Laboratory of Neurobiology of Movement Disorders INM

Pozzilli, Italy

Laboratory of Neurobiology of Movement Disorders INM

Pozzilli, Italy

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Pasquali L.,University of Pisa | Ruggieri S.,Laboratory of Neurobiology of Movement Disorders INM | Murri L.,University of Pisa | Paparelli A.,University of Pisa | And 2 more authors.
Parkinsonism and Related Disorders | Year: 2010

In eukaryotic cells intracellular components are mainly degraded by autophagy and the ubiquitin-proteasome system. Autophagy is more flexible compared with the ubiquitin-proteasome system and it is involved in the degradation of long-lived proteins and organelles, such as mitochondria, which cannot be degraded by the ubiquitin-proteasome. Although autophagy is able to compensate for ubiquitin-proteasome dysfunction, the opposite does not occur. Autophagy is frequently involved in neurodegeneration; however, there is no consensus on its role in cell survival, as it can be either neuroprotective or neurotoxic. With respect to dopaminergic neurons, there is evidence that autophagy occurs during damage to substantia nigra neurons such as in Parkinson's disease. Moreover, a variety of inherited forms of Parkinson's disease are characterized by mutated proteins that belong to the autophagy pathway. Inhibition of autophagy precipitates dopaminergic cell death, whereas autophagy activation rescues the death of nigral dopaminergic neurons induced by proteasome inhibitors. Taken together, this evidence suggests that autophagy improves the survival of dopaminergic cells. © 2009 Elsevier Ltd. All rights reserved.


Giannessi F.,University of Pisa | Scavuzzo M.C.,University of Pisa | Giambelluca M.A.,University of Pisa | Fornai F.,University of Pisa | And 3 more authors.
Systems Biology in Reproductive Medicine | Year: 2015

Several studies reported that chronic alcohol consumption alters the intestinal mucosa barrier, and subsequent entrance of endotoxins into the bloodstream. In many tissues endotoxin exposure causes the expression of calprotectin (CP) and the receptor for advanced glycation -end products (RAGE). In this study we investigated whether chronic alcohol administration causes expression of CP and RAGE in mouse testis. The distribution of free and loosely bound Zn2+ (FLB-Zn2+) in the testicular tissues was also evaluated. Alcohol-induced testicular damage was documented by measuring testosterone blood levels and by light and electron microscope studies. Twenty mice were treated daily for three weeks with 3.0g/kg of a 25% solution of alcohol. Ten mice were treated in the same period of time with a solution of maltose dextrins, isocaloric to alcohol. Twenty untreated mice were used as controls. Alcohol treated mice showed diffuse expression of CP and RAGE in the interstitial cells. RAGE was found also in the basal compartment of the seminiferous tubules. Depletion of FLB-Zn2+ was observed in the adluminal compartment of the seminiferous tubules. Expression of CP and RAGE was not found in control mice and maltose dextrin treated mice. Our results indicated novel mechanisms by which alcohol acts in testis. Indeed, CP and RAGE may cause the generation of oxidants and inflammatory mediators, with negative impact on testicular functions. Depletion of FLB-Zn2+ may contribute to the dysregulation of spermatogenesis. © 2015 Informa Healthcare USA, Inc.

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