Diphlorethohydroxycarmalol inhibits melanogenesis via protein kinase A/cAMP response element‐binding protein and extracellular signal‐regulated kinase‐mediated microphthalmia‐associated transcription factor downregulation in α‐melanocyte stimulating hormone‐stimulated B16F10 melanoma cells and zebrafish

2021 ◽  
Author(s):  
Yuling Ding ◽  
Yunfei Jiang ◽  
Seung Tae Im ◽  
Seungwon Myung ◽  
Hyun‐Soo Kim ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Camp Response Element Binding ◽  
B16f10 Melanoma ◽  
Camp Response Element ◽  
Extracellular Signal Regulated Kinase ◽  
Melanocyte Stimulating Hormone ◽  
Extracellular Signal ◽  
B16f10 Melanoma Cells ◽  
Element Binding Protein ◽  
Kinase A

scholarly journals Stimulation of Phosphorylation of ERK and CREB by Phellopterin and Auraptene Isolated from Citrus junos

2014 ◽  
Vol 9 (10) ◽  
pp. 1934578X1400901 ◽  
Author(s):  
Mitsuhiro Nakamura ◽  
Tomoko Suzuki ◽  
Mai Takagi ◽  
Hirotoshi Tamura ◽  
Toshiya Masuda
Keyword(s):  
Camp Response Element Binding ◽  
Long Term Memory ◽  
Camp Response Element ◽  
Extracellular Signal Regulated Kinase ◽  
Cellular Processes ◽  
Extracellular Signal ◽  
Citrus Junos ◽  
Element Binding Protein ◽  
Methyl Ferulate

Bioactive compounds from citrus fruits contribute many benefits to human health. Extracellular signal-regulated kinase (ERK) signaling plays an important role in the regulation of multiple cellular processes. Activation of the ERK-cAMP response element binding protein (CREB) signaling is required for long-term memory formation. In this study, auraptene, phellopterin, thymol, coniferyl alcohol 9-methyl ether and methyl ferulate were isolated from Citrus junos. Among the five compounds isolated, auraptene and phellopterin increased the phosphorylation of ERK and CREB. This study provides, to our knowledge, the first evidence that phellopterin potently stimulates the phosphorylation of ERK and CREB. Phellopterin could be a novel neuroprotective agent.

scholarly journals Extracellular Signal-Regulated Kinase 5 in the Cerebrospinal Fluid-Contacting Nucleus Contributes to Neuropathic Pain in Rats

2015 ◽  
Vol 6;18 (6;11) ◽  
pp. E1073-E1082
Author(s):  
Li-Cai Zhang
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Allodynia ◽  
Chronic Constriction Injury ◽  
Camp Response Element Binding ◽  
Camp Response Element ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Element Binding Protein ◽  
Thermal Hypersensitivity

Background: The activation of mitogen-activated protein kinases (MAPKs) have been observed in synaptic plasticity processes of learning and memory in neuropathic pain. Cerebrospinal fluidcontacting nucleus (CSF-CN) has been identified with the onset and persistence of neuropathic pain. However, whether extracellular signal-regulated protein kinase 5 (ERK5), a member of MAPKs, in CSF-CN participates in neuropathic pain has not been studied yet. Objective: The aim of the present study was to identify the role of ERK5 in CSF-CN on the formation and development of neuropathic pain, and to investigate its possible mechanism. Study Design: Controlled animal study. Setting: University laboratory. Methods: After a chronic constriction injury (CCI) model was produced, BIX02188 was dissolved in 1% DMSO and injected into the lateral ventricles LV in a volume of 3 μl with different doses (0.1 μg, 1 μg, 10 μg). Mechanical allodynia and thermal hypersensitivity behavioral test, immunofluorescence, and western blot technique were used in this research. Result: Following CCI, mechanical allodynia and thermal hypersensitivity were developed within a day, peaked at 14 days, and persisted for 21 days. ERK5 was remarkably activated by CCI in CSFCN. Moreover, selective inhibiting of p-ERK5 expression in CSF-CN by BIX02188 could significantly relieve CCI-induced mechanical allodynia and thermal hypersensitivity, accompanying with the decreased phosphorylation of cAMP response-element binding protein (CREB) in CSF-CN. Limitations: More underlying mechanism(s) of the role of ERK5 in CSF-CN on the formation and development of neuropathic pain will be needed to explore in future research. Conclusion: These findings suggest activation of ERK5 in CSF-CN might contribute to the onset and development of neuropathic pain and its role might be partly accomplished by p-CREB. Key words: Neuropathic pain, extracellular signal-regulated kinase 5, distal cerebrospinal fluidcontacting neurons, cerebrospinal fluid-contacting nucleus, chronic constriction injury, cAMP response-element binding protein

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