Calcitonin gene related peptide gene expression in collagen-induced arthritis

1995 ◽  
Vol 73 (7) ◽  
pp. 1015-1019 ◽  
Author(s):  
Eberhard Weihe ◽  
Donatus Nohr ◽  
Martin K.-H. Schäfer ◽  
Stefan Persson ◽  
Johanna Källström ◽  
...  
Keyword(s):  
Gene Expression ◽  
Motor Neurons ◽  
Calcitonin Gene Related Peptide ◽  
Motor Dysfunction ◽  
Mrna Levels ◽  
Related Peptide ◽  
Inflammatory Conditions ◽  
Systemic Corticosteroids ◽  
Calcitonin Gene ◽  
Peptide Gene

Changes in calcitonin gene related peptide (CGRP) gene expression in spinal motoneurons and dorsal root ganglia (DRG) of rats subjected to collagen II induced arthritis (CIA) were evaluated by semiquantitative in situ hybridization. The effects of systemic treatment with the corticosteroid budesonide on basal CGRP expression and on changes under inflammatory conditions were examined. CIA caused a significant increase in CGRP mRNA levels in DRG. Budesonide reduced the constitutive CGRP mRNA levels in DRG, compared with untreated control rats, and reversed the CIA-induced increase. In contrast, CIA caused a marked decrease of CGRP mRNA levels in motoneurons. Budesonide had no effect on constitutive CGRP mRNA levels in motoneurons and attenuated the decrease in CGRP mRNA levels in motoneurons of rats subjected to CIA. Thus, peripheral inflammation and systemic corticosteroids have differential effects on CGRP expression in sensory and motor neurons. This may be relevant for the pathophysiology and pharmacotherapy of chronic inflammatory pain and motor dysfunction in chronic arthritis.Key words: calcitonin gene related peptide, neuropeptides, sensory, spinal motoneuron, arthritis, glucocorticoids, pain.

scholarly journals Retinoic acid repression of cell-specific helix-loop-helix-octamer activation of the calcitonin/calcitonin gene-related peptide enhancer.

1993 ◽  
Vol 13 (10) ◽  
pp. 6079-6088 ◽  
Author(s):  
T M Lanigan ◽  
L A Tverberg ◽  
A F Russo
Keyword(s):  
Retinoic Acid ◽  
Acid Treatment ◽  
Calcitonin Gene Related Peptide ◽  
Retinoid X Receptor ◽  
Mrna Levels ◽  
Retinoic Acid Treatment ◽  
Enhancer Activity ◽  
Related Peptide ◽  
Helix Loop Helix ◽  
Calcitonin Gene

We have investigated the mechanism underlying repression of calcitonin/calcitonin gene-related peptide (CT/CGRP) gene expression by retinoic acid. Retinoic acid treatment of the CA77 thyroid C-cell line decreased CT/CGRP promoter activity two- to threefold, which correlates well with the decrease in calcitonin and CGRP mRNA levels. Repression is mediated through the nuclear retinoic acid receptors (RAR) on the basis of the retinoid specificity, the sensitivity of repression (half-maximal repression at 0.2 nM), and the additional repression caused by cotransfection of an alpha-RAR expression vector. The sequences required for retinoic acid repression were localized to an 18-bp element containing cell-specific enhancer activity. The enhancer binds helix-loop-helix (HLH) and octamer transcription factors that act synergistically to activate transcription. Retinoic acid repression requires both these factors since mutations in either motif resulted in the loss of repression. Furthermore, repression was observed only in cell lines containing enhancer activity. We have used electrophoretic mobility shift assays to show that repression does not involve direct DNA binding of RAR or RAR-retinoid X receptor heterodimers. Instead, repression appears to involve interactions with the stimulatory enhancer factors. Following retinoic acid treatment, there was a specific decrease in an enhancer complex containing both HLH and octamer proteins. Formation of the HLH-octamer complex was also specifically blocked by the addition of exogenous RAR-retinoid X receptor protein. These results demonstrate that RAR can repress CT/CGRP gene transcription by interfering with combinatorial activation by cell-specific HLH and octamer proteins.

The localization of calcitonin gene related peptide (CGRP) receptor in rat stomach, and the role of CGRP on the secretion and gene expression of somatostatin

2000 ◽  
Vol 118 (4) ◽  
pp. A1103
Author(s):  
Kousaku Kawashima ◽  
Shunji Ishihara ◽  
Nobuyuki Moriyama ◽  
Hiroshi Suetsugu ◽  
Hideaki Kazumori ◽  
...  
Keyword(s):  
Gene Expression ◽  
Calcitonin Gene Related Peptide ◽  
Cgrp Receptor ◽  
Rat Stomach ◽  
Related Peptide ◽  
Calcitonin Gene

scholarly journals Induction of calcitonin gene-related peptide expression in rats by cortical spreading depression

Cephalalgia ◽  
2016 ◽  
Vol 39 (3) ◽  
pp. 333-341 ◽  
Author(s):  
Yan Wang ◽  
Anne E Tye ◽  
Junli Zhao ◽  
Dongqing Ma ◽  
Ann C Raddant ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Calcitonin Gene Related Peptide ◽  
Rat Cerebral Cortex ◽  
Mrna Levels ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peptide Expression ◽  
Cortical Regions

Objective The neuropeptide calcitonin gene-related peptide (CGRP) has now been established as a key player in migraine. However, the mechanisms underlying the reported elevation of CGRP in the serum and cerebrospinal fluid of some migraineurs are not known. A candidate mechanism is cortical spreading depression (CSD), which is associated with migraine with aura and traumatic brain injury. The aim of this study was to investigate whether CGRP gene expression may be induced by experimental CSD in the rat cerebral cortex. Methods CSD was induced by topical application of KCl and monitored using electrophysiological methods. Quantitative PCR and ELISA were used to measure CGRP mRNA and peptide levels in discrete ipsilateral and contralateral cortical regions of the rat brain 24 hours following CSD events and compared with sham treatments. Results The data show that multiple, but not single, CSD events significantly increase CGRP mRNA levels at 24 hours post-CSD in the ipsilateral rat cerebral cortex. Increased CGRP was observed in the ipsilateral frontal, motor, somatosensory, and visual cortices, but not the cingulate cortex, or contralateral cortices. CSD also induced CGRP peptide expression in the ipsilateral, but not contralateral, cortex. Conclusions Repeated CSD provides a mechanism for prolonged elevation of CGRP in the cerebral cortex, which may contribute to migraine and post-traumatic headache.

Sign in / Sign up

Export Citation Format

Share Document