ライフサイエンスコーパス: CGRP

1 CGRP caused sustained excitation of neurons in slices of

2 CGRP dilated dural, but not pial, vessels and significan

3 CGRP in concert with IL-33 and neuromedin U (NMU) suppor

4 CGRP induced marked changes in ILC2 expression programs

5 CGRP pathway blockers might thus aggravate coincidental

6 CGRP potently inhibited alarmin-driven type 2 cytokine p

7 CGRP(+) SP(-) boutons were prevalent in lateral lamina I

8 CGRP(PBN) neurons are also activated in Apc(min/+) mice,

9 CGRP-based agents induce effects at nanomolar concentrat

10 CGRP-containing nerves innervate dermal blood vessels an

11 CGRP-mediated vasodilation is, however, a critical rescu

12 cells and expression-levels of spinal PAR-2, CGRP and c-Fos in the EA group were greater (P < 0.01) t

13 distribution and expression-levels of PAR-2, CGRP and c-Fos on day 22.

14 gulate HSCs indirectly via the niche(3,4,6), CGRP acts directly on HSCs via receptor activity modifyi

15 iography was performed with [(3)H]MK-3207 (a CGRP receptor antagonist).

16 ed the effect of fremanezumab (TEV-48125), a CGRP-mAb, on the activity of second-order trigeminovascu

17 rugs, the 5-HT1B/D agonist sumatriptan and a CGRP-blocking monoclonal antibody, attenuated the periph

18 distinct subset of ILCs scored highly for a CGRP-specific gene signature after in vivo alarmin stimu

19 study, we show that, if given enough time, a CGRP-mAb can prevent the activation and sensitization of

20 he CGRP pathway was shown in skin by using a CGRP receptor antagonist.

21 on at the site of intradermally administered CGRP led to a similar bias in CD4(+) T cells from draini

22 acerbation with migraine-like features after CGRP, compared with 6 patients (20%) after placebo (p <

23 ensity scores was significantly larger after CGRP, compared with placebo (p < 0.001).

24 nised monoclonal antibodies directed against CGRP and its receptor followed from these findings.

25 l calcitonin gene-related polypeptide-alpha (CGRP) in both the peripheral cortex of the femur and the

26 alpha-CGRP antagonized KLRG1(+) ILC2s proliferation but promot

27 g-lasting (t(1/2) >/=7 hours) acylated alpha-CGRP analogue (alphaAnalogue) could alleviate and revers

28 Genetic perturbation of alpha-CGRP increased the proportion of intestinal KLRG1(+) ILC

29 alpha-calcitonin gene-related peptide (alpha-CGRP) has been limited because of its peptide nature and

30 alpha-calcitonin gene-related peptide (alpha-CGRP), in intestinal KLRG1(+) ILC2s.

31 Our work highlights a model where alpha-CGRP-mediated neuronal signaling is critical for suppres

32 Although CGRP receptor blockade reduced certain proinflammatory g

33 In comparison, although CGRP infusion gave rise to the expected dilatation of du

34 transient receptor potential vanilloid 1 and CGRP.

35 Downregulation of spinal PAR-2 and CGRP levels by EA attenuates the ileitis and resultant V

36 uates VH through spinal PAR-2 activation and CGRP release, goats received an injection of 2,4,6-trini

37 ignificantly higher proportions of CALR+ and CGRP+ varicosities colocalized in baskets than in circul

38 calcitonin gene-related peptide (CGRP), and CGRP treatment inhibited osteoclastogenesis in vitro.

39 for functional connectivity between CSD and CGRP has triggered scientific interest in the possibilit

40 l colon and their morphological features and CGRP immunoreactivity characterized.

41 RP+ axons, but not varicose CGRP+ fibers and CGRP+ baskets.

42 f other submucosal neurons (NOS-, GABA-, and CGRP-expressing), are also deficient.

43 ciation between periodontal inflammation and CGRP in chronic migraine.

44 ated in the pathophysiology of migraine, and CGRP-based therapeutics are efficacious for the treatmen

45 t mechanisms through which periodontitis and CGRP are linked in these patients deserves further inves

46 d elucidated by the CGRP receptor antagonist CGRP(8-37).

47 d by the anti-CGRP monoclonal antibody (anti-CGRP-mAb) fremanezumab.

48 proach to migraine treatment, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs) were developed to

49 y, a new class of such drugs, humanized anti-CGRP monoclonal antibodies (CGRP-mAbs), were found to be

50 and efficacy of TEV-48125, a monoclonal anti-CGRP antibody, in the preventive treatment of high-frequ

51 rstanding of the mechanism of action of anti-CGRP-mAbs in migraine prevention.SIGNIFICANCE STATEMENT

52 ven recent clinical trials showing that anti-CGRP monoclonal antibodies can reduce and even prevent m

53 nd how these events are affected by the anti-CGRP monoclonal antibody (anti-CGRP-mAb) fremanezumab.

54 elated peptide (CGRP) monoclonal antibodies (CGRP-mAbs) are capable of preventing migraine.

55 d that humanized CGRP monoclonal antibodies (CGRP-mAbs) prevent activation and sensitization of high-

56 , humanized anti-CGRP monoclonal antibodies (CGRP-mAbs) were developed to reduce the availability of

57 , humanized anti-CGRP monoclonal antibodies (CGRP-mAbs), were found to be effective in reducing the f

58 Because CGRP(PBN) neurons respond broadly to multi-modal threats

59 e consists of major vasodilatation caused by CGRP (and possibly substance P) released from sensory-mo

60 ggests that these events are not mediated by CGRP, a conclusion with important implications for our u

61 L-4, we demonstrated that IL-6 production by CGRP-treated pDMECs was involved in these effects.

62 that virtually all NTS-->lPBN and lPBN-->CeA CGRP projections coexpress vesicular glutamate transport

63 isolated rat periosteum-derived stem cells, CGRP induces CALCRL- and RAMP1-dependent activation of c

64 gions that regulate arousal (locus ceruleus, CGRP(+) parabrachial neurons).

65 TN, C1 neurons innervate the locus ceruleus, CGRP(+) processes within the parabrachial complex, and l

66 rmed dense, basket-like varicosity clusters (CGRP+ baskets) that enveloped myenteric nerve cell bodie

67 In conclusion, CGRP+ baskets in mouse colon are formed by intrinsic ent

68 ng fibers were identified: fibers containing CGRP and fibers containing VIP but not CGRP.

69 rly half originate in DRG neurons containing CGRP and TRPV1; that nerve bundles traverse suboccipital

70 To define CGRP receptor binding sites, in vitro autoradiography wa

71 Actions of nerve-derived CGRP on ECs may have important regulatory effects on the

72 -84 or RAMP2 Glu-101 contacting the distinct CGRP/AM C-terminal residues.

73 In females, dural CGRP causes priming to a pH 7.0 solution after animals r

74 response was observed only in females; dural CGRP at doses from 1 pg to 3.8 mug produce no responses

75 um nitroprusside (0.1 mg/kg) following dural CGRP.

76 These data further implicate dural CGRP signaling in the pathophysiology of migraine and pr

77 males but only priming to subthreshold dural CGRP (0.1 pg) in females.

78 ut only causes priming to subthreshold dural CGRP (0.1 pg) in females.

79 y, the sexually dimorphic responses to dural CGRP were not specific to rats as similar female-specifi

80 of migraine and propose a model where dural CGRP-based mechanisms contribute to the sexual disparity

81 s and monoclonal antibodies targeting either CGRP or its receptor.

82 smaller vasodilatation caused by endogenous CGRP that is only visible after inhibition of Y1 NPY rec

83 ogether, these data indicate that endogenous CGRP is a critical negative regulator of ILC2 responses

84 K and DBH neurons in the NTS directly engage CGRP(PBN) neurons to promote anorexia.

85 These findings establish CGRP(PBN) neurons as key mediators of cancer-induced app

86 wo separate populations that directly excite CGRP(PBN) neurons.

87 thway appears critical, nerve growth factor, CGRP, and substance P all appear to be required.

88 ra mater as a primary location of action for CGRP in migraine and suggest that female-specific mechan

89 However, the location of action for CGRP in migraine remains unclear.

90 n DRG and spinal cord sections colabeled for CGRP and SP.

91 mples and serum concentrations were done for CGRP, interleukin (IL)-6 and IL-10.

92 re, mouse distal colon was immunolabeled for CGRP, a marker of putative IPANs.

93 RAMP1/2 alter CLR selectivity for CGRP/AM in part by RAMP1 Trp-84 or RAMP2 Glu-101 contact

94 Furthermore, CGRP-targeted therapies might provide a novel mechanism-

95 sCT and AC413 supported a shared non-helical CGRP-like conformation for their TN(T/V)G motif prior to

96 However, CGRP-positive nerves were significantly more superficial

97 erability of fremanezumab, a fully humanised CGRP antibody, in patients with migraine who had previou

98 ATEMENT Recently, we reported that humanized CGRP monoclonal antibodies (CGRP-mAbs) prevent activatio

99 root ganglia (DRG), there is an increase in CGRP(+), TH(+), and Iba1(+) (macrophage) labeling, but n

100 regions in the brainstem may be involved in CGRP signaling.

101 vels of the neurochemical SP, a reduction in CGRP fibers and changes in pERK/ERK and pAKT/AKT ratios.

102 At the ankle there is increased CGRP(+), TH(+), and GAP-43(+) fiber synovial innervation

103 n spinal cord nociceptive neurons, increased CGRP release from sciatic nerves and DRGs, and a reducti

104 taglandin (indomethacin) synthesis increased CGRP EC50 in both age groups.

105 ing NO and prostaglandin synthesis increased CGRP EC50 in Young and Old MAs.

106 arrier, which suggests that drugs inhibiting CGRP signaling may not be able to penetrate the central

107 ution after animals recover from the initial CGRP-induced allodynia.

108 al and intranasal gepants and the injectable CGRP monoclonal antibodies (mAbs) are described, as are

109 way and the possibility that this injectable CGRP analogue may be effective in cardiac disease.

110 ately half (48%) of nerve cell bodies inside CGRP+ baskets lacked both NOS and CALR, while two overla

111 , but was seen after intracerebroventricular CGRP injection.

112 tility changes after intracerebroventricular CGRP.

113 In addition, as with intracerebroventricular CGRP, there was no general increase in anxiety as measur

114 low light was not seen after intraperitoneal CGRP injection, but was seen after intracerebroventricul

115 After intraperitoneal CGRP, motility was decreased in the dark only, similar t

116 in an open-field assay after intraperitoneal CGRP.

117 n is indicated by the ability of intravenous CGRP to trigger migraine in humans and the efficacy of C

118 5 days in organ culture caused loss of large CGRP+ axons, but not varicose CGRP+ fibers and CGRP+ bas

119 or-bound structure of the homologous ligands CGRP and AM.

120 Binding of one of the three peptide ligands, CGRP, adrenomedullin (AM), and intermedin/adrenomedullin

121 As the main CGRP-mAb site of action appears to be situated outside t

122 ated protein (peptidergic nociceptor marker; CGRP), and/or neurofilament 200 (myelinated axon marker;

123 ree plasma levels that provided near maximal CGRP receptor coverage.

124 Acute responses to meningeal CGRP are female-specific and sensitization to CGRP after

125 nce led to the development of small molecule CGRP receptor antagonists and monoclonal antibodies targ

126 chemistry required to advance small molecule CGRP receptor antagonists, also called gepants, includin

127 investigated whether gepants, small molecule CGRP receptor antagonists, worsen cerebral ischemia.

128 Because the sensory neuropeptide CGRP (calcitonin gene-related peptide) regulates host re

129 rsal horn that co-expressed the neuropeptide CGRP.

130 n of osteoclastogenesis via the neuropeptide CGRP.

131 ither peptidergic (CGRP+) or nonpeptidergic (CGRP-).

132 ining CGRP and fibers containing VIP but not CGRP.

133 In most PBN subdivisions, more than 50% of CGRP cells dually projected to muscle + WAT and muscle +

134 Similarly, 31-68% of CGRP cells projected both to WAT + BAT.

135 d further explore the mechanism of action of CGRP-mAbs, we tested the effect of fremanezumab on the c

136 Using pharmacological tools, the actions of CGRP were probed and elucidated by the CGRP receptor ant

137 We show here that application of CGRP to the cranial meninges causes behavioral responses

138 Sprouting and arborization of CGRP+TrkA+ sensory nerve fibers within the reactive peri

139 were developed to reduce the availability of CGRP, and were found effective in reducing the frequency

140 y help to explain the therapeutic benefit of CGRP-mAb in reducing headaches of intracranial origin su

141 Providing clinically effective blockade of CGRP signaling required surmounting multiple challenging

142 pes of noxious stimuli caused a depletion of CGRP from corneal nerves, indicating that all modalities

143 Whereas the distribution of CGRP receptor proteins was similar in SMCs, RAMP1 associ

144 The distribution of CGRP-positive nerves did not differ significantly betwee

145 hat female-specific mechanisms downstream of CGRP receptor activation contribute to the higher preval

146 With no difference in efficacy, the EC50 of CGRP as a vasodilator was approximately 6-fold greater i

147 rve function and diminished effectiveness of CGRP as a vasodilator is multifaceted and may adversely

148 d the vascular and behavioral the effects of CGRP.

149 igger migraine in humans and the efficacy of CGRP receptor antagonists that evidently do no penetrate

150 Inactivation of CGRP(PBN) neurons before tumor implantation prevents ano

151 Inactivation of CGRP(PBN) neurons in Apc(min/+) mice permits hyperphagia

152 We also demonstrate that inactivation of CGRP(PBN) neurons prevents lethargy, anxiety and malaise

153 during C rodentium infection, independent of CGRP receptor signaling.

154 Indeed, a single injection of CGRP induced much of the genetic program elicited in mSC

155 Peripheral (intraperitoneal) injection of CGRP resulted in light-aversive behavior in wild-type CD

156 therapeutics that inhibit the interaction of CGRP with its receptor in migraineurs.

157 tween periodontitis and peripheral levels of CGRP in a cohort of patients with chronic migraine.

158 ociated with increased circulating levels of CGRP in chronic migraineurs.

159 ive an intravenous infusion of 1.5mug/min of CGRP or placebo (isotonic saline) over 20 minutes on two

160 ma or IL-4 were decreased by the presence of CGRP-treated pDMECs.

161 To determine central projections of CGRP(+) SP(-) neurons, Neurobiotin (NB) was applied to t

162 shared and distinct signaling properties of CGRP, AM, and AM2/IMD.

163 To address the role of CGRP both within and outside the CNS, we used CGRP-induc

164 and small intestine, we assessed the role of CGRP receptor signaling during C rodentium infection.

165 Therefore, to elucidate the role of CGRP, it is critical to identify the regions within the

166 that act peripherally, the relevant sites of CGRP action remain unknown.

167 t while three partially separable subsets of CGRP(PBN) neurons broadly collateralize to their respect

168 ; and demonstrate that up- or down-tuning of CGRP signals augments or diminishes, respectively, IL-33

169 We also determined their potency on CGRP-induced relaxations in mouse and human vessels, in

170 t was 10-fold more potent than rimegepant on CGRP-induced relaxations in mouse aorta.

171 Parabrachial CGRP neurons receive diverse threat-related signals and

172 ogether, these results demonstrate that PBel CGRP neurons mediate a gastrointestinal distress signal

173 forebrain sites under the control of a PBel(CGRP) switch that is necessary to arouse animals from hy

174 HT(2a) receptors which are expressed by PBel(CGRP) neurons.

175 mogenetic and optogenetic activation of PBel(CGRP) neurons caused wakefulness, whereas optogenetic in

176 ness, whereas optogenetic inhibition of PBel(CGRP) neurons prevented arousal to CO2, but not to an ac

177 Optogenetic inhibition of PBel(CGRP) terminals identified a network of forebrain sites

178 aining calcitonin gene related peptide (PBel(CGRP) neurons) are critical for causing arousal during h

179 l for modulating the sensitivity of the PBel(CGRP) neurons that cause arousal to rising levels of blo

180 PBN CGRP neurons become active in response to anorexigenic h

181 ppetite-suppressing effects and activate PBN CGRP neurons.

182 and to decrease activity in anorexigenic PBN CGRP neurons, thereby increasing food intake during home

183 on stimulation reduces Fos expression in PBN CGRP neurons across all conditions.

184 ing chemogenetic-mediated stimulation of PBN CGRP neurons.

185 gene-related protein (CGRP)-expressing PBN (CGRP(PBN)) neurons; however, the molecular identity of t

186 ors for the calcitonin gene-related peptide (CGRP) and adrenomedulin (AM) recently published.

187 ca-encoding calcitonin gene-related peptide (CGRP) and its cognate receptor components.

188 europeptide calcitonin gene-related peptide (CGRP) and its receptor.

189 ted against calcitonin gene-related peptide (CGRP) and substance P could neutralise their actions.

190 The calcitonin gene-related peptide (CGRP) family of G protein-coupled receptors (GPCRs) is f

191 europeptide calcitonin gene-related peptide (CGRP) from dorsal root ganglion neurons, and reduced inf

192 europeptide calcitonin gene-related peptide (CGRP) has a key role in migraine.

193 E STATEMENT Calcitonin gene-related peptide (CGRP) has long been implicated in the pathophysiology of

194 tal role of calcitonin gene-related peptide (CGRP) in migraine pathophysiology was identified over 30

195 nt role for calcitonin gene-related peptide (CGRP) in migraine pathophysiology.

196 europeptide calcitonin gene-related peptide (CGRP) is a central player in migraine pathogenesis, yet

197 Calcitonin gene-related peptide (CGRP) is a key element in migraine pathophysiology.

198 europeptide calcitonin gene-related peptide (CGRP) is a key player in migraine.

199 Calcitonin gene-related peptide (CGRP) is a neuropeptide with well-established immunomodu

200 Calcitonin gene-related peptide (CGRP) is a potent vasodilator involved in migraine patho

201 europeptide calcitonin gene-related peptide (CGRP) is associated with activation of the trigeminovasc

202 E STATEMENT Calcitonin gene-related peptide (CGRP) monoclonal antibodies (CGRP-mAbs) are capable of p

203 xia made by calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) that tra

204 s targeting calcitonin gene-related peptide (CGRP) or its receptor have shown efficacy in the prevent

205 Calcitonin gene-related peptide (CGRP) pathway inhibitors are emerging treatments for mig

206 The calcitonin gene-related peptide (CGRP) pathway is a promising target for preventive thera

207 The calcitonin gene-related peptide (CGRP) pathway is important in migraine pathophysiology.

208 (lPBN) and calcitonin-gene related peptide (CGRP) projections from the lPBN to the central nucleus o

209 l-molecule, calcitonin gene-related peptide (CGRP) receptor antagonist under investigation for treatm

210 HTL22562, a calcitonin gene-related peptide (CGRP) receptor antagonist.

211 tionship to calcitonin gene-related peptide (CGRP) staining in the dorsal horn.

212 Calcitonin gene-related peptide (CGRP) stimulated CLR endocytosis and activated protein k

213 lication of calcitonin gene-related peptide (CGRP) to the rat dura mater produces cutaneous periorbit

214 eactive for calcitonin gene-related peptide (CGRP), a marker for polymodal nociceptors, suggesting th

215 ody against calcitonin gene-related peptide (CGRP), a marker of nociceptive sensory nerves.

216 y releasing calcitonin gene-related peptide (CGRP), a neuropeptide that modulates M cells and SFB lev

217 Calcitonin gene-related peptide (CGRP), adrenomedullin (AM), and adrenomedullin 2/interme

218 ylin (Amy), calcitonin gene-related peptide (CGRP), and adrenomedullin (AM) peptides.

219 uropeptide, calcitonin gene-related peptide (CGRP), and CGRP treatment inhibited osteoclastogenesis i

220 expressing calcitonin gene-related peptide (CGRP), and in central processes of these cells in the su

221 y targeting calcitonin gene-related peptide (CGRP), is being investigated as a preventive treatment f

222 tide (VIP), calcitonin-gene related peptide (CGRP), substance P (SP), neuropeptide tyrosine (NPY), an

223 Calcitonin gene-related peptide (CGRP), the most abundant neuropeptide in primary afferen

224 CO2 express calcitonin gene-related peptide (CGRP), we hypothesized that CGRP may provide a molecular

225 vasodilator calcitonin gene-related peptide (CGRP), which induces headache in humans.

226 n contrast, calcitonin gene-related peptide (CGRP)-expressing neurons in the parabrachial nucleus (PB

227 hology, and calcitonin gene-related peptide (CGRP)-immunoreactivity of uterine spinal afferent ending

228 latation to calcitonin gene-related peptide (CGRP).

229 stained for calcitonin gene-related peptide (CGRP).

230 ecretion of calcitonin gene-related peptide (CGRP).

231 reactive to calcitonin gene-related peptide (CGRP).

232 e (CRH) and calcitonin gene-related peptide (CGRP).

233 tor for the calcitonin-gene-related peptide (CGRP); and demonstrate that up- or down-tuning of CGRP s

234 activity to calcitonin-gene-related-peptide (CGRP).

235 ensory neurons that were either peptidergic (CGRP+) or nonpeptidergic (CGRP-).

236 begin to address the mechanism of peripheral CGRP action, we used transgenic CGRP-sensitized mice tha

237 noclonal antibody, attenuated the peripheral CGRP-induced light aversion and motility behaviors.

238 he regions within the brainstem that process CGRP signaling.

239 sly undefined role of magnesium in promoting CGRP-mediated osteogenic differentiation, which suggests

240 d risk of ischemic events or on prophylactic CGRP inhibition.

241 n involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRP(PBN)) neurons; however, the m

242 sensory nerve density was reduced and RAMP1 (CGRP receptor component) associated with nuclear regions

243 conformation of peptides that require RAMPs; CGRP, AM, and amylin.

244 ering RAMPs to CTR enhanced binding of rAmy, CGRP, and the AMY antagonist AC413.

245 d with fewer activated microglia and reduced CGRP expression in the dorsal horn caudal to the lesion.

246 plexes and was also conserved in the related CGRP receptor.

247 Quantitative analysis revealed CGRP+ varicosities were most abundant in baskets, follow

248 belling revealed reduced density of sensory (CGRP) but not sympathetic (tyrosine hydroxylase) innerva

249 th periodontitis had greater levels of serum CGRP (19.7 +/- 6.5 versus 15.3 +/- 6.2 pg/mL, P < 0.0001

250 fter in vivo alarmin stimulation, suggesting CGRP regulated this response.

251 dels of migraine, CSD induction and systemic CGRP infusion.

252 shows that therapeutic approaches targeting CGRP have the potential to transform the clinical manage

253 nd the brain by distinct mechanisms and that CGRP actions may be transmitted to the CNS via indirect

254 These data are the first to demonstrate that CGRP-induced headache-like behavioral responses at doses

255 related peptide (CGRP), we hypothesized that CGRP may provide a molecular identifier of the CO2 arous

256 scientific interest in the possibility that CGRP antagonism may disrupt vascular responses to CSD an

257 In this study, we report that CGRP can act in both the brain and the periphery of the

258 In the current paper, we report that CGRP-mAbs prevent the activation of Adelta but not C-typ

259 We show that CGRP(PBN) neurons are activated in mice implanted with L

260 Our data showed that CGRP-evoked 5-HT release reduced taste-evoked ATP secret

261 These results suggest that CGRP can act in both the periphery and the brain by dist

262 fully human monoclonal antibody against the CGRP receptor, for migraine prevention.

263 fully human monoclonal antibody against the CGRP receptor, in patients with chronic migraine.

264 ns of CGRP were probed and elucidated by the CGRP receptor antagonist CGRP(8-37).

265 this study was to better understand how the CGRP-mAb fremanezumab (TEV-48125) modulates meningeal se

266 ed responses to alarmins in mice lacking the CGRP receptor.

267 s indicates the therapeutic potential of the CGRP pathway and the possibility that this injectable CG

268 anethidine, although not by the 1 mum of the CGRP receptor antagonist BIBN4096bs.

269 itized mice that have elevated levels of the CGRP receptor hRAMP1 subunit in nervous tissue (nestin/h

270 f sensory nerves or knockdown in vivo of the CGRP-receptor-encoding genes Calcrl or Ramp1 substantial

271 We show that the CGRP family of receptors displays both ligand- and RAMP-

272 the alphaAnalogue to act selectively via the CGRP pathway was shown in skin by using a CGRP receptor

273 The structure of 8 complexed with the CGRP receptor was determined at a 1.6 angstrom resolutio

274 dation reduced the efficacy of dilatation to CGRP by approximately 30% in Old MAs yet increased this

275 othelial denudation attenuated dilatation to CGRP in Old MAs yet enhanced dilatation to CGRP in Young

276 o CGRP in Old MAs yet enhanced dilatation to CGRP in Young MAs while abolishing all dilatations to AC

277 ts with persistent PTH are hypersensitive to CGRP, which underscores its pathophysiological importanc

278 ed nerve axons and endings immunoreactive to CGRP.

279 murine dermal microvascular ECs (pDMECs) to CGRP followed by coculture with LCs, responsive CD4(+) T

280 Collectively, these data point to CGRP as a context-dependent negative regulatory factor t

281 GRP are female-specific and sensitization to CGRP after two distinct stimuli are also female-specific

282 f peripheral CGRP action, we used transgenic CGRP-sensitized mice that have elevated levels of the CG

283 the nociceptive neuronal markers IB4, TRPV1, CGRP, and substance P.

284 ation of RTX caused downregulation of TRPV1, CGRP, and IB4 binding and upregulation of VIP in the cor

285 GRP both within and outside the CNS, we used CGRP-induced light-aversive behavior in mice as a measur

286 Although migraine can be treated using CGRP antagonists that act peripherally, the relevant sit

287 loss of large CGRP+ axons, but not varicose CGRP+ fibers and CGRP+ baskets.

288 fibers containing immunoreactivity for VIP, CGRP, SP, or nNOS were found.

289 ximal vagina and reduced proportions of VIP, CGRP, and SP containing nerve fibers in the distal epith

290 Most spinal afferent endings were CGRP-immunoreactive and morphologically classified as "s

291 jority of spinal afferent nerve endings were CGRP-immunoreactive.

292 tified in the stomach, and most of them were CGRP immunoreactive.

293 ts a type II turn (Gly(28)-Thr(31)), whereas CGRP and AM adopt type I turns.

294 We examined whether CGRP regulates the outcome of Ag presentation by Langerh

295 a and pia, we determined the extent to which CGRP contributes to the induction of arterial dilatation

296 PISA was independently associated with CGRP in patients with chronic migraine (beta = 0.003; 95

297 2C showed colocalization of subunit C2I with CGRP-positive sensory neurons and fibers but not with Ch

298 haracterized further by triple labeling with CGRP, nitric oxide synthase (NOS) and calretinin (CALR)

299 PISA correlated positively with CGRP (r = 0.236; P = 0.017) and IL-6 (r = 0.262; P = 0.0

300 Without CGRP signaling, ILC2 responses and worm expulsion were e