scholarly journals Hepatocyte nuclear factor 4α is implicated in endoplasmic reticulum stress-induced acute phase response by regulating expression of cyclic adenosine monophosphate responsive element binding protein H

Hepatology ◽  
2008 ◽  
Vol 48 (4) ◽  
pp. 1242-1250 ◽  
Author(s):  
Jennifer Luebke-Wheeler ◽  
Kezhong Zhang ◽  
Michele Battle ◽  
Karim Si-Tayeb ◽  
Wendy Garrison ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Acute Phase Response ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Element Binding Protein ◽  
Hepatocyte Nuclear Factor 4Α ◽  
Responsive Element

scholarly journals Polydeoxyribonucleotide Attenuates Airway Inflammation Through A2AR Signaling Pathway in PM10-Exposed Mice

2021 ◽  
Vol 25 (Suppl 1) ◽  
pp. S19-26 ◽  
Author(s):  
Lakkyong Hwang ◽  
Jun-Jang Jin ◽  
Il-Gyu Ko ◽  
Suyeon Kim ◽  
Young-A Cho ◽  
...  
Keyword(s):  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Chronic Obstructive ◽  
Nuclear Factor ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α ◽  
Element Binding Protein ◽  
Responsive Element

Purpose: Inhalation of air containing high amounts of particular matter (PM) causes various respiratory disorders including asthma, chronic obstructive pulmonary disease, and lung cancer. The changes of expression of inflammatory factors by polydeoxyribonucleotide (PDRN) administration in the PM10-exposed trachea inflammation model were evaluated.Methods: PM<sub>10</sub> was administered to mouse trachea to induce acute inflammatory damage, and changes in inflammatory factors were observed after administration of PDRN and 3,7-dimethyl-1-propargylxanthine (DMPX) for 3 days daily. Expression of inflammatory cytokines, adenosine A<sub>2A</sub> receptor (A<sub>2A</sub>R), protein kinase A (PKA), 3΄,5΄-cyclic adenosine monophosphate responsive element binding protein (CREB) were detected by enzyme‐linked immunosorbent assay, immunofluorescence, and western blot assay.Results: PM-exposed trachea showed increased tumor necrosis factor (TNF)-α and interleukin (IL)-1β expression, and expression of TNF-α and IL-1β was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased nuclear factor (NF)-κB phosphorylation, and phosphorylation of nuclear factor-kappa B was inhibited by PDRN treatment in PM-exposed mice. PM-exposed trachea showed increased expression of A<sub>2A</sub>R, but PDRN treatment more enhanced A<sub>2A</sub>R expression in PM-exposed mice. PKA phosphorylation was not changed and CREP phosphorylation was decreased, however PDRN treatment increased phosphorylation of PKA and CREB in PM-exposed mice. DMPX treatment blocked all the effects of PDRN on PM-exposed mice, demonstrating that the action of PDRN occurs via A<sub>2A</sub>R.Conclusions: PDRN treatment attenuated inflammation in the trachea of the PM<sub>10</sub>-exposed mice. This improving effect of PDRN can be ascribed to the activation of A<sub>2A</sub>R through the cAMP-PKA pathway.

scholarly journals Sargahydroquinoic Acid Suppresses Hyperpigmentation by cAMP and ERK1/2-Mediated Downregulation of MITF in α-MSH-Stimulated B16F10 Cells

Foods ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2254
Author(s):  
Mohammed Shariful Azam ◽  
Bonggi Lee ◽  
Jae-Il Kim ◽  
Chang Geun Choi ◽  
Jinkyung Choi ◽  
...  
Keyword(s):  
Docking Simulation ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Regulatory Subunit ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Creb Activation ◽  
B16f10 Cells ◽  
Element Binding Protein ◽  
Responsive Element

Hyperpigmentation diseases of the skin require topical treatment with depigmenting agents. We investigated the hypopigmented mechanisms of sargahydroquinoic acid (SHQA) in alpha-melanocyte-stimulating hormone (α-MSH)-stimulated B16F10 cells. SHQA reduced cellular tyrosinase (TYR) activity and melanin content in a concentration-dependent manner and attenuated the expression of TYR and tyrosinase-related protein 1 (TRP1), along with their transcriptional regulator, microphthalmia-associated transcription factor (MITF). SHQA also suppressed α-MSH-induced cellular production of cyclic adenosine monophosphate (cAMP), which inhibited protein kinase A (PKA)-dependent cAMP-responsive element-binding protein (CREB) activation. Docking simulation data showed a potential binding affinity of SHQA to the regulatory subunit RIIβ of PKA, which may also adversely affect PKA and CREB activation. Moreover, SHQA activated ERK1/2 signaling in B16F10 cells, stimulating the proteasomal degradation of MITF. These data suggest that SHQA ameliorated hyperpigmentation in α-MSH-stimulated B16F10 cells by downregulating MITF via PKA inactivation and ERK1/2 phosphorylation, indicating that SHQA is a potent therapeutic agent against skin hyperpigmentation disorders.

scholarly journals Therapeutic targeting of the pathological triad of extrasynaptic NMDA receptor signaling in neurodegenerations

2017 ◽  
Vol 214 (3) ◽  
pp. 569-578 ◽  
Author(s):  
Hilmar Bading
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Histone Deacetylases ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Cell Loss ◽  
Nuclear Accumulation ◽  
Receptor Signaling ◽  
Element Binding Protein ◽  
Responsive Element

Activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegeneration and cell death. The disease mechanism involves a pathological triad consisting of mitochondrial dysfunction, loss of integrity of neuronal structures and connectivity, and disruption of excitation–transcription coupling caused by CREB (cyclic adenosine monophosphate–responsive element-binding protein) shut-off and nuclear accumulation of class IIa histone deacetylases. Interdependency within the triad fuels an accelerating disease progression that culminates in failure of mitochondrial energy production and cell loss. Both acute and slowly progressive neurodegenerative conditions, including stroke, Alzheimer’s disease, amyotrophic lateral sclerosis, and Huntington’s disease, share increased death signaling by extrasynaptic NMDA receptors caused by elevated extracellular glutamate concentrations or relocalization of NMDA receptors to extrasynaptic sites. Six areas of therapeutic objectives are defined, based on which a broadly applicable combination therapy is proposed to combat the pathological triad of extrasynaptic NMDA receptor signaling that is common to many neurodegenerative diseases.

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