Erratum to “Calpains and neuronal damage in the ischemic brain: The swiss knife in synaptic injury” [Progress in Neurobiology 143 (2016) 1–35]

Curcio, M. Joan; Salazar, Ivan L.; Mele, Miranda; Canzoniero, Lorella M.T.; Duarte, Carlos B.

doi:10.1016/j.pneurobio.2016.08.004

Cited by 2 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies have addressed that CAST/calpain system was involved in cell death following glutamate excitotoxicity ( Miao et al, 2012 ; Curcio et al, 2015 ; Yan et al, 2016 ). Calpains are calcium-dependent cysteine proteases, which ubiquitously exist in organisms ( Curcio et al, 2016 ; Machado et al, 2017 ). The activity of calpains are physiologically regulated by its specific endogenous inhibitor, calpastatin (CAST) ( Averna et al, 2001 ; Volbracht et al, 2005 ).…”

Section: Introductionmentioning

confidence: 99%

“…The activity of calpains are physiologically regulated by its specific endogenous inhibitor, calpastatin (CAST) ( Averna et al, 2001 ; Volbracht et al, 2005 ). The CAST/calpain system has drawn more attention since it was implicated in a variety of calcium-related cellular processes, such as survival, proliferation, differentiation, apoptosis, and signal transduction ( Senter et al, 1991 ; Curcio et al, 2016 ; Martensson et al, 2017 ). Recent studies have specifically addressed whether the CAST/calpain system plays a role in cell death following glutamate excitotoxicity ( Miao et al, 2012 ; Curcio et al, 2015 ; Yan et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway

Wang

Liao

Wang

et al. 2018

Front. Cell. Neurosci.

View full text Add to dashboard Cite

The purpose of the current study was to investigate whether peptidyl-prolyl cis/trans isomerase NIMA-interacting 1 (Pin1) can interact with calpastatin (CAST) and regulate CAST/calpain2, under excessive glutamate conditions, and subsequently regulate necrosis in rat retinal neurons. Glutamate triggered CAST/calpain2-mediated necrosis regulation in primary cultured retinal neurons, as demonstrated by propidium iodide-staining and lactate dehydrogenase assay. Co-IP results and a computer simulation suggested that Pin1 could bind to CAST. Western blot, real-time quantitative polymerase chain reaction, immunofluorescence, and phosphorylation analysis results demonstrated that CAST was regulated by Pin1, as proven by the application of juglone (i.e., a Pin1 specific inhibitor). The retinal ganglion cell 5 cell line, combined with siRNA approach and flow cytometry, was then used to verify the regulatory pathway of Pin1 in CAST/calpain2-modulated neuronal necrosis that was induced by glutamate. Finally, in vivo studies further confirmed the role of Pin1 in CAST/calpain2-modulated necrosis following glutamate excitation, in the rat retinal ganglion cell and inner nuclear layers. In addition, a flash electroretinogram study provided evidence for the recovery of impaired visual function, which was induced by glutamate, with juglone treatment. Our work aims to investigate the involvement of the Pin1-CAST/calpain2 pathway in glutamate-mediated excitotoxicity.

show abstract