β-Amyloid peptide-induced death of PC 12 cells and cerebellar granule cell neurons is inhibited by long-term lithium treatment

Wei, Huafeng; Leeds, Peter; Qian, Yanning; Wu, Wei; Chen, Ren‐Wu; Chuang, De‐Maw

doi:10.1016/s0014-2999(00)00127-8

Cited by 119 publications

(80 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In a rat model of Huntington's disease, subcutaneous administration of lithium reduces the size of quinolinic acid-induced lesion and protects striatal neurons from apoptotic death (Wei et al, 2001). Long-term lithium treatment also protects cerebellar granule cell neurons from ␤-amyloid peptide-induced death (Wei et al, 2000). Lithium can prevent potassium efflux-induced neuronal cell apoptosis, with the induction of caspase-3 expression (Li and El-Mallahk, 2000).…”

Section: Discussionmentioning

confidence: 99%

Lithium Chloride Reinforces the Regeneration-Promoting Effect of Chondroitinase ABC on Rubrospinal Neurons after Spinal Cord Injury

Yick¹,

So²,

Cheung³

et al. 2004

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Lithium Chloride Reinforces the Regeneration-Promoting Effect of Chondroitinase ABC on Rubrospinal Neurons after Spinal Cord Injury

Yick¹,

So²,

Cheung³

et al. 2004

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…28 PI-and FDA-positive cells were counted in three representative highpower fields of independent cultures and cell death was determined by the ratio of the number of PI-positive cells/PI þ FDA-stained-positive cells. 30 Determination of mitochondrial function. Neuronal survival was assessed by using 3-(4,5-dimethylthiazol-2-yl)-2,5, diphenyltetrazolium bromide (MTT).…”

Section: Methodsmentioning

confidence: 99%

Endoplasmic reticulum refilling and mitochondrial calcium extrusion promoted in neurons by NCX1 and NCX3 in ischemic preconditioning are determinant for neuroprotection

Sisalli¹,

Secondo²,

Esposito³

et al. 2014

Cell Death Differ

View full text Add to dashboard Cite

Ischemic preconditioning (IPC), an important endogenous adaptive mechanism of the CNS, renders the brain more tolerant to lethal cerebral ischemia. The molecular mechanisms responsible for the induction and maintenance of ischemic tolerance in the brain are complex and still remain undefined. Considering the increased expression of the two sodium calcium exchanger (NCX) isoforms, NCX1 and NCX3, during cerebral ischemia and the relevance of nitric oxide (NO) in IPC modulation, we investigated whether the activation of the NO/PI3K/Akt pathway induced by IPC could regulate calcium homeostasis through changes in NCX1 and NCX3 expression and activity, thus contributing to ischemic tolerance. To this aim, we set up an in vitro model of IPC by exposing cortical neurons to a 30-min oxygen and glucose deprivation (OGD) followed by 3-h OGD plus reoxygenation. IPC was able to stimulate NCX activity, as revealed by Fura-2AM single-cell microfluorimetry. This effect was mediated by the NO/PI3K/ Akt pathway since it was blocked by the following: (a) the NOS inhibitors L-NAME and 7-Nitroindazole, (b) the IP3K/Akt inhibitors LY294002, wortmannin and the Akt-negative dominant, (c) the NCX1 and NCX3 siRNA. Intriguingly, this IPC-mediated upregulation of NCX1 and NCX3 activity may control calcium level within endoplasimc reticulum (ER) and mitochondria, respectively. In fact, IPC-induced NCX1 upregulation produced an increase in ER calcium refilling since this increase was prevented by siNCX1. Moreover, by increasing NCX3 activity, IPC reduced mitochondrial calcium concentration. Accordingly, the inhibition of NCX by CGP37157 reverted this effect, thus suggesting that IPC-induced NCX3-increased activity may improve mitochondrial function during OGD/reoxygenation. Collectively, these results indicate that IPC-induced neuroprotection may occur through the modulation of calcium homeostasis in ER and mitochondria through NO/PI3K/Akt-mediated NCX1 and NCX3 upregulation.

show abstract

“…Not only is GSK3 intimately involved in many aspects of amyloid precursor protein metabolism and Aβ production, but GSK3 also contributes to Aβ-induced neuronal toxicity. Aβ is well-known to cause neuronal death when applied to cultured cells or to brain in vivo, and inhibition of GSK3 by a variety of methods significantly attenuates the neurotoxicity caused by Aβ [79][80][81][82][83][84][85]]. This appears not to be a "bystander" effect of GSK3 because treatment with Aβ activates GSK3 in a number of conditions, indicating a direct link between Aβ-induced GSK3 activation and neurotoxicity [79,86,87].…”

Section: Neurodegenerative Diseases: Gsk3 and Admentioning

confidence: 97%

Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics

2006

View full text Add to dashboard Cite

Deciphering what governs inflammation and its effects on tissues is vital for understanding many pathologies. The recent discovery that glycogen synthase kinase-3 (GSK3) promotes inflammation reveals a new component of its well-documented actions in several prevalent diseases which involve inflammation, including mood disorders, Alzheimer's disease, diabetes, and cancer. Involvement in such disparate conditions stems from the widespread influences of GSK3 on many cellular functions, with this review focusing on its regulation of inflammatory processes. GSK3 promotes the production of inflammatory molecules and cell migration, which together make GSK3 a powerful regulator of inflammation, while GSK3 inhibition provides protection from inflammatory conditions in animal models. The involvement of GSK3 and inflammation in these diseases are highlighted. Thus, GSK3 may contribute not only to primary pathologies in these diseases, but also to the associated inflammation, suggesting that GSK3 inhibitors may have multiple effects influencing these conditions.

show abstract

β-Amyloid peptide-induced death of PC 12 cells and cerebellar granule cell neurons is inhibited by long-term lithium treatment

Cited by 119 publications

References 22 publications

Lithium Chloride Reinforces the Regeneration-Promoting Effect of Chondroitinase ABC on Rubrospinal Neurons after Spinal Cord Injury

Lithium Chloride Reinforces the Regeneration-Promoting Effect of Chondroitinase ABC on Rubrospinal Neurons after Spinal Cord Injury

Endoplasmic reticulum refilling and mitochondrial calcium extrusion promoted in neurons by NCX1 and NCX3 in ischemic preconditioning are determinant for neuroprotection

Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics

Contact Info

Product

Resources

About