p38 and c-Jun N-Terminal Kinase Mitogen-Activated Protein Kinase Signaling Pathways Play Distinct Roles in the Response of Organogenesis-Stage Embryos to a Teratogen

Yan, Jin; Hales, Barbara F.

doi:10.1124/jpet.108.139907

Cited by 12 publications

(12 citation statements)

References 39 publications

(42 reference statements)

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“…In accordance with already published data the time frame and concentration used were enough to let the inhibitor diffuse and inhibit JNK2930. In line with the evidences that L-JNKi1 does not affect JNK phosphorylation31, pre-incubation of synaptosomes with L-JNKi1 resulted in increased JNK activation when NMDA stimulus was applied (+49 ± 10% vs control = 100%. * p < 0.05).…”

Section: Resultssupporting

confidence: 87%

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Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

Nisticò

Florenzano

Mango

et al. 2015

Sci Rep

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Activation of c-Jun N-terminal kinase (JNK) signaling pathway is a critical step for neuronal death occurring in several neurological conditions. JNKs can be activated via receptor tyrosine kinases, cytokine receptors, G-protein coupled receptors and ligand-gated ion channels, including the NMDA glutamate receptors. While JNK has been generally associated with postsynaptic NMDA receptors, its presynaptic role remains largely unexplored. Here, by means of biochemical, morphological and functional approaches, we demonstrate that JNK and its scaffold protein JIP1 are also expressed at the presynaptic level and that the NMDA-evoked glutamate release is controlled by presynaptic JNK-JIP1 interaction. Moreover, using knockout mice for single JNK isoforms, we proved that JNK2 is the essential isoform in mediating this presynaptic event. Overall the present findings unveil a novel JNK2 localization and function, which is likely to play a role in different physiological and pathological conditions.

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Section: Resultssupporting

confidence: 87%

“…This peptide competes with the JNK binding domain (JBD) disrupting the interaction between JIP1 and JNK, consequently the downstream activity of JNK is blocked31. Our data strongly suggest that presynaptic JNK signaling pathway might be selectively engaged following NMDA receptor activation.…”

Section: Discussionmentioning

confidence: 71%

Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

Nisticò

Florenzano

Mango

et al. 2015

Sci Rep

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“…17 Phosphorylated p38 (phospho-p38) was also found to be increased in neural tube sections of embryos of diabetic dams as evidenced by greater immunoreactive intensity with IHC and by Western blot (P < .001; Figure 7A, B, and C). No change in total p38 was observed.…”

Section: Resveratrol Prevents Diabetes-induced Activation Of Jnk1/2mentioning

confidence: 98%

“…16 Mitogenactivated protein kinases (MAPKs) play a major role in growth, differentiation, and development, and their activation has been shown as a determinant of the fate of embryonic organogenesis when exposed to insult. 17 Previous work from our laboratory has shown that RA affects MAPK signaling via PI3K (Phosphatidylinositol 3-kinases) and Rac1 during neuronal cell differentiation. 18 In addition, diabetes inhibits the activation of Rac1 and reduces the expression of neuronal markers in rat embryonic day 16 (E16) cortical neurons.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

et al. 2012

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Diabetes induces impairments in gene expression during embryonic development that leads to premature and improper tissue specialization. Retinoic acid receptors (RARs and retinoid X receptor [RXRs]) and mitogen-activated protein kinases (MAPKs) play crucial roles during embryonic development, and their suppression or activation has been shown as a determinant of the fate of embryonic organogenesis. We studied the activation of RARs and MAPKs in embryonic day 12 (E12) in embryos of rats under normal, diabetic, and diabetic treated with resveratrol ([RSV]; 100 mg/kg body weight) conditions. We found downregulation of RARs and RXRs expressions as well as their DNA-binding activities in the embryos exhibiting developmental delays due to diabetes. Furthermore, the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was decreased and phosphorylation of c-Jun N-terminal kinase (JNK) 1/2 and p38 was increased. Interestingly, embryos of diabetic rats treated with RSV showed normalized patterns of RARs, RXRs, neuronal markers, and ERK, JNK and p38 phosphorylation.

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“…109 MAPKs also contribute to growth, differentiation and developmental processes; their activity determines the fate of embryonic organogenesis when the embryo faces teratogenic conditions. 110 Hyperglycemia increases ROS, which modulate MAPK signaling. 111 In the embryo, oxidative stress results in DNA, protein and lipid modifications that disrupt normal development.…”

Section: Diabetes Impairs Rho Gtpase Signaling Could Resveratrol Revmentioning

confidence: 99%

Diabetic complications in pregnancy: is resveratrol a solution?

Singh

Kumar²,

LaVoie

et al. 2013

Exp Biol Med (Maywood)

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Diabetes is a metabolic disorder that, during pregnancy, may affect fetal development. Fetal outcome depends on the type of diabetes present, the concentration of blood glucose and the extent of fetal exposure to elevated or frequently fluctuating glucose concentrations. The result of some diabetic pregnancies will be embryonic developmental abnormalities, a condition referred to as diabetic embryopathy. Tight glycemic control in type 1 diabetes during pregnancy using insulin therapy together with folic acid supplementation are partially able to prevent diabetic embryopathy; however, the protection is not complete and additional interventions are needed. Resveratrol, a polyphenol found largely in the skins of red grapes, is known to have antidiabetic action and is in clinical trials for the treatment of diabetes, insulin resistance, obesity and metabolic syndrome. Studies of resveratrol in a rodent model of diabetic embryopathy reveal that it significantly improves the embryonic outcome in terms of diminishing developmental abnormalities. Improvements in maternal and embryonic outcomes observed in rodent models may arise from resveratrol’s antioxidative potential, antidiabetic action and antidyslipidemic nature. Whether resveratrol will have similar actions in human diabetic pregnancy is unknown. Here, we review the potential therapeutic use of resveratrol in diabetes and diabetic pregnancy.

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p38 and c-Jun N-Terminal Kinase Mitogen-Activated Protein Kinase Signaling Pathways Play Distinct Roles in the Response of Organogenesis-Stage Embryos to a Teratogen

Cited by 12 publications

References 39 publications

Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

Diabetic complications in pregnancy: is resveratrol a solution?

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