Maurizio Parola

Publications (112) View all

• Article: Corrigendum to Silibinin improves hepatic and myocardial injury in mice with nonalcoholic steatohepatitis [Dig. Liver Dis. 44 (2012) 334-342]

  F. Salamone, F. Galvano, A. Marino Gammazza, C. Paternostro, D. Tibullo, F. Bucchieri, A. Mangiameli, M. Parola, E. Bugianesi, G. Li Volti
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  ABSTRACT: Export Date: 3 May 2013, Source: Scopus, CODEN: DLDIF, :doi 10.1016/j.dld.2012.04.004, Language of Original Document: English, Correspondence Address: Salamone, F.; Dipartimento di Medicina Interna, Università di Catania, Via Santa Sofia 78, 95123 Catania, Italy; email: federicosalamone@yahoo.it
  Digestive and Liver Disease. 01/2012; 44(8):709.
• Article: Human-induced pluripotent stem cells as a source of hepatocyte-like cells: new kids on the block.

  C Busletta, E Novo, M Parola
  Hepatology International 07/2011; · 2.64 Impact Factor
• Article: Calcium-dependent diuretic system in preascitic liver cirrhosis.

  G Sansoè, M Aragno, C E Tomasinelli, L Valfrè di Bonzo, F Wong, M Parola
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  ABSTRACT: Extracellular Ca(++) activates cell membrane calcium-sensing receptors (CaRs), leading to renal tubule production of prostaglandins E(2) (PGE(2)), which decrease both sodium reabsorption in the thick ascending limb of Henle's loop and free-water reabsorption in collecting ducts. To assess the activity of this diuretic system in experimental cirrhosis, we evaluated renal function, hormonal status, PGE(2) urinary excretion, and renal tissue concentrations of Na(+)-K(+)-2Cl(-) co-transporters (BSC-1) and CaRs in three groups of rats: one group of controls receiving 5% glucose solution (vehicle) intravenously and two groups of rats with CCl(4)-induced preascitic cirrhosis receiving either vehicle or 0.5mg i.v. Poly-l-Arginine (PolyAg), a CaR-selective agonist. Compared to controls, cirrhotic rats showed reduced urine volume and sodium excretion (p<0.05). Western blot analysis revealed reduced CaRs and increased BSC-1 protein content in kidneys of cirrhotic rats compared with controls (all p<0.01). PolyAg-treated cirrhotic rats had their urine and sodium excretion returned to normal; PolyAg also increased renal plasma flow, PGE(2) urinary excretion, and free-water clearance in cirrhotic rats (all p<0.01 v. untreated cirrhotic animals). In preascitic cirrhosis, sodium retention may be linked to down-regulation of renal CaRs and up-regulation of tubular sodium-retaining channels. Calcimimetic drugs normalize preascitic sodium retention.
  Journal of Hepatology 11/2010; 53(5):856-62. · 9.26 Impact Factor
• Article: Human mesenchymal stem cells as a two-edged sword in hepatic regenerative medicine: engraftment and hepatocyte differentiation versus profibrogenic potential.

  L Valfrè di Bonzo, I Ferrero, C Cravanzola, K Mareschi, D Rustichell, E Novo, F Sanavio, S Cannito, E Zamara, M Bertero, A Davit, S Francica, F Novelli, S Colombatto, F Fagioli, M Parola
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  ABSTRACT: Mesenchymal stem cells from bone marrow (MSCs) may have the potential to differentiate in vitro and in vivo into hepatocytes. We investigated whether transplanted human MSCs (hMSCs) may engraft the liver of non-obese diabetic severe combined immuno-deficient (NOD/SCID) mice and differentiate into cells of hepatic lineage. Ex vivo expanded, highly purified and functionally active hMSCs from bone marrow were transplanted (caudal vein) in sublethally irradiated NOD/SCID mice that were either exposed or not to acute liver injury or submitted to a protocol of chronic injury (single or chronic intraperitoneal injection of CCl(4), respectively). Chimeric livers were analysed for expression of human transcripts and antigens. Liver engraftment of cells of human origin was very low in normal and acutely injured NOD/SCID mice with significantly higher numbers found in chronically injured livers. However, hepatocellular differentiation was relatively rare, limited to a low number of cells (ranging from less than 0.1% to 0.23%) as confirmed by very low or not detectable levels of human transcripts for alpha-fetoprotein, CK18, CK19 and albumin in either normal or injured livers. Finally, a significant number of cells of human origin exhibited a myofibroblast-like morphology. Transplanted hMSCs have the potential to migrate into normal and injured liver parenchyma, particularly under conditions of chronic injury, but differentiation into hepatocyte-like cells is a rare event and pro-fibrogenic potential of hMSC transplant should be not under-evaluated.
  Gut 03/2008; 57(2):223-31. · 10.11 Impact Factor
• Source

  Available from: Antonio Mazzocca

  Article: Overexpression of Bcl-2 by activated human hepatic stellate cells: resistance to apoptosis as a mechanism of progressive hepatic fibrogenesis in humans.

  E Novo, F Marra, E Zamara, L Valfrè di Bonzo, L Monitillo, S Cannito, I Petrai, A Mazzocca, A Bonacchi, R S M De Franco, S Colombatto, R Autelli, M Pinzani, M Parola
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  ABSTRACT: Myofibroblast-like cells, originating from activation of hepatic stellate cells (HSC/MFs), play a key role in liver fibrosis, a potentially reversible process that may rely on induction of HSC/MFs apoptosis. While this possibility has been shown in cultured rat HSC, very limited data are currently available for human HSC/MFs. Cultured human HSC/MFs were exposed to several proapoptotic stimuli, including those known to induce apoptosis in rat HSC/MFs, and induction of cell death and related mechanisms were investigated using morphology, molecular biology, and biochemical techniques. In this study we report that fully activated human HSC/MFs did not undergo spontaneous apoptosis and survived to prolonged serum deprivation, Fas activation, or exposure to nerve growth factor, tumour necrosis factor alpha (TNF-alpha), oxidative stress mediators, doxorubicin, and etoposide. Induction of caspase dependent, mitochondria driven apoptosis in HSC/MFs was observed only when protein synthesis or transcription were inhibited. Importantly, the process of HSC activation was accompanied by changes in expression of a set of genes involved in apoptosis control. In particular, activated human HSC/MFs in culture overexpressed Bcl-2. The role of Bcl-2 was crucial as Bcl-2 silenced cells became susceptible to TNF-alpha induced apoptosis. Finally, Bcl-2 was markedly expressed in HSC/MFs present in liver tissue obtained from patients with hepatitis C virus related cirrhosis. Human activated HSC/MFs are resistant to most proapoptotic stimuli due to Bcl-2 overexpression and this feature may play a key role in the progression of fibrosis in chronic liver diseases.
  Gut 09/2006; 55(8):1174-82. · 10.11 Impact Factor