Evaluation of the Expression Levels of Cannabinoid Type-1 (CB1) Receptor and Phosphorylated Extracellular Signal-Regulated Kinase (p-ERK) in Gliomas

2021 ◽  
Author(s):  
Nader Choucair ◽  
Zahraa Sakr ◽  
Hassane Kheir Eddine ◽  
Mariana Zaarour ◽  
Hayat Harati ◽  
...  
Keyword(s):  
Therapeutic Effects ◽  
Cb1 Receptors ◽  
Normal Brain ◽  
Clinicopathologic Features ◽  
Expression Levels ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Low Expression ◽  
Brain Tissues

Abstract Background Gliomas are the most frequent primary brain tumors and one of the most aggressive forms of cancer. Recently, numerous studies have focused on cannabinoids as a new cancer-therapeutic approach due to their antineoplastic effects through activation of the cannabinoid receptors, CB1 and CB2. The aim of this study was to investigate the expression levels of cannabinoid type-1 (CB1) receptors and phosphorylated extracellular signal-regulated kinase (p-ERK) in human glioma samples and evaluate their clinicopathologic significance. Materials and Methods We analyzed the expressions of CB1 receptors (CB1R) and p-ERK in 61 paraffin-embedded gliomas and 4 normal brain tissues using automated immunohistochemical assay. CB1R and p-ERK expressions were categorized into high versus low expression levels. Statistical analyses were performed to evaluate the association between CB1R and p-ERK expression levels and the clinicopathologic features and overall survival. Results Our results showed that CB1R is down-expressed in glioma tissues compared to normal brain tissues. However, the low expression of CB1R was found to be not related to the malignancy grade of gliomas. Conversely, higher expression of p-ERK was noted in gliomas compared to normal brain tissues, with no association observed with tumor grades. In addition, CB1R expression was not observed to be associated with clinicopathologic features of gliomas, except for p-ERK expression. Conclusion Our findings indicate a down-expression of CB1R and overexpression of p-ERK in glioma tissues when compared to non-cancerous brain tissues. This change in CB1R expression in gliomas may contribute to further research on the therapeutic effects of cannabinoids in human gliomas.

scholarly journals Nav1.7 via Promotion of ERK in the Trigeminal Ganglion Plays an Important Role in the Induction of Pulpitis Inflammatory Pain

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Shukai Sun ◽  
Jiangxing Sun ◽  
Wenkai Jiang ◽  
Wei Wang ◽  
Longxing Ni
Keyword(s):  
Trigeminal Ganglion ◽  
Inflammatory Pain ◽  
Pain Threshold ◽  
Expression Levels ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Pulp Exposure ◽  
Mechanical Pain Threshold ◽  
Hematoxylin Eosin ◽  
Inhibitor Dose

The trigeminal ganglion (TG) refers to sensory neurons bodies that innervate the spinal cord and peripheral axons that innervate teeth. The tetrodotoxin-sensitive sodium (NA) channels (Nav1.7) play important roles in the pathophysiology of pain. In this study, we investigated the TG expression of Nav1.7 and extracellular signal-regulated kinase (ERK) in a rat model of pulpitis to explore the correlation between these channels and inflammatory pain. Pulpitis was confirmed by hematoxylin-eosin staining. In this study, we demonstrated that the reflex of rats to mechanical stimulation increases after pulp exposure and that the exposed rat molar pulp can upregulate the expression of Nav1.7 and ERK in the rat TG. Three days after rat pulp exposure, the expression levels of the two ion channels in the TG increased. TG target injection of PF04856264, a Nav1.7 inhibitor, dose-dependently increased the mechanical pain threshold and was able to inhibit ERK expression. TG target injection of PD98059, an ERK inhibitor, dose-dependently increased the mechanical pain threshold. These factors simultaneously resulted in the highest production. In this study, with the established link to inflammatory pain, we found that Nav1.7 and ERK both play important roles in the induction of inflammatory pain caused by pulpitis. We also found a correlation between the expression levels of Nav1.7 and ERK and the degree of inflammatory pain. Furthermore, ERK signaling pathways were promoted by the Nav1.7 in TG after pulpitis.

Angiotensin II downregulates ACE2-mediated enhancement of MMP-2 activity in human cardiofibroblasts

2013 ◽  
Vol 91 (6) ◽  
pp. 435-442 ◽  
Author(s):  
Tang-Ching Kuan ◽  
Mu-Yuan Chen ◽  
Yan-Chiou Liao ◽  
Li Ko ◽  
Yi-Han Hong ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathway ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Lentiviral Infection ◽  
And Control

Angiotensin converting enzyme II (ACE2) is a component of the renin-angiotensin system (RAS) that negatively regulates angiotensin II (Ang II). Ang II, in turn, affects the expression of matrix metalloproteinases (MMPs) to induce heart remodeling. The specific mechanisms by which ACE2 regulates MMP-2, however, remain unclear. The aim of this study was to investigate the regulatory relationships between Ang II, ACE2, and MMP-2. ACE2 expression was upregulated and downregulated in human cardiofibroblasts (HCFs) by lentiviral infection. Effects on MMP-2 activity, shed ACE2 activity, extracellular signal-regulated kinase (ERK) signaling pathway, and ADAM metallopeptidase domain 17 (ADAM17) expression were assessed. ACE2 increased MMP-2 activity, and Ang II inhibited this effect through the Ang II type-1 receptor (AT1R) and ERK1/2 signaling pathway. Ang II also reduced the effect of ACE2 on ERK1/2 levels, the activity of shed ACE2, and adam17 expression in HCFs. Additionally, these Ang II-mediated reductions could be attenuated by AT1R antagonist valsartan. In conclusion, these data help to clarify how ACE2 and Ang II interact to regulate MMP-2 and control tissue remodeling in heart disease.

Melatonin Receptor Type 1 Signals to Extracellular Signal-Regulated Kinase 1 and 2 via Giand GsDually Coupled Pathways in HEK-293 Cells

Biochemistry ◽  
2014 ◽  
Vol 53 (17) ◽  
pp. 2827-2839 ◽  
Author(s):  
Linjie Chen ◽  
Xiaobai He ◽  
Yaping Zhang ◽  
Xiaopan Chen ◽  
Xiangru Lai ◽  
...  
Keyword(s):  
Receptor Type ◽  
Melatonin Receptor ◽  
Hek 293 ◽  
Extracellular Signal Regulated Kinase ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Extracellular Signal

scholarly journals Extracellular Signal-Regulated Kinase Mediates Ebastine-Induced Human Follicle Dermal Papilla Cell Proliferation

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Fu-Ming Tsai ◽  
Chao-Hsu Li ◽  
Lu-Kai Wang ◽  
Mao-Liang Chen ◽  
Ming-Cheng Lee ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Allergic Inflammation ◽  
Dermal Papilla ◽  
Dermal Papilla Cells ◽  
Expression Levels ◽  
Extracellular Signal Regulated Kinase ◽  
Hair Regrowth ◽  
Extracellular Signal ◽  
Elevated Expression ◽  
H1 Receptor Antagonist

Ebastine is a second-generation histamine H1 receptor antagonist that is used to attenuate allergic inflammation. Ebastine has also shown to affect hair loss; however, the immunoregulatory effect of ebastine cannot completely exclude the possibility of spontaneous hair regrowth in ebastine-treated mice. In this study, we examined the effects of ebastine on the growth of human follicle dermal papilla cells (HFDPC) using a WST-1 cell proliferation assay and a bromodeoxyuridine incorporation assay. Ebastine was shown to significantly increase the proliferation of HFDPC. The expression levels of cell-cycle regulatory proteins and an antiapoptotic protein were increased in ebastine-treated HFDPC. Furthermore, elevated expression levels of phospho-AKT and phospho-p44/42 extracellular signal-regulated kinase (ERK) were observed in ebastine-treated HFDPC. Ebastine-mediated HFDPC growth was completely reversed by blocking ERK kinase. The results from our present study suggest that the regulation of HFDPC proliferation by ebastine might be directly involved in hair regrowth through the ERK signaling pathway.

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