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Journals / Journal of Neurological Sciences (Turkish) / 2012 / Cilt: 29 - Sayı: 3

C-Jun N-Terminal Kinaz Sıçan Trigeminal Ganglionunda in Vitro Olarak Kalsitonin Gene-bağlı Peptid Yapımını Düzenler

C-Jun N-Terminal Kinase Mediates Calcitonin Gene-Related Peptide Expression in Rat Trigeminal Ganglion in Vitro

Guo-Gang LUO
Bo-Bo YUAN
Xing-Yun YUAN
Kang HUO
Wen-Jing FAN
Min She LU
Yong-Xiao CAO
Yaping ZHANG
Pages
566–575
Publication Date
2022-10-19
DOI
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

Real-time polymerase chain reaction(RT-PCR) and Western blotting were used to evaluate the CGRP-mRNA expression andphosphorylated JNK (pJNK) protein in rat TG after the organ culture.Results and Conclusions: The JNK inhibitor significantly reduced the organ culture andcytokines-induced up-regulation of CGRP-mRNA expression compared with control(P

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Calcitonin gene-related peptide (CGRP) plays a prominent role in migrainepathophysiology.
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Key Findings & Data:Using an in-vitro model of organculture of rat trigeminal ganglion (TG), the present study aims to investigate the role of c-JunN-terminal kinase (JNK) in regulation of CGRP.Methods: The TG was isolated from Sprague-Dawley (SD) rats and then organ cultured inpresence of inflammatory cytokines tumor necrosis factor-alpha (TNF-α) (50μg/L) orinterleukin-1β (IL-1β) (25μg/L) with and without a specific JNK inhibitor SP600125 (10-5M)or an anti-migraine drug sumatriptan (0.5g/L) for 24h.
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Conclusion & Impact:Real-time polymerase chain reaction(RT-PCR) and Western blotting were used to evaluate the CGRP-mRNA expression andphosphorylated JNK (pJNK) protein in rat TG after the organ culture.Results and Conclusions: The JNK inhibitor significantly reduced the organ culture andcytokines-induced up-regulation of CGRP-mRNA expression compared with control(P
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: Calcitonin gene-related peptide (CGRP) plays a prominent role in migrainepathophysiology. However, the underlying molecular mechanisms that are responsible forregulating CGRP expression are not fully understood. Using an in-vitro model of organculture of rat trigeminal ganglion (TG), the present study aims to investigate the role of c-JunN-terminal kinase (JNK) in regulation of CGRP.Methods: The TG was isolated from Sprague-Dawley (SD) rats and then organ cultured inpresence of inflammatory cytokines tumor necrosis factor-alpha (TNF-α) (50μg/L) orinterleukin-1β (IL-1β) (25μg/L) with and without a specific JNK inhibitor SP600125 (10-5M)or an anti-migraine drug sumatriptan (0.5g/L) for 24h. Real-time polymerase chain reaction(RT-PCR) and Western blotting were used to evaluate the CGRP-mRNA expression andphosphorylated JNK (pJNK) protein in rat TG after the organ culture.Results and Conclusions: The JNK inhibitor significantly reduced the organ culture andcytokines-induced up-regulation of CGRP-mRNA expression compared with control(P

Özet

Amaç: Kalsitonin gene-bağlı peptid (CGRP) migren patofizyolojisinde önemli bir rol oynar.Bununla beraber CGRP oluşumunun düzenlenmesinde altta yatan moleküler mekanizma tamolarak anlaşılmış değildir. Bu çalışmada sıçan trigeminal ganglion (TG) organ kültürü in vitromodeli kullanılarak c-Jun N-terminal kinazın CGRP regülasyonundaki rolü araştırılmaktadır.Yöntem: Sprague-Dawley (SD) sıçanlarının TG'ları izole edildi ve ortamda yangısalsitokinler tümör nekroz faktörü-alfa (TNF-α) (50μg/L) ya da interlökin-1β (IL-1β) (25μg/L) ile bir spesifik JNK inhibitörü SP600125 (10-5M) birlikte veya olmaksızın ya da bir migrenilacı olan sumatriptan (0.5g/L) bir gün boyu uygulandı. Organ kültürü sonrası sıçan TG'ndafosforilize olan JNK (pJNK) proteini ve CGRP-mRNA miktarı değerlendirilmesi için gerçekzamanlı polimeraz zincir reaksiyonu (RT-PCR) ve Western blotting kullanıldı.Sonuç ve Yorum: JNK inhibitörü, transkripsiyonel bir mekanizmayı işaret edercesine, organkültürü ve sitokinin oluşturduğu CGRP-mRNA miktarının regülasyonunu kontrollere göreönemli ölçüde azalttı (P

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Cite This Article

LUO, G., YUAN, B., YUAN, X., HUO, K., FAN, W., LU, M. S., CAO, Y., ZHANG, Y. (2022). C-Jun N-Terminal Kinaz Sıçan Trigeminal Ganglionunda in Vitro Olarak Kalsitonin Gene-bağlı Peptid Yapımını Düzenler. Journal of Neurological Sciences (Turkish), Cilt: 29 - Sayı: 3, 566–575. https://ajindex.com/articles/565254

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References (16)

  1. Bigal ME, Lipton RB. The ep idemiology, burden, and comorbidities of migraine. Neurol Clin 2009; 27:321-34
  2. Bogoyevitch MA, Ngoei KR, Zhao TT, Yeap YY, Ng DC. c-Jun N-terminal kinase (JNK) signaling: recent advances and challenges. Biochim Biophys Acta. 2010; 1804:463-75
  3. Bowen EJ, Schmidt TW, Firm CS, Russo AF, Durham PL. Tumor necrosis f actor-alpha stimulation of calcitonin gene-related peptide exp ression and secretion f rom rat trigeminal ganglion neurons. J Neurochem 2006; 96: 65-77
  4. Crown ED. The role of mitogen activated p rotein kinase signaling in microglia and neurons in the initiation and maintenance of chronic pain. Exp Neurol. 2012; 234:330-9
  5. De Corato A, Lisi L, Capuano A, Tringali G, Tramutola A, Navarra P, Dello Russo C. Trigeminal satellite cells exp ress f unctional calcitonin gene- related peptide receptors, whose activation enhances interleukin-1β p ro-inf lammatory eff ects. J Neuroimmunol 2011; 237:39-46
  6. De Corato A, Capuano A, Currò D, Tringali G, Navarra P, Dello Russo C. Trigeminal satellite cells modulate neuronal responses to triptans: relevance f or migraine therapy. Neuron Glia Biol 2012; 10:1- 8
  7. Durham PL, Russo AF. New insights into the molecular actions of serotonergic antimigraine drugs. Pharmacol Ther. 2002; 94:77-92
  8. Durham PL. Calcitonin gene-related peptide (CGRP) and migraine. Headache 2006; 46: S3-8
  9. Durham PL, Vause CV. CGRP receptor antagonists in the treatment of migraine. CNS Drugs 2010; 24:539-48
  10. Gao YJ, Ji RR. Activation of JNK pathway in persistent pain. Neurosci Lett 2008; 437:180-3
  11. Huang GJ, Huang SS, Deng JS. Anti-Inf lammatory activities of inotilone f rom phellinus linteus through the inhibition of MMP-9, NF-κB, and MAPK activation in vitro and in vivo. PLoS One. 2012; 7:e35922
  12. Ji RR, Gereau RW 4th, Malcangio M, Strichartz GR. MAP kinase and pain. Brain Res Rev. 2009; 60:135- 48
  13. Katsarava Z, Buse DC, Manack AN, Lipton RB. Def ining the diff erences between ep isodic migraine and chronic migraine. Curr Pain Headache Rep 2012; 16:86-92
  14. Kuris A, Xu CB, Zhou MF, Taj ti J, Uddman R, Edvinsson L. Enhanced exp ression of CGRP in rat trigeminal ganglion neurons during cell and organ culture. Brain Res 2007; 1173: 6-13
  15. Luo GG, Cao YX, Xu CB, Ma AQ, Edvinsson L. ERK1/2 pathway involved in the exp ression of ETB receptors of the culturing smooth muscle cells of rat mesenteric artery. Acta Pharm Sin 2006; 41: 257- 62
  16. Luo GG, Jamali R, Cao YX, Edvinsson