Cathepsin D plays a crucial role in the trimethyltin-induced hippocampal neurodegeneration process

Ceccariglia, Sabrina; D’Altocolle, Anna; Fa, Aurora Del; Pizzolante, Fabrizio; Caccia, Elisabetta; Michetti, Fabrizio; Gangitano, Carlo

doi:10.1016/j.neuroscience.2010.11.024

Cited by 28 publications

(17 citation statements)

References 64 publications

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“…In addition, the involvement of LAMP1 and both PS1 and PS2 [26] in intracellular Ca 2+ homeostasis [80,81] appears to be in line with the hypothesis that TMT-induced neuronal damage could be largely dependent on calcium homeostasis dysregulation [82–85]. …”

Section: Different Models Used To Investigate Tmt-induced Gene Expmentioning

confidence: 57%

Gene Expression Profiling as a Tool to Investigate the Molecular Machinery Activated during Hippocampal Neurodegeneration Induced by Trimethyltin (TMT) Administration

Lattanzi

Corvino

Maria

et al. 2013

IJMS

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Trimethyltin (TMT) is an organotin compound exhibiting neurotoxicant effects selectively localized in the limbic system and especially marked in the hippocampus, in both experimental animal models and accidentally exposed humans. TMT administration causes selective neuronal death involving either the granular neurons of the dentate gyrus or the pyramidal cells of the Cornu Ammonis, with a different pattern of localization depending on the different species studied or the dosage schedule. TMT is broadly used to realize experimental models of hippocampal neurodegeneration associated with cognitive impairment and temporal lobe epilepsy, though the molecular mechanisms underlying the associated selective neuronal death are still not conclusively clarified. Experimental evidence indicates that TMT-induced neurodegeneration is a complex event involving different pathogenetic mechanisms, probably acting differently in animal and cell models, which include neuroinflammation, intracellular calcium overload, and oxidative stress. Microarray-based, genome-wide expression analysis has been used to investigate the molecular scenario occurring in the TMT-injured brain in different in vivo and in vitro models, producing an overwhelming amount of data. The aim of this review is to discuss and rationalize the state-of-the-art on TMT-associated genome wide expression profiles in order to identify comparable and reproducible data that may allow focusing on significantly involved pathways.

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Section: Different Models Used To Investigate Tmt-induced Gene Expmentioning

confidence: 57%

Gene Expression Profiling as a Tool to Investigate the Molecular Machinery Activated during Hippocampal Neurodegeneration Induced by Trimethyltin (TMT) Administration

Lattanzi

Corvino

Maria

et al. 2013

IJMS

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“…The activation of lysosomes and CathD has already been observed in some in vitro and in vivo models of several neurodegenerative diseases . A previous study showed that the expression of CathD was markedly increased in trimethyltin‐induced hippocampal neurodegeneration in Sprague Dawley rats, and it played a crucial role in this process . However, the role of CathD in neuroinflammation and the underlying mechanisms involved have not been completely elucidated.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of cathepsin D protects dopaminergic neurons against neuroinflammation‐mediated neurotoxicity through inhibition of NF‐κB signalling pathway in Parkinson's disease model

Gan

Xia

Hang

et al. 2019

Clin Exp Pharma Physio

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“…In many instances, leakage of lysosomal enzymes is believed to precede release of cytochrome c, loss of mitochondrial membrane potential and morphologic manifestations of apoptosis (Chwieralski et al, 2006;Benes et al, 2008;Boya and Kroemer, 2008). These phenomena have been described in in vitro paradigms using a variety of toxic insults (Roberg and Ollinger, 1998;Yang et al, 1998;Ditaranto et al, 2001;Johansson et al, 2003;Vene et al, 2007;Gowran and Campbell, 2008;Tofighi et al, 2011) and in some animal models of neurodegenerative disorders (Yamashima et al, 1998;Vitner et al, 2010;Ceccariglia et al, 2011). However, it remains unclear whether increased levels/ activities of the enzymes observed in kainic acid-treated hippocampi are involved in the protection or degeneration of neurons.…”

Section: Discussionmentioning

confidence: 99%

Increased levels and activity of cathepsins B and D in kainate-induced toxicity

et al. 2015

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Cathepsin D plays a crucial role in the trimethyltin-induced hippocampal neurodegeneration process

Cited by 28 publications

References 64 publications

Gene Expression Profiling as a Tool to Investigate the Molecular Machinery Activated during Hippocampal Neurodegeneration Induced by Trimethyltin (TMT) Administration

Gene Expression Profiling as a Tool to Investigate the Molecular Machinery Activated during Hippocampal Neurodegeneration Induced by Trimethyltin (TMT) Administration

Knockdown of cathepsin D protects dopaminergic neurons against neuroinflammation‐mediated neurotoxicity through inhibition of NF‐κB signalling pathway in Parkinson's disease model

Increased levels and activity of cathepsins B and D in kainate-induced toxicity

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