C-jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis

Willaime‐Morawek, Sandrine; Brami‐Cherrier, Karen; Mariani, Jean; Caboche, Jocelyne; Brugg, Bernard

doi:10.1016/s0306-4522(02)00996-x

Cited by 67 publications

(46 citation statements)

References 57 publications

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“…A study on the apoptotic regulators of cortical neurons concluded that neurodegenerative pathways were prone to translocate intracellular p-p38 and p-JNK to nuclei. 36 As seen in Figure 3C(b), the insult with Aβ decreased the quantity of p-ERK5. After rescue with free NGF, the increase in the expression of p-ERK5 was unclear ( Figure 3C[c]).…”

mentioning

confidence: 68%

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer’s disease treatment

Kuo¹,

Lin²,

Li³

et al. 2017

IJN

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Curcumin (CRM) and nerve growth factor (NGF) were entrapped in liposomes (LIP) with surface wheat germ agglutinin (WGA) to downregulate the phosphorylation of kinases in Alzheimer’s disease (AD) therapy. Cardiolipin (CL)-conjugated LIP carrying CRM (CRM-CL/LIP) and also carrying NGF (NGF-CL/LIP) were used with AD models of SK-N-MC cells and Wistar rats after an insult with β-amyloid peptide (Aβ). We found that CRM-CL/LIP inhibited the expression of phosphorylated p38 (p-p38), phosphorylated c-Jun N-terminal kinase (p-JNK), and p-tau protein at serine 202 and prevented neurodegeneration of SK-N-MC cells. In addition, NGF-CL/LIP could enhance the quantities of p-neurotrophic tyrosine kinase receptor type 1 and p-extracellular signal-regulated kinase 5 for neuronal rescue. Moreover, WGA-grafted CRM-CL/LIP and WGA-grafted NGF-CL/LIP significantly improved the permeation of CRM and NGF across the blood–brain barrier, reduced Aβ plaque deposition and the malondialdehyde level, and increased the percentage of normal neurons and cholinergic activity in the hippocampus of AD rats. Based on the marker expressions and in vivo evidence, current LIP carriers can be promising drug delivery systems to protect nervous tissue against Aβ-induced apoptosis in the brain during the clinical management of AD.

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mentioning

confidence: 68%

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer’s disease treatment

Kuo¹,

Lin²,

Li³

et al. 2017

IJN

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“…Involvement of MAPK subfamilies (P44/42 MAP kinase, c-JNK, and p38 kinase) in ceramide-induced apoptosis have been reported in various cell types, including astrocytes (Blazquez et al 2000, Oh et al 2006, neuronal cells (Verheij et al 1996, Willaime et al 2001, Willaime-Morawek et al 2003, lung cancer-derived cells (Kurinna et al 2004) and vascular smooth muscle cells (Loidl et al 2004). The P44/42 MAP kinase pathway plays a major role in regulating cell growth, survival and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Ceramide inhibition of chondrocyte proliferation and bone growth is IGF-I independent

MacRae¹,

Burdon²,

Ahmed³

et al. 2006

Journal of Endocrinology

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Proinflammatory cytokines inhibit growth plate development. However, their underlying mechanisms of action are unclear. These effects may be mediated by ceramide, a sphingosine-based lipid second messenger, which is elevated in a number of chronic inflammatory diseases. To test this hypothesis, we determined the effects of C2-ceramide, a cell permeable ceramide analogue, on the growth of the ATDC5 chondrogenic cell line and on cultured fetal mice metatarsals. In ATDC5 cells, C2-ceramide significantly induced apoptosis at both 40 (82%; P!0 . 05) and 25 mM (53%; P!0 . 05). At 40 mM, C2-ceramide significantly reduced proliferation ([ 3 H]-thymidine uptake/mg protein) (62%; P!0 . 05). C2-ceramide did not markedly alter the differentiation state of the cells as judged by the expression of markers of chondrogenesis and differentiation (sox 9, collagen II and collagen X). The IGF-I signalling pathway is the major autocrine/paracrine regulator of bone growth. Both in the presence and absence of IGF-I, C2-ceramide (25 mM) induced an equivalent reduction in proliferation (60%; P!0 . 001). Similarly, C2-ceramide (40 mM) induced a 31% reduction in fetal metatarsal growth both in the presence and absence of IGF-I (both P!0 . 001). Furthermore, C2-ceramide reduced ADCT5 proliferation in the presence of AG1024, an IGF-I and insulin receptor blocker. Therefore, C2-ceramide-dependent inhibition appears to be independent of IGF-mediated stimulation of bone growth. Indeed, biochemical studies demonstrated that C2-ceramide (25 mM) pretreatment did not alter IGF-I-stimulated phosphorylation of insulin receptor substrate-1, Akt or P44/42 MAP kinase. In conclusion, C2-ceramide inhibits proliferation and induces apoptosis in growth plate chondrocytes through an IGF-I independent mechanism.

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“…Ceramide accumulation, which can occur via enhanced de novo synthesis using palmitate or increased sphingomyelin breakdown, has been linked to both insulin resistance and apoptosis [42][43][44][45]. In pancreatic β cells and bovine retinal pericytes, saturated fatty acids not only increase ceramide levels, but inhibition of ceramide production prevents saturated fatty acid-induced apoptosis [26,46].…”

Section: Intracellular Signals Mediating Saturated Fatty Acid-inducedmentioning

confidence: 99%

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

Gentile

Pagliassotti

2008

The Journal of Nutritional Biochemistry

210

156

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C-jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis

Cited by 67 publications

References 57 publications

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer’s disease treatment

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer’s disease treatment

Ceramide inhibition of chondrocyte proliferation and bone growth is IGF-I independent

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

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C-jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis

Cited by 67 publications

References 57 publications

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer&rsquo;s disease treatment

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer&rsquo;s disease treatment

Ceramide inhibition of chondrocyte proliferation and bone growth is IGF-I independent

The role of fatty acids in the development and progression of nonalcoholic fatty liver disease

Contact Info

Product

Resources

About

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer’s disease treatment

Wheat germ agglutinin-conjugated liposomes incorporated with cardiolipin to improve neuronal survival in Alzheimer’s disease treatment