Glial-derived neurotrophic factor (GDNF) prevents ethanol (EtOH) induced B92 glial cell death by both PI3K/AKT and MEK/ERK signaling pathways

Villegas, Santiago Nahuel; Njaine, Brian; Linden, Rafael; Carri, Néstor Gabriel

doi:10.1016/j.brainresbull.2006.08.014

Cited by 42 publications

(25 citation statements)

References 88 publications

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“…RET activates the PI3K/AKT, MEK/ERK, and SRC pathways, and NCAM activates the FYN/FAK pathway. Through these downstream targets, GDNF prevents apoptosis and promotes proliferation and differentiation in neurons (33,34,(38)(39)(40), ureteric bud (35,36), and spermatogonial SCs (37). Our results show that GDNF and its receptor, GFRα1, are found primarily in SSCs, suggesting that GDNF mainly acts as an autocrine factor.…”

Section: Sca1mentioning

confidence: 58%

“…Of interest is GDNF, which showed a more than 2-fold elevation in SSCs by microarray and was 4-fold higher in SSCs by qPCR when compared with the Lin -CD24 + c-Kit -Sca1 -population ( Figure 5A). GDNF preferentially binds to the GDNF family receptor α 1 (GFRα1), which mediates the activation of the RET receptor tyrosine kinase and functions through the PI3K/AKT, MEK/ERK and SRC pathways in neurons (33,34), ureteric buds (35,36), and spermatogonial SCs (37). Recent studies indicated that the neural cell adhesion molecule (NCAM) and the downstream targets FYN/FAK may function as alternative pathways for GDNF in regulating axonal guidance and corneal regeneration (38)(39)(40)(41).…”

Section: Gdnf Does Not Function As a Radio Protector In Smgmentioning

confidence: 99%

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Neurotrophic factor GDNF promotes survival of salivary stem cells

Xiao¹,

Lin²,

Cao³

et al. 2014

J. Clin. Invest.

116

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Section: Sca1mentioning

confidence: 58%

Section: Gdnf Does Not Function As a Radio Protector In Smgmentioning

confidence: 99%

Neurotrophic factor GDNF promotes survival of salivary stem cells

Xiao¹,

Lin²,

Cao³

et al. 2014

J. Clin. Invest.

116

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“…GDNF preferentially binds to the GFRα1 coreceptor, and then GDNF-GFRα1 complex interacts with receptor tyrosine kinase RET triggering its dimerization, kinase activation and phosphorylation at RET intracellular tyrosine residues. Further actions in neurons go through the MEK/ERK, SRC, PLCγ, and PI3K/AKT pathways (McAlhany et al, 2000; Airaksinen and Saarma, 2002; Villegas et al, 2006). GDNF can bind to the neural cell adhesion molecule (NCAM)-GFRα1 complex and activate the downstream targets Src-type kinases FYN/FAK in regulating axonal guidance and corneal regeneration (You et al, 2001; Paratcha et al, 2003; Euteneuer et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Evidence for an Additive Neurorestorative Effect of Simultaneously Administered CDNF and GDNF in Hemiparkinsonian Rats: Implications for Different Mechanism of Action

Voutilainen

Lorenzo

Stepanova

et al. 2017

eNeuro

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Parkinson’s disease (PD) is a neurodegenerative disorder associated with a progressive loss of dopaminergic (DAergic) neurons of the substantia nigra (SN) and the accumulation of intracellular inclusions containing α-synuclein. Current therapies do not stop the progression of the disease, and the efficacy of these treatments wanes over time. Neurotrophic factors (NTFs) are naturally occurring proteins promoting the survival and differentiation of neurons and the maintenance of neuronal contacts. CDNF (cerebral dopamine NTF) and GDNF (glial cell line-derived NTF) are able to protect DAergic neurons against toxin-induced degeneration in experimental models of PD. Here, we report an additive neurorestorative effect of coadministration of CDNF and GDNF in the unilateral 6-hydroxydopamine (6-OHDA) lesion model of PD in rats. NTFs were given into the striatum four weeks after unilateral intrastriatal injection of 6-OHDA (20 µg). Amphetamine-induced (2.5 mg/kg, i.p.) rotational behavior was measured every two weeks. Number of tyrosine hydroxylase (TH)-positive cells from SN pars compacta (SNpc) and density of TH-positive fibers in the striatum were analyzed at 12 weeks after lesion. CDNF and GDNF alone restored the DAergic function, and one specific dose combination had an additive effect: CDNF (2.5µg) and GDNF (1µg) coadministration led to a stronger trophic effect relative to either of the single treatments alone. The additive effect may indicate different mechanism of action for the NTFs. Indeed, both NTFs activated the survival promoting PI3 kinase (PI3K)-Akt signaling pathway, but only CDNF decreased the expression level of tested endoplasmatic reticulum (ER) stress markers ATF6, glucose-regulated protein 78 (GRP78), and phosphorylation of eukaryotic initiation factor 2α subunit (eIF2α).

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“…GDNF preferentially binds to the GFRα1, which then activates the receptor tyrosine kinase RET or the neural cell adhesion molecule (Zhou et al 2003). The PI3K/AKT, MEK/ERK, SRC/c-Jun kinase, FYN/focal adhesion kinase pathways have all been reported to be downstream of the GDNF signal (Charoy et al 2012; Euteneuer et al 2013; McAlhany et al 2000; Oatley et al 2007; Paratcha et al 2003; Tang et al 2002; Villegas et al 2006). …”

Section: Gdnf Familymentioning

confidence: 99%

Neurotrophic Factors and Their Potential Applications in Tissue Regeneration

Xiao¹,

2015

Arch. Immunol. Ther. Exp.

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Neurotrophic factors are growth factors that can nourish neurons and promote neuron survival and regeneration. They have been studied as potential drug candidates for treating neurodegenerative diseases. Since their identification, there are more and more evidences to indicate that neurotrophic factors are also expressed in non-neuronal tissues and regulate the survival, anti-inflammation, proliferation and differentiation in these tissues. This mini review summarizes the characteristics of the neurotrophic factors and their potential clinical applications in the regeneration of neuronal and non-neuronal tissues.

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Glial-derived neurotrophic factor (GDNF) prevents ethanol (EtOH) induced B92 glial cell death by both PI3K/AKT and MEK/ERK signaling pathways

Cited by 42 publications

References 88 publications

Neurotrophic factor GDNF promotes survival of salivary stem cells

Neurotrophic factor GDNF promotes survival of salivary stem cells

Evidence for an Additive Neurorestorative Effect of Simultaneously Administered CDNF and GDNF in Hemiparkinsonian Rats: Implications for Different Mechanism of Action

Neurotrophic Factors and Their Potential Applications in Tissue Regeneration

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