1980 University of Rome “La Sapienza” : Doctor of Biology cum laude
1988 University of Yeshiva, New York , NY, USA: Specialization in Pharmacology with honors

Chronology of Employment
1980-1983: Fellow, Institute of Biochemistry, University of Rome “La Sapienza”, Rome, Italy
1983-1994: Researcher, University of Rome “Tor Vergata”,Rome, Italy
1986-1988: Research associate, Yeshiva University, New York, NY (USA)
1994-2002: Full Professor, University of Chieti “G.D’Annunzio” Chieti, Italy
2002- to present: Full Professor, University of Rome “Tor Vergata”,Rome, Italy
2007-to present: Head of laboratory “Biochemistry of Ageing” IRCCS San Raffaele, Rome, Italy


1982-to present: Member of the Italian Society of Biochemistry
1983-to present: Enlisted in National Order of Biologist
1993-to present: Member of the national Interuniversity Consortium I.N.B.B. (Institute National Biostructure and Biosistems)
2002-to present: Member of the National Health committee on the evaluation of voluntary copper risk assessment

Reactive oxygen species and oxidative state are slowly gaining acceptance in having a physiological relevance rather than just being the culprits in patho-physiological processes. The control of the redox environment of the cell provides for additional regulation in relation to critical cellular signal transduction pathways. Indeed, several kinases and nuclear transcription factors are sensitive to redox-mediated regulation. Conversely, aberrant regulation of oxidative state manifesting as oxidative stress can predispose a cell to adverse outcome. The main interest of my research group is to make clear that oxidative state plays a key role in the regulation and control of numerous signal transduction pathways in the cell and that elucidating the mechanisms behind oxidative stress-mediated cell death or proliferation is important in identifying potential putative targets for the treatment of neuropathologies as well as cancer.
Glutathione, a pivotal constituent of antioxidant defense and enzyme cofactor, is involved in several cellular functions. The study of the changes of the levels and redox status of this tripeptide in association with several physio-pathological situations is also deeply studied in my laboratory. In particular we investigate its role in i) redox regulation of viral replication; ii) modulation of cellular redox state, mediated by membrane transduction; iii) involvement in apoptotic/autophagic processes.
Nitric oxide (NO) is a diatomic free radical that plays an important role in the homeostatic regulation of the central nervous, immune, and cardiovascular systems. In addition to its interaction with guanylate cyclase, which results in the production of the second messenger cyclic GMP, there is now a large body of literature indicating that many of the effects associated with the production of NO are due to the nitrosation of cysteine residues in proteins. We study the primary chemical pathways that may account for protein nitrosation in cells and tissues. Prototypical examples of protein nitrosation include p21(ras) subfamily of small monomeric GTPases and the cysteine-containing aspartate-specific proteases (caspases) which are implicated in cell cycle regulation and apoptosis. Overall, in addition to the well characterized NO/O(2) reaction, there may exist multiple pathways accounting for protein nitrosation in cells. These include acid- and free radical-mediated mechanisms. Although protein nitrosation may not be limited to cysteine residues, there is now ample evidence that nitrosation reactions, in a fashion similar to oxidative modifications, may modulate the structure, activity, association, and localization of a specific subset of proteins in cells and tissues.

Ciriolo,M.R. Redox control of apoptosis. Antiox.Redox Signal 7, 430-433 (2005).

Filomeni,G., Aquilano,K., Civitareale,P., Rotilio,G. and Ciriolo,M.R. Activation of c-jun-N-terminal kinase is required for apoptosis triggered by GSSG in neuroblastoma cells. Free Rad.Biol.Med. 39, 345-354 (2005).

Filomeni, G., Cardaci, S., Da Costa Ferreira, A.M. Rotilio, G. and Ciriolo M.R. Metabolic oxidative stress elicited by the copper (II) complex [Cu(isaepy)2] triggers apoptosis in SH-SY5Y cells through the induction of AMPK/ p38MAPK/p53 signalling axis. Biochem J. May 06, 2011

Filomeni,G., Rotilio,G. and Ciriolo,M.R. Disulfide relays and phosphorylative cascade: partners in redox-mediated signaling pathways. Cell Death Differ. 12, 1555-1563 (2005).

Filomeni,G., Aquilano,K., Rotilio,G. and Ciriolo,M.R. Glutathione-related systems and modulation of extracellular signal-regulated kinases are involved in resistance of AGS cells to diallyl disulfide-induced apoptosis. Cancer Res. 65, 11735-11742 (2005).

Aquilano,K., Vigilanza,P., Rotilio,G. and Ciriolo,M.R. Mitochondrial damage due to SOD1 deficiency in SH-SY5Y neuroblastoma cells: a rationale for the redundancy of SOD1. FASEB J. 20, 1683-1685 (2006).

Filomeni,G., Cerchiaro,G., Da Costa Ferreira,A.M., De Martino,A., Pedersen,J.Z., Rotilio,G. and Ciriolo,M.R. Pro-apoptotic activity of novel isatin-Schiff base copper(II) complexes depends on oxidative stress induction and organelle-selective damage. J.Biol.Chem. 282, 12010-12021 (2007).

Vigilanza,P., Aquilano,P., Rotilio,G. and Ciriolo,M.R. Transient cytoskeletal alterations after SOD1 depletion in neuroblastoma cells. Cell.Mol. Life Sci. 65, 991-1004 (2008).

Baldelli,S., Aquilano,K., Rotilio,G. and Ciriolo,M.R. GSH and Cu,Zn superoxide dismutase are modulated by overexpression of neuronal nitric oxide synthase. Int. J. Biochem. Cell Biol. 40, 2660-2670 (2008).

Cardaci,S., Filomeni,G., Rotilio,G. and Ciriolo,M.R. ROS mediate p53 activation and apoptosis induced by sodium nitroprusside in SH-SY5Y cells. Mol.Pharmacol. 74, 1234-1245 (2008).

Aquilano,K., Baldelli,S., Rotilio,G. and Ciriolo,M.R. t-resveratrol inhibits H2O2-induced adenocarcinoma gastric cells proliferation via inactivation of MEK1/2-ERK1/2-C-Jun signaling axis. Biochem. Pharmacol. 77, 337-347 (2009).

Aquilano, K., Vigilanza, P., Filomeni, G., Rotilio, G. and Ciriolo, M.R. Tau dephosphorylation and microfilaments disruption are upstream events of the anti-proliferative effects of DADS in SH-SY5Y cells. J. Cell.Mol.Med. (2008).

Filomeni,G., Piccirillo,S., Graziani,I., Cardaci,S., Da Costa Ferreira,AM., Rotilio,G. and Ciriolo,M.R. The isatin-Schiff base copper(II) complex acts as delocalized lipophilic cation, yields widespread mitochondrial oxidative damage and induces AMPK dependent apoptosis. Carcinogenesis. 30, 1115-1124 (2009).

Piccirillo,S., Filomeni,G., Brüne,B., Rotilio, G. and Ciriolo, M.R. Redox mechanisms involved in the selective activation of Nrf2-mediated resistance versus p53-dependent apoptosis in AGS cells. J Biol Chem 284, 27721-27733 (2009).

Filomeni, G., Desideri, E., Piccirillo, S., Graziani, I., Rotilio, G. and Ciriolo, M.R. Carcinoma cells activate AMP-activated protein kinase-dependent autophagy as survival response to kaempferol-mediated energetic impairment. Autophagy 6, 202-216 (2010).

Aquilano, K., Vigilanza, P., Baldelli, S., Pagliei, B., Rotilio, G. and Ciriolo, M.R. Peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1{alpha}) and sirtuin 1 (SIRT1) reside in mitochondria: possible direct function in mitochondrial biogenesis. J.Biol.Chem 285, 21590-21599 (2010).

Filomeni, G., Graziani, I., De Zio, D., Dini, L., Centonze, D., Rotilio, G. and Ciriolo, M.R. Neuroprotection of kaempferol by autophagy in models of rotenone-mediated acute toxicity: possible implications for Parkinson's disease. Neurobiology of Aging (2010).

Filomeni, G., Desideri, E., Cardaci, S., Rotilio, G. and Ciriolo, M.R. Under the ROS…Thiol network is the principal suspect for autophagy commitment. Autophagy 6, 999-1005 (2010).

Cardaci, S., Filomeni, G., Rotilio, G. and Ciriolo, M.R. p38MAPK/p53 signaling axis mediates neuronal apoptosis in response to tetrahydrobiopterin-induced oxidative stress and glucose uptake inhibition: implication for neurodegeneration Biochem. J. 430, 439-451(2010).

Vigilanza, P., Aquilano, K., Baldelli, S., Rotilio, G. and Ciriolo M.R. Modulation of intracellular glutathione affects adipogenesis in 3T3-L1 cells. J Cell Physiol. 226, 2016-2024 (2011)

Baldelli, S., Aquilano, K., Rotilio, G. and Ciriolo M.R. Neuronal nitric oxide synthase interacts with Sp1 through the PDZ domain inhibiting Sp1-mediated copper-zinc superoxide dismutase expression. Int J Biochem Cell Biol. 43, 163-169 (2011).

Aquilano, K., Baldelli, S., Cardaci, S., Rotilio, G. and Ciriolo M.R. Nitric oxide is the primary mediator of cytotoxicity induced by GSH depletion in neuronal cells. J Cell Sci. March 01, 2011

No projects are available to students for the current accademic year.