Cristina Cecchi

Summary

Affiliation: University of Florence
Country: Italy

Publications

  1. doi request reprint Neuronal differentiation of human mesenchymal stromal cells increases their resistance to Aβ42 aggregate toxicity
    Cristina Cecchi
    Department of Biochemical Sciences, and Research Centre on the Molecular Basis of Neurodegeneration CIMN, Florence, Italy
    J Alzheimers Dis 27:651-64. 2011
  2. doi request reprint A protective role for lipid raft cholesterol against amyloid-induced membrane damage in human neuroblastoma cells
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134 Florence, Italy
    Biochim Biophys Acta 1788:2204-16. 2009
  3. doi request reprint Seladin-1/DHCR24 protects neuroblastoma cells against Abeta toxicity by increasing membrane cholesterol content
    C Cecchi
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    J Cell Mol Med 12:1990-2002. 2008
  4. ncbi request reprint Replicating neuroblastoma cells in different cell cycle phases display different vulnerability to amyloid toxicity
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134, Florence, Italy
    J Mol Med (Berl) 86:197-209. 2008
  5. ncbi request reprint Increased susceptibility to amyloid toxicity in familial Alzheimer's fibroblasts
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    Neurobiol Aging 28:863-76. 2007
  6. ncbi request reprint Differing molecular mechanisms appear to underlie early toxicity of prefibrillar HypF-N aggregates to different cell types
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Italy
    FEBS J 273:2206-22. 2006
  7. doi request reprint Differentiation increases the resistance of neuronal cells to amyloid toxicity
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134, Florence, Italy
    Neurochem Res 33:2516-31. 2008
  8. ncbi request reprint Lipid rafts mediate amyloid-induced calcium dyshomeostasis and oxidative stress in Alzheimer's disease
    Elisa Evangelisti
    Department of Biochemical Sciences, University of Florence, 50134, Florence, Italy
    Curr Alzheimer Res 10:143-53. 2013
  9. doi request reprint Protective effect of new S-acylglutathione derivatives against amyloid-induced oxidative stress
    Anna Pensalfini
    Department of Biochemical Sciences, University of Florence, 50134 Florence, Italy
    Free Radic Biol Med 44:1624-36. 2008
  10. doi request reprint Membrane cholesterol enrichment prevents Aβ-induced oxidative stress in Alzheimer's fibroblasts
    Anna Pensalfini
    Department of Biochemical Sciences, University of Florence, 50134 Florence, Italy
    Neurobiol Aging 32:210-22. 2011

Collaborators

Detail Information

Publications28

  1. doi request reprint Neuronal differentiation of human mesenchymal stromal cells increases their resistance to Aβ42 aggregate toxicity
    Cristina Cecchi
    Department of Biochemical Sciences, and Research Centre on the Molecular Basis of Neurodegeneration CIMN, Florence, Italy
    J Alzheimers Dis 27:651-64. 2011
    ..These findings extend our knowledge of stem cell vulnerability to amyloid species, which remains a controversial issue, and confirm that amyloid-GM1 interactions play an important role in cell impairment...
  2. doi request reprint A protective role for lipid raft cholesterol against amyloid-induced membrane damage in human neuroblastoma cells
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134 Florence, Italy
    Biochim Biophys Acta 1788:2204-16. 2009
    ..Our data suggest that cholesterol reduces amyloid-induced membrane modifications at the lipid raft level by altering raft physicochemical features...
  3. doi request reprint Seladin-1/DHCR24 protects neuroblastoma cells against Abeta toxicity by increasing membrane cholesterol content
    C Cecchi
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    J Cell Mol Med 12:1990-2002. 2008
    ..Our findings extend recently reported data indicating that seladin-1 overexpression directly enhances the resistance to Abeta toxicity featuring seladin-1/DHCR 24 as a possible new susceptibility gene for sporadic AD...
  4. ncbi request reprint Replicating neuroblastoma cells in different cell cycle phases display different vulnerability to amyloid toxicity
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134, Florence, Italy
    J Mol Med (Berl) 86:197-209. 2008
    ..The high vulnerability of S cells to aggregate toxicity extends previous data suggesting that neuronal loss in AD could result from mitotic reactivation of terminally differentiated neurons with arrest in the S phase...
  5. ncbi request reprint Increased susceptibility to amyloid toxicity in familial Alzheimer's fibroblasts
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    Neurobiol Aging 28:863-76. 2007
    ..These findings provide compelling evidence that cells bearing increased membrane lipoperoxidation are more susceptible to aggregate toxicity as a result of their reduced ability to counteract amyloid oligomeric attack...
  6. ncbi request reprint Differing molecular mechanisms appear to underlie early toxicity of prefibrillar HypF-N aggregates to different cell types
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Italy
    FEBS J 273:2206-22. 2006
    ....
  7. doi request reprint Differentiation increases the resistance of neuronal cells to amyloid toxicity
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134, Florence, Italy
    Neurochem Res 33:2516-31. 2008
    ..Finally, increasing the content of membrane cholesterol resulted in a remarkable reduction of vulnerability and ability to bind the aggregates in either undifferentiated and differentiated cells...
  8. ncbi request reprint Lipid rafts mediate amyloid-induced calcium dyshomeostasis and oxidative stress in Alzheimer's disease
    Elisa Evangelisti
    Department of Biochemical Sciences, University of Florence, 50134, Florence, Italy
    Curr Alzheimer Res 10:143-53. 2013
    ..These findings suggest a specific role for raft domains as primary mediators of amyloid toxicity in AD neurons...
  9. doi request reprint Protective effect of new S-acylglutathione derivatives against amyloid-induced oxidative stress
    Anna Pensalfini
    Department of Biochemical Sciences, University of Florence, 50134 Florence, Italy
    Free Radic Biol Med 44:1624-36. 2008
    ..Hence, we put forward these derivatives as new antioxidant compounds which could be excellent candidates for therapeutic treatment of AD and other oxidative stress-related diseases...
  10. doi request reprint Membrane cholesterol enrichment prevents Aβ-induced oxidative stress in Alzheimer's fibroblasts
    Anna Pensalfini
    Department of Biochemical Sciences, University of Florence, 50134 Florence, Italy
    Neurobiol Aging 32:210-22. 2011
    ..These results identify membrane cholesterol as being key to Aβ42 oligomer accumulation at the cell surfaces and to the following Aβ42-induced cell death in AD neurons...
  11. doi request reprint Curcumin protects cardiac cells against ischemia-reperfusion injury: effects on oxidative stress, NF-kappaB, and JNK pathways
    Claudia Fiorillo
    Department of Biochemical Sciences University of Florence, 50134 Florence, Italy
    Free Radic Biol Med 45:839-46. 2008
    ....
  12. doi request reprint A comparison of the biochemical modifications caused by toxic and non-toxic protein oligomers in cells
    Mariagioia Zampagni
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    J Cell Mol Med 15:2106-16. 2011
    ....
  13. doi request reprint Lipid rafts are primary mediators of amyloid oxidative attack on plasma membrane
    Mariagioia Zampagni
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134, Florence, Italy
    J Mol Med (Berl) 88:597-608. 2010
    ..These data identify lipid rafts as key mediators of oxidative damage as a result of their ability to recruit aggregates to the cell surface...
  14. doi request reprint Membrane lipid composition and its physicochemical properties define cell vulnerability to aberrant protein oligomers
    Elisa Evangelisti
    Department of Biochemical Sciences and Research Centre on the Molecular Basis of Neurodegeneration CIMN, University of Florence, Florence, Italy
    J Cell Sci 125:2416-27. 2012
    ..We identified that the degree of toxicity of the oligomeric species is the result of a complex interplay between the structural and physicochemical features of both the oligomers and the cell membrane...
  15. doi request reprint Novel S-acyl glutathione derivatives prevent amyloid oxidative stress and cholinergic dysfunction in Alzheimer disease models
    Mariagioia Zampagni
    Department of Biochemical Sciences, University of Florence, 50134 Florence, Italy
    Free Radic Biol Med 52:1362-71. 2012
    ..Collectively, these findings suggest that acyl-SG thioesters could prove useful as a tool for controlling AD-induced cerebral deterioration...
  16. ncbi request reprint Beneficial effects of poly (ADP-ribose) polymerase inhibition against the reperfusion injury in heart transplantation
    Claudia Fiorillo
    Dipartimento di Scienze Biochimiche, Universita di Firenze, Viale Morgagni 50, 50134, Fireze, Italia
    Free Radic Res 37:331-9. 2003
    ..These latter allow irreversible damages triggered during the ischemic phase to proceed towards apoptosis instead of towards necrosis, as it appears to happen when the energetic pools are depleted by high PARP activity...
  17. doi request reprint SIRT1 modulates MAPK pathways in ischemic-reperfused cardiomyocytes
    Matteo Becatti
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    Cell Mol Life Sci 69:2245-60. 2012
    ..These results reveal a new protective mechanism elicited by Resv-induced SIRT1 activation in IR tissues and suggest novel potential therapeutic targets to manage IR-induced cardiac dysfunction...
  18. doi request reprint Glycosaminoglycans (GAGs) suppress the toxicity of HypF-N prefibrillar aggregates
    Theodora Saridaki
    Department of Biochemical Sciences, University of Florence, Viale Morgagni 50, 50134 Florence, Italy
    J Mol Biol 421:616-30. 2012
    ....
  19. doi request reprint A causative link between the structure of aberrant protein oligomers and their toxicity
    Silvia Campioni
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    Nat Chem Biol 6:140-7. 2010
    ..Our findings suggest that structural flexibility and hydrophobic exposure are primary determinants of the ability of oligomeric assemblies to cause cellular dysfunction and its consequences, such as neurodegeneration...
  20. ncbi request reprint Patterns of cell death triggered in two different cell lines by HypF-N prefibrillar aggregates
    Monica Bucciantini
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    FASEB J 19:437-9. 2005
    ....
  21. doi request reprint Protective properties of novel S-acyl-glutathione thioesters against ultraviolet-induced oxidative stress
    Daniel Wright
    Department of Biochemical Sciences, University of Florence, Firenze, Florence, Italy
    Photochem Photobiol 89:442-52. 2013
    ..Taken together, our findings suggest that acyl-SG thioesters may be therapeutically effective in the treatment of UV-related skin disorders and oxidative stress-mediated conditions in general...
  22. ncbi request reprint Oxidative stress and reduced antioxidant defenses in peripheral cells from familial Alzheimer's patients
    Cristina Cecchi
    Department of Biochemical Sciences, University of Florence, Florence, Italy
    Free Radic Biol Med 33:1372-9. 2002
    ..These results support the hypothesis that oxidative damage to lipid, protein, and DNA is an important early event in the pathogenesis of AD...
  23. doi request reprint Extracellular chaperones prevent Aβ42-induced toxicity in rat brains
    Roberta Cascella
    Department of Biomedical Experimental and Clinical Sciences, University of Florence, V le GB Morgagni 50, 50134, Italy
    Biochim Biophys Acta 1832:1217-26. 2013
    ..These findings elect them as novel neuroprotectors against amyloid-induced injury and excellent candidates for the design of therapeutic strategies against AD...
  24. pmc Molecular mechanisms used by chaperones to reduce the toxicity of aberrant protein oligomers
    Benedetta Mannini
    Department of Biochemical Sciences, University of Florence, 50134 Florence, Italy
    Proc Natl Acad Sci U S A 109:12479-84. 2012
    ....
  25. doi request reprint The amyloid-cell membrane system. The interplay between the biophysical features of oligomers/fibrils and cell membrane defines amyloid toxicity
    Cristina Cecchi
    Department of Biomedical Experimental and Clinical Sciences and Research Centre on the Molecular Basis of Neurodegeneration, University of Florence, Florence, Italy
    Biophys Chem 182:30-43. 2013
    ..Finally, a recent view describes amyloid toxicity as an emerging property dependent on a complex interplay between the biophysical features of early aggregates and the interacting cell membranes taken as a whole system. ..
  26. ncbi request reprint Insights into the molecular basis of the differing susceptibility of varying cell types to the toxicity of amyloid aggregates
    Cristina Cecchi
    Department of Biochemical Sciences
    J Cell Sci 118:3459-70. 2005
    ..Our data depict membrane destabilization and the subsequent early derangement of ion balance and intracellular redox status as key events in targeting exposed cells to apoptotic death...
  27. ncbi request reprint Poly(ADP-ribose) polymerase activation and cell injury in the course of rat heart heterotopic transplantation
    Claudia Fiorillo
    Dipartimento di Scienze Biochimiche, Universita di Firenze, Italy
    Free Radic Res 36:79-87. 2002
    ..Our results suggest that during heart transplantation, the activation of PARP, causing energy depletion, results in myocardial cell injury whose dominant feature, at least in our experimental model, is necrosis rather than apoptosis...
  28. ncbi request reprint Over-expression of amyloid precursor protein in HEK cells alters p53 conformational state and protects against doxorubicin
    Daniela Uberti
    Department of Biomedical Sciences and Biotechnologies, University of Brescia, Brescia, Italy
    J Neurochem 103:322-33. 2007
    ....