Modulation of PKA, PKC, CAMKII, ERK 1/2 pathways is involved in the acute antidepressant-like effect of (octylseleno)-xylofuranoside (OSX) in mice

Brod, Lucimar M. Pinto; Fronza, Mariana G.; Vargas, Jaqueline Pinto; Lüdtke, Diogo S.; Brüning, César Augusto; Savegnago, Lucielli

doi:10.1007/s00213-016-4505-5

Cited by 14 publications

(5 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our study found the potential target of miR-1275 (17)(18)(19). Furthermore, many studies have shown that PKCα can play a role in diagnosing cancers (20). In pancreatic cancer, PKCα expression was thought to be directly correlated with tumorigenicity and survival rate (21).…”

Section: Discussionmentioning

confidence: 75%

MicroRNA-1275 targets PKCα to depress proliferation and the invasion of pancreatic cancer cells

Liu¹,

Ji²,

Liu³

et al. 2018

Transl. Cancer Res

View full text Add to dashboard Cite

Background: Pancreatic cancer (PC) is one of the cancers with the highest mortality rate in the world.Therefore, it is urgent to understand the potential molecular mechanisms of PC progression and to detect novel and original strategies for a targeted therapy. Many reports show that a lot of cancers are regulated by miR-1275; however, the role which miR-1275 plays in PC remains unknown. Our study was conducted to explore miR-1275 expression and role in PC.Methods: qRT-PCR was used to detect the expression of miR-1275 in both PC tissues and cell lines. The function of miR-1275 in PC cells was evaluated by luciferase assays through transfection with miR-1275 mimics and inhibitor. Western blot analysis was employed to test the target gene expression of miR-1275.Results: Reduced miR-1275 expression in the PC tissues was observed in comparison with the matched non-cancerous tissues. Furthermore, over-expression of miR-1275 significantly inhibited cell proliferation, metastasis, and invasion in the PC cells. In addition, we found that protein kinase C (PKCα) is negatively controlled by miR-1275 at the posttranscriptional level, through a pathognostic target spot within the 3'-UTR. In PC and cell lines, the expression of PCKα is usually up-regulated and adversely related to miR-1275 expression. Conclusions:The results of our data are first to show that miR-1275 was a new suppressor and negative regulator of PKCα expression in PC, possibly furnishing a new method for PC therapy.

show abstract

Section: Discussionmentioning

confidence: 75%

MicroRNA-1275 targets PKCα to depress proliferation and the invasion of pancreatic cancer cells

Liu¹,

Ji²,

Liu³

et al. 2018

Transl. Cancer Res

View full text Add to dashboard Cite

show abstract

“…Disruption in cyclic cAMP-PKA signaling has been implicated in stress maladaptation, anxiety, and depression [ 23 ]. Chronic treatment with fluoxetine enhances cAMP levels, subsequently activates PKA, and upregulates CREB signaling in the hippocampus, cortex, and hypothalamus of the chronically stressed rats [ 27 ]. The previous studies showed that Yueju treatment induced an upregulation of PKA-CREB signaling expression in the KM mice [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Repeated Yueju, But Not Fluoxetine, Induced Sustained Antidepressant Activity in a Mouse Model of Chronic Learned Helplessness: Involvement of CaMKII Signaling in the Hippocampus

Zou

Huang

Yang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Objective. Depression is characterized with long disease length, whereas one major disadvantage of current mainstream treatment of depression is a high rate of relapse and recurrence. A sustained antidepressant activity is proposed to facilitate the prevention of relapse/recurrence. Here we compared the long-term antidepressant effect of Yueju, a traditional Chinese medicine formula, and a conventional antidepressant, fluoxetine, as well as revealing the underlying mechanism of long-term antidepressant effect of Yueju. Methods. Clinical long-term depression condition was modelled by using chronic learned helplessness (cLH) protocol in ICR strain mice. The short-term and long-term antidepressant effects of drugs were assessed with learned helplessness (LH), tail suspension test (TST), forced swim test (FST), and novelty-suppressed feeding (NSF) test. The expression of PKA, CaMKII signaling, and NR1, the NMDA receptor subunit, in hippocampus was determined. A CaMKII inhibitor (KN-62) was used to assess the role of CaMKII signaling in antidepressant effects of Yueju or fluoxetine. Results. In the mice exposed to chronic learned helplessness (cLH) procedure, administration of Yueju or fluoxetine for 3 weeks elicited comparable antidepressant effects, indicated by learned helplessness test, as well as TST and NSF. However, 5 days after termination of the 3-week-long drug administration, only mice previously treated with Yueju still showed the alleviation of depressive-like behaviors. At this time, the downregulation of PKA and p-CaMKII/CaMKII and upregulation of NMDA receptor subunit NR1 in the hippocampus were normalized in animals previously treated with Yueju. In contrast, none of the expressions of these proteins were changed in mice previously treated with fluoxetine. Interestingly, an administration of KN-62 blunted the antidepressant effect of Yueju. Conclusion. These findings showed the sustained antidepressant efficacy of chronic treatment with routine dose of Yueju and the CaMKII signaling activation may play a critical role in the sustained antidepressant response.

show abstract

“…Flavonoid restored the decrease in the phosphorylation of CaMKII caused by chronic glucocorticoid administration [ 140 ]. Studies using ursolic acid, creatine, ferulic acid, or (octylseleno)-xylofuranoside showed that the reduction of immobility time in the tail suspension test in mice might be reversed by administration of KN-62 (a CaMKII inhibitor) [ 141 , 142 , 143 , 144 , 145 ]. Similarly, the antidepressant-like effect of memantine and 7-fluoro-1,3-diphenylisoquinoline-1-amine in forced swim test in mice was blocked by KN-62 [ 146 , 147 ].…”

Section: Depression-like State In Rodentsmentioning

confidence: 99%

The Calcium/Calmodulin-Dependent Kinases II and IV as Therapeutic Targets in Neurodegenerative and Neuropsychiatric Disorders

Sałaciak

Koszałka

Żmudzka

et al. 2021

IJMS

View full text Add to dashboard Cite

CaMKII and CaMKIV are calcium/calmodulin-dependent kinases playing a rudimentary role in many regulatory processes in the organism. These kinases attract increasing interest due to their involvement primarily in memory and plasticity and various cellular functions. Although CaMKII and CaMKIV are mostly recognized as the important cogs in a memory machine, little is known about their effect on mood and role in neuropsychiatric diseases etiology. Here, we aimed to review the structure and functions of CaMKII and CaMKIV, as well as how these kinases modulate the animals’ behavior to promote antidepressant-like, anxiolytic-like, and procognitive effects. The review will help in the understanding of the roles of the above kinases in the selected neurodegenerative and neuropsychiatric disorders, and this knowledge can be used in future drug design.

show abstract

Modulation of PKA, PKC, CAMKII, ERK 1/2 pathways is involved in the acute antidepressant-like effect of (octylseleno)-xylofuranoside (OSX) in mice

Abstract: The results demonstrated that OSX showed an antidepressant-like effect in the TST in mice through the activation of protein kinases PKA, PKC, CAMKII and ERK1/2 that are involved in intracellular signalling pathways.

Cited by 14 publications

References 69 publications

MicroRNA-1275 targets PKCα to depress proliferation and the invasion of pancreatic cancer cells

MicroRNA-1275 targets PKCα to depress proliferation and the invasion of pancreatic cancer cells

Repeated Yueju, But Not Fluoxetine, Induced Sustained Antidepressant Activity in a Mouse Model of Chronic Learned Helplessness: Involvement of CaMKII Signaling in the Hippocampus

The Calcium/Calmodulin-Dependent Kinases II and IV as Therapeutic Targets in Neurodegenerative and Neuropsychiatric Disorders

Contact Info

Product

Resources

About