUnder hypertonic conditions the induction of SLC38A2/SNAT2 leads to the stimulation of transport system A and to the increase in the cell content of amino acids. In hypertonically stressed human fibroblasts transfection with two siRNAs for SNAT2 suppressed the increase in SNAT2 mRNA and the stimulation of system A transport activity. Under the same condition, the expansion of the intracellular amino acid pool was significantly lowered and cell volume recovery markedly delayed. It is concluded that the up-regulation of SNAT2 is essential for the rapid restoration of cell volume after hypertonic stress.

Small interfering RNAmedicine.medical_specialtyAmino Acid Transport System AGlutamineCellBiophysicsStimulationBiologyTransfectionBiochemistryStructural BiologyOsmotic PressureCell volumeInternal medicineGeneticsmedicineHumansRNA MessengerAmino AcidsRNA Small InterferingMolecular BiologyCell Sizechemistry.chemical_classificationSaline Solution HypertonicCell BiologyFibroblastsAmino acidCell biologyUp-RegulationGlutaminemedicine.anatomical_structureEndocrinologychemistryHypertonic StresssiRNATonicityRNA InterferenceIntracellularFEBS letters
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INFγ stimulates arginine transport through system y+L in human monocytes

2004

Freshly isolated human monocytes transport L-arginine mostly through a sodium independent, NEM insensitive pathway inhibited by L-leucine in the presence, but not in the absence of sodium. Interferon-gamma (IFNgamma) stimulates this pathway, identifiable with system y+L, and markedly enhances the expression of SLC7A7, the gene that encodes for system y+L subunit y+LAT1, but not of SLC7A6, that codes for the alternative subunit y+LAT2. System y+ plays a minor role in arginine uptake by monocytes and the expression of system y+-related genes, SLC7A1 and SLC7A2, is not changed by IFNgamma. These results demonstrate that system y+L is sensitive to IFNgamma.

ArginineSodiumProtein subunitBiophysicschemistry.chemical_elementBiologyLPI - Lysinuric protein intoleranceArginineMonocyteBiochemistryMonocytesInterferon-gammaInterferon γLeucineStructural BiologyArginine transportSystem y+L.GeneticsmedicineHumansMolecular BiologyGeneLysinuric protein intoleranceCells CulturedArginine transportReverse Transcriptase Polymerase Chain ReactionFusion Regulatory Protein 1 Light ChainsMonocyteSodiumAmino Acid Transport System y+LBiological TransportCell BiologyMolecular biologyRecombinant ProteinsKineticsmedicine.anatomical_structurechemistryEthylmaleimideAmino Acid Transport Systems BasicInterferon-γFEBS Letters
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In human endothelial cells rapamycin causes mTORC2 inhibition and impairs cell viability and function.

2008

Aim Drug-eluting stents are widely used to prevent restenosis but are associated with late endothelial damage. To understand the basis for this effect, we have studied the consequences of a prolonged incubation with rapamycin on the viability and functions of endothelial cells. Methods and results Human umbilical vein or aorta endothelial cells were exposed to rapamycin in the absence or in the presence of tumour necrosis factor α (TNFα). After a 24 h-incubation, rapamycin (100 nM) caused a significant cell loss associated with the increase of both apoptosis and necrosis, as quantified by propidium iodide staining, caspase 3 activity, and lactate dehydrogenase release. Rapamycin also impair…

Time FactorsPhysiologyApoptosismTORC1Polymerase Chain Reactionchemistry.chemical_compoundCell MovementStress FibersMicroscopy ConfocalCaspase 3TOR Serine-Threonine KinasesNitric Oxide Synthase Type IIIRibosomal Protein S6 Kinases 70-kDaUp-RegulationEndothelial stem cellmedicine.anatomical_structureBiochemistryCardiology and Cardiovascular MedicineE-SelectinEndotheliumNitric Oxide Synthase Type IIICell SurvivalBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyMechanistic Target of Rapamycin Complex 1Nitric OxideTacrolimusNecrosisTheophyllinePhysiology (medical)medicineHumansImmunoprecipitationViability assayPropidium iodideProtein kinase BAdaptor Proteins Signal TransducingSirolimusDose-Response Relationship DrugL-Lactate DehydrogenaseTumor Necrosis Factor-alphaEndothelial CellsProteinsCardiovascular AgentsRegulatory-Associated Protein of mTORMolecular biologyRapamycin-Insensitive Companion of mTOR ProteinchemistryMultiprotein ComplexesTOR Serine-Threonine KinasesCarrier ProteinsProtein KinasesTranscription FactorsCardiovascular research
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Stanozolol promotes osteogenic gene expression and apposition of bone mineral in vitro

2018

Abstract Stanozolol (ST) is a synthetic androgen with high anabolic potential. Although it is known that androgens play a positive role in bone metabolism, ST action on bone cells has not been sufficiently tested to support its clinical use for bone augmentation procedures. Objective: This study aimed to assess the effects of ST on osteogenic activity and gene expression in SaOS-2 cells. Material and Methods: SaOS-2 deposition of mineralizing matrix in response to increasing doses of ST (0-1000 nM) was evaluated through Alizarin Red S and Calcein Green staining techniques at 6, 12 and 24 days. Gene expression of runt-related transcription factor 2 (RUNX2), vitamin D receptor (VDR), osteopon…

0301 basic medicineTime FactorsBone matrixCore Binding Factor Alpha 1 SubunitReal-Time Polymerase Chain ReactionCalcitriol receptorBone remodelingCalcificationAndrology03 medical and health sciencesAnabolic AgentsCalcification PhysiologicOsteogenesisCell Line TumorBone cellHumansOsteonectinOsteopontinGeneral DentistryBone mineralAnalysis of VarianceOsteoblastsbiologyChemistryReproducibility of Resultslcsh:RK1-715RUNX2Apposition030104 developmental biologylcsh:DentistryLinear Modelsbiology.proteinAndrogensReceptors CalcitriolOriginal ArticleOsteopontinGene expressionOsteonectinStanozolol
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The synthesis of SNAT2 transporters is required for the hypertonic stimulation of system A transport activity

2004

AbstractIn cultured human fibroblasts incubated under hypertonic conditions, the stimulation of system A for neutral amino acid transport, associated to the increased expression of the mRNA for SNAT2 transporter, leads to an expanded intracellular amino acid pool and to the recovery of cell volume. A protein of nearly 60 kDa, recognized by an antiserum against SNAT2, is increased both in the pool of biotinylated membrane proteins and in the total cell lysate of hypertonically stressed cells. The increased level of SNAT2 transporters in hypertonically stressed cells is confirmed by immunocytochemistry. DRB, an inhibitor of transcription, substantially inhibits the increase of SNAT2 proteins …

LysisAmino Acid Transport System AProlineTranscription GeneticGlutamineBlotting WesternHypertonic SolutionsBiophysicsStimulationBiologyHuman fibroblastBiochemistrySubstrate SpecificityAmino acid starvationHypertonic stressCell volumeNeutral amino acid transportHumansBiotinylationRNA MessengerCells CulturedCell Sizechemistry.chemical_classificationRadioisotopesCell MembraneBiological TransportPhosphorusCell BiologyFibroblastsImmunohistochemistryAmino acidGlutamineMolecular WeightKineticschemistryBiochemistryMembrane proteinHypertonic StressIntracellularDichlororibofuranosylbenzimidazoleBiochimica et Biophysica Acta (BBA) - Biomembranes
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Rapamycin stimulates arginine influx through CAT2 transporters in human endothelial cells

2007

In endothelial cells Tumor Necrosis Factor-alpha (TNFalpha) stimulates arginine transport through the increased expression of SLC7A2/CAT2 transcripts. Here we show that also rapamycin, an inhibitor of mTOR kinase, stimulates system y(+)-mediated arginine uptake in human endothelial cells derived from either saphenous (HSVECs) or umbilical veins (HUVECs). When used together with TNFalpha, rapamycin produces an additive stimulation of arginine transport in both cell models. These effects are observed also upon incubation with AICAR, a stimulator of Adenosine-Monophosphate-dependent-Protein Kinase (AMPK) that produces a rapamycin-independent inhibition of the mTOR pathway. Rapamycin increases …

CAT transporterArginineBlotting WesternBiophysicsBiologyArginineNitric OxideBiochemistryWestern blotSLC7A genemedicineHumansAmino AcidsPI3K/AKT/mTOR pathwayDNA PrimersSirolimusArginine transportmedicine.diagnostic_testKinaseReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAMPKEndothelial CellsBiological TransportCell BiologySystem y+Molecular biologyImmunohistochemistryGene Expression RegulationmTORAmino Acid Transport Systems BasicTumor necrosis factor alphaIntracellularBiochimica et Biophysica Acta (BBA) - Biomembranes
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The stimulation of arginine transport by TNFα in human endothelial cells depends on NF-κB activation

2004

In human saphenous vein endothelial cells (HSVECs), tumor necrosis factor-alpha (TNFalpha) and bacterial lipopolysaccharide (LPS), but neither interferon gamma (IFNgamma) nor interleukin 1beta (IL-1beta), stimulate arginine transport. The effects of TNFalpha and LPS are due solely to the enhancement of system y+ activity, whereas system y+L is substantially unaffected. TNFalpha causes an increased expression of SLC7A2/CAT-2B gene while SLC7A1/CAT-1 expression is not altered by the cytokine. The suppression of PKC-dependent transduction pathways, obtained with the inhibitor chelerytrhine, the inhibitor peptide of PKCzeta isoform, or chronic exposure to phorbol esters, does not prevent TNFalp…

MAPK/ERK pathwayLipopolysaccharidesmedicine.medical_specialtyUmbilical VeinsTime FactorsCAT transporterArginineTranscription Geneticp38 mitogen-activated protein kinasesmedicine.medical_treatmentBiophysicsPharmacologyBiologyArgininePolymerase Chain Reactionp38 Mitogen-Activated Protein KinasesBiochemistryInterferon-gammaInternal medicineCationsmedicineTNFαHumansInterferon gammaRNA MessengerCationic Amino Acid Transporter 2Cells CulturedProtein Kinase CArginine transportReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaNF-kappa BBiological TransportCell BiologyCytokineEndocrinologySLC7 geneAmino Acid Transport Systems BasicCytokinesTumor necrosis factor alphaEndothelium VascularSignal transductionMitogen-Activated Protein KinasesPeptidesmedicine.drugInterleukin-1Signal TransductionNFκBBiochimica et Biophysica Acta (BBA) - Biomembranes
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Effects of zoledronic acid and dexamethasone on early phases of socket healing after tooth extraction in rats : a preliminary macroscopic and microsc…

2018

Background The exact pathogenesis of medication-related osteonecrosis of the jaw (MRONJ) is still unknown. The aim of this paper was to investigate the effects of zoledronic acid and dexamethasone on the early phases of socket healing in rats subjected to tooth extractions. Material and Methods Thirty male Sprague-Dawley rats were divided into 2 groups: pharmacologically treated group (T, n=20) and non-pharmacologically treated group (C, n=10). T group rats received 0.1 mg/Kg of zoledronic acid (ZOL) and 1 mg/Kg of dexamethasone (DEX) three times a week for 10 consecutive weeks. C group rats were infused with vehicle. After 9 weeks from the first infusion, first maxillary molars were extrac…

MolarMalemedicine.medical_specialtyConnective tissueZoledronic AcidDexamethasoneBone remodelingRats Sprague-Dawley03 medical and health sciences0302 clinical medicineOsteoclastInternal medicinemedicineAnimalsHumansTooth SocketGeneral DentistryDexamethasoneDental alveolusOral Medicine and PathologyBone Density Conservation AgentsDiphosphonatesbusiness.industryResearchOsteonecrosis030206 dentistrymedicine.disease:CIENCIAS MÉDICAS [UNESCO]Ratsmedicine.anatomical_structureZoledronic acidEndocrinologyOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASTooth ExtractionSurgerybusinessOsteonecrosis of the jawmedicine.drug
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Stanozolol promotes osteogenic gene expression and apposition of bone mineral in vitro

2018

Abstract Stanozolol (ST) is a synthetic androgen with high anabolic potential. Although it is known that androgens play a positive role in bone metabolism, ST action on bone cells has not been sufficiently tested to support its clinical use for bone augmentation procedures. Objective: This study aimed to assess the effects of ST on osteogenic activity and gene expression in SaOS-2 cells. Material and Methods: SaOS-2 deposition of mineralizing matrix in response to increasing doses of ST (0-1000 nM) was evaluated through Alizarin Red S and Calcein Green staining techniques at 6, 12 and 24 days. Gene expression of runt-related transcription factor 2 (RUNX2), vitamin D receptor (VDR), osteopon…

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