ERK/MAPK signalling in the developing brain: Perturbations and consequences

Iroegbu, Joy D.; Ijomone, Olayemi K.; Femi-Akinlosotu, Omowumi; Ijomone, Omamuyovwi M.

doi:10.1016/j.neubiorev.2021.10.009

Cited by 76 publications

(32 citation statements)

References 146 publications

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“…The molecular mechanisms of melatonin protecting against cell death have been extensively described 114 . Phosphatidylinositide‐3‐kinase/Akt (PI3K/Akt) and extracellular signal‐regulated kinase/MAP kinase (ERK/MAPK) pathways are two critical signals in regulating cell survival 115–117 . Gianesini et al 118 have demonstrated that melatonin binds to MT1/MT2 heteromers to suppress proapoptotic gene transcription through PI3K/AKT pathway in protecting photoreceptors.…”

Section: Discussionmentioning

confidence: 99%

“…114 Phosphatidylinositide-3-kinase/Akt (PI3K/Akt) and extracellular signal-regulated kinase/MAP kinase (ERK/MAPK) pathways are two critical signals in regulating cell survival. [115][116][117] Gianesini et al 118 have demonstrated that melatonin binds to MT1/MT2 heteromers to suppress proapoptotic gene transcription through PI3K/AKT pathway in protecting photoreceptors. The work of Sánchez-Bretaño et al 28,119 have shown that MT1/MT2 signaling prevents photoreceptor death by inhibiting caspase-3-dependent apoptosis induced by oxidative stress via AKT-FOXO1-Fas/ FasL-caspase-3 pathway as well.…”

Section: Discussionmentioning

confidence: 99%

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Anti‐PANoptosis is involved in neuroprotective effects of melatonin in acute ocular hypertension model

Shi

et al. 2022

Journal of Pineal Research

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Acute ocular hypertension (AOH) is the most important characteristic of acute glaucoma, which can lead to retinal ganglion cell (RGC) death and permanent vision loss. So far, approved effective therapy is still lacking in acute glaucoma. PANoptosis (pyroptosis, apoptosis, and necroptosis), which consists of three key modes of programmed cell death-apoptosis, necroptosis, and pyroptosis -may contribute to AOH-induced RGC death. Previous studies have demonstrated that melatonin (N-acetyl-5-methoxytryptamine) exerts a neuroprotective effect in many retinal degenerative diseases. However, whether melatonin is anti-PANoptotic and neuroprotective in the progression of acute glaucoma remains unclear. Thus, this study aimed to explore the role of melatonin in AOH retinas and its underlying mechanisms. The results showed that melatonin treatment attenuated the loss of ganglion cell complex thickness, retinal nerve fiber layer thickness, and RGC after AOH injury, and improved the amplitudes of a-wave, b-wave, and oscillatory potentials in the electroretinogram. Additionally, the number of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells was decreased, and the upregulation of cleaved caspase-8, cleaved caspase-3, Bax, and Bad and downregulation of Bcl-2 and p-Bad were inhibited after melatonin administration. Meanwhile, both the expression and activation of MLKL, RIP1, and RIP3, along with the number of PI-positive cells, were reduced in melatonintreated mice, and p-RIP3 was in both RGC and microglia/macrophage after AOH injury. Furthermore, melatonin reduced the expression of NLRP3, ASC,

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Anti‐PANoptosis is involved in neuroprotective effects of melatonin in acute ocular hypertension model

Shi

et al. 2022

Journal of Pineal Research

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“…The results, obtained 1, 2 and 3 days after treatments, showed that the levels of ERK1/2 phosphorylation decline during NSCs differentiation [ 23 ]. In contrast, the activation of the ERK1/2 signaling pathway is proved fundamental for the neurite outgrowth and the correct neurogenesis [ 24 ]. Indeed, the Western blot analysis confirmed an increased amount of p-ERK in treated cells compared to the control ( Figure 5 i).…”

Section: Discussionmentioning

confidence: 99%

Cannabidiol Promotes Neuronal Differentiation Using Akt and Erk Pathways Triggered by Cb1 Signaling

et al. 2022

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Recently, the scientific community has started to focus on the neurogenic potential of cannabinoids. The phytocompound cannabidiol (CBD) shows different mechanism of signaling on cannabinoid receptor 1 (CB1), depending on its concentration. In this study, we investigated if CBD may induce in vitro neuronal differentiation after treatment at 5 µM and 10 µM. For this purpose, we decided to use the spinal cord × neuroblastoma hybrid cell line (NSC-34) because of its proliferative and undifferentiated state. The messenger RNAs (mRNAs) expression profiles were tested using high-throughput sequencing technology and Western blot assay was used to determine the number of main proteins in different pathways. Interestingly, the treatment shows different genes associated with neurodifferentiation statistically significant, such as Rbfox3, Tubb3, Pax6 and Eno2. The CB1 signaling pathway is responsible for neuronal differentiation at 10 µM, as suggested by the presence of p-ERK and p-AKT, but not at 5 µM. A new correlation between CBD, neurodifferentiation and retinoic acid receptor-related orphan receptors (RORs) has been observed.

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“…Numerous previous studies have reported that p38 and JNK are involved in ccRCC survival and growth and play a significant regulatory role in ccRCC tumorigenesis, metastasis, and angiogenesis [ 32 – 34 ], which is consistent with our findings. Notably, ERK is a key downstream factor of MAPK and is involved in ccRCC progression [ 35 , 36 ]. However, no significant changes in ERK expression were observed in the present study.…”

Section: Discussionmentioning

confidence: 99%

Lysosomal-Associated Transmembrane Protein 5 Promotes Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma

Huang

et al. 2022

Journal of Oncology

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Clear cell renal cell carcinoma (ccRCC) is the most aggressive and deadly cancer of the urinary system and is regulated by multiple signaling pathways. However, the specific molecular mechanisms underlying ccRCC have not been fully studied or demonstrated. This study aimed to elucidate the function of lysosomal-associated transmembrane protein 5 (LAPTM5) in ccRCC cell lines and animal models and determine the potential underlying mechanisms. Our results demonstrated that LAPTM5 expression in patients with ccRCC was significantly higher in the tumor group than that in the adjacent nontumor group. Moreover, LAPTM5 promoted proliferation, migration, and invasion of ccRCC cells through the gain and loss of the function of LAPTM5 in 786-0 and Caki-1 cell lines. Similar results regarding LAPTM5 overexpression were obtained in BALB/c nude mice. In addition, LAPTM5 activated the Jun N-terminal kinase (JNK)/p38 signaling cascade by interacting with Ras-related C3 botulinum toxin substrate 1 (RAC1). Treatment with an RAC1 inhibitor eliminated the effects of LAPTM5 in ccRCC. In conclusion, these results indicate that LAPTM5 may be a new therapeutic target for ccRCC via activation of the RAC1-JNK/p38 axis.

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ERK/MAPK signalling in the developing brain: Perturbations and consequences

Cited by 76 publications

References 146 publications

Anti‐PANoptosis is involved in neuroprotective effects of melatonin in acute ocular hypertension model

Anti‐PANoptosis is involved in neuroprotective effects of melatonin in acute ocular hypertension model

Cannabidiol Promotes Neuronal Differentiation Using Akt and Erk Pathways Triggered by Cb1 Signaling

Lysosomal-Associated Transmembrane Protein 5 Promotes Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma

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