ライフサイエンスコーパス: GHRH

1 GHRH agonists have been shown to promote islet graft sur

2 GHRH and its mRNA are also found in human cancers of the

3 GHRH and its receptors are expressed in experimental mod

4 GHRH and the GHRH receptor (GHRHR) mRNAs are detectable

5 GHRH antagonist MZ-J-7-114 (5 mug/day) significantly sup

6 GHRH antagonists could offer a new therapeutic modality

7 GHRH antagonists including MZ-J-7-46 and MZ-J-7-114 acyl

8 GHRH antagonists inhibit growth of various experimental

9 GHRH augmented and GHRH antagonist suppressed lipid and

10 GHRH induced a significant increase in levels of ERK, bu

11 GHRH knockout mice are remarkably long-lived, exhibiting

12 GHRH receptor is expressed on both adrenal cells and isl

13 GHRH stimulated and GHRH antagonist inhibited the expres

14 GHRH stimulated the growth of BPH-1 and primary prostate

15 GHRH was well tolerated and effectively increased levels

16 GHRH, GHRH receptor, and its main splice variant SV1 wer

17 GHRH-A markedly improved cardiac function as shown by ec

18 GHRH-A stimulated CSCs proliferation ex vivo, in a manne

19 GHRH-R and its splice variant, SV1, were present in 22Rv

20 GHRH-R is expressed in ckit(+) CSCs isolated from mouse,

21 In this study, we administered a GHRH antagonist (JV-1-42) and showed that, after i.v. in

22 Here, we microinjected a GHRH antagonist or GHRHR small interfering RNA (siGHRHR)

23 Here we show that a GHRH-agonist (GHRH-A; JI-38) reverses ventricular remode

24 H), we hypothesized that pretreatment with a GHRH agonist, JI-34, might increase the susceptibility o

25 These results show that treatment with a GHRH antagonist has positive effects on some aspects of

26 Treatment of T1D rats with a GHRH antagonist, MIA-602, at a dose that did not affect

27 2) also were observed after treatment with a GHRH antagonist.

28 In vivo long-acting GHRH treatment also induced pituitary DNA damage in mice

29 not known whether peripherally administered GHRH antagonists can cross the blood-brain barrier.

30 Furthermore, Cdk4 siRNA does not affect GHRH-induced proliferation of mouse embryonic fibroblast

31 Here we show that a GHRH-agonist (GHRH-A; JI-38) reverses ventricular remodeling and enhan

32 The concentrations of serum IGF-1 and GHRH, bFGF, and VEGF in tumor tissue were measured by ra

33 The effects of MZ-5-156, MZ-J-7-138 and GHRH on cell proliferation were evaluated in vitro.

34 idant effects of GHRH antagonist MIA-690 and GHRH agonist MR-409, on isolated mouse prefrontal cortex

35 easing hormone (GHRH) antagonist MIA-690 and GHRH agonist MR-409, previously synthesized and develope

36 GHRH augmented and GHRH antagonist suppressed lipid and protein oxidative s

37 DMS-153 tumors expressed mRNAs for GHRH and GHRH receptor splice variants 1 and 2, suggesting that G

38 growth hormone-releasing hormone (GHRH) and GHRH receptor (GHRH-R) are regulated in an autocrine fas

39 in, insulin-like growth factor-1 (IGF1), and GHRH receptor, and also stimulated insulin secretion in

40 he expression of mRNA for SVs of pGHRH-R and GHRH was likewise found in xenografts of human non-Hodgk

41 xpression of mRNA for N-cadherin, Snail, and GHRH GHRH antagonist reduced the average volume of spher

42 GHRH stimulated and GHRH antagonist inhibited the expression of the major an

43 ected with the empty vector did not show any GHRH binding.

44 el that can be used to explore links between GHRH repression, downregulation of the somatotropic axis

45 n the periphery was not reliably affected by GHRH administration and did not account for treatment ne

46 nonmyocyte mitosis was markedly increased by GHRH-A.

47 I and were, at least partially, nullified by GHRH antagonism, confirming a receptor-mediated mechanis

48 The inhibitory effect produced by GHRH antagonist can result in part from inactivation of

49 Lack of AR in GHRH cells (GHRH(DeltaAR) mice) induced no changes in body length, b

50 mice with deletion of ERalpha in GHRH cells (GHRH(DeltaERalpha)), which displayed reduced body length

51 In MPM cells, GHRH antagonists also regulated activity and expression

52 In conclusion, GHRH antagonists in combination with docetaxel synergist

53 H460 NSCLC cells contained GHRH peptide, and its growth was significantly inhibited

54 RL and HT cells contained GHRH peptide, and their growth in vitro was significantl

55 Our data suggest that endogenous cortical GHRH activates local cortical cells to affect EEG delta

56 tidase domain of botulinum toxin serotype D (GHRH-LHN/D, where HN/D indicates endopeptidase and trans

57 owever, the electrical patterns that dictate GHRH neuron functions have remained elusive.

58 th factor 1 (IGF1) was not reduced by either GHRH antagonists.

59 g diverse tumoral growth factors, especially GHRH itself, which acts as a potent autocrine/paracrine

60 one possible mechanism to explain favorable GHRH effects on cognition in adults with MCI and in heal

61 neurons in brain slices from male and female GHRH-GFP mice.

62 c expression of Ghrh mRNA, although very few GHRH neurons were found to coexpress TH- and GH-induced

63 one-releasing hormone (GHRH), as well as for GHRH itself, in human lung microvascular endothelial cel

64 The mRNA expression for GHRH receptor splice variants was found in all these mod

65 growth hormone-releasing hormone (GHRH) for GHRH-neurons and somatostatin (Sst) for Sst-neurons.

66 affinity binding sites for GHRH and mRNA for GHRH and splice variant-1 of the GHRH receptors were fou

67 DMS-153 tumors expressed mRNAs for GHRH and GHRH receptor splice variants 1 and 2, suggesti

68 The receptor for GHRH was detectable on myocytes, supporting direct activ

69 ct effects mediated by tumoral receptors for GHRH.

70 High-affinity binding sites for GHRH and mRNA for GHRH and splice variant-1 of the GHRH

71 presence of high-affinity binding sites for GHRH on RL and HT tumors.

72 Specific high-affinity binding sites for GHRH were found on MX-1 tumor membranes using ligand com

73 (K(d) = 0.58 +/- 0.17 nM) binding sites for GHRH with a maximal binding capacity (B(max)) of 103 +/-

74 le mice undergoes a shift in phenotype, from GHRH to Kiss1, during pubertal transition.

75 ctioning of these pituitary cell-types (e.g. GHRH/ghrelin/somatostatin/insulin/IGF-I-receptors/Pit-1)

76 GHRH, GHRH receptor, and its main splice variant SV1 were foun

77 The expression of GHRH, GHRH receptors, and their main splice variant, SV1, in P

78 findings demonstrate that within the heart, GHRH agonists can activate cardiac repair after MI, sugg

79 t with the growth hormone-releasing hormone (GHRH) agonist, JI-36, significantly enhanced graft funct

80 kolin or a long-acting GH-releasing hormone (GHRH) analog increased GH production and DNA damage meas

81 CJC-1295, a synthetic GH-releasing hormone (GHRH) analog, rescued the growth deficit displayed by Br

82 Because growth hormone-releasing hormone (GHRH) and GHRH receptor (GHRH-R) are regulated in an aut

83 nsation by Growth hormone-releasing hormone (GHRH) and Growth hormone (GH), underappreciated findings

84 analogs of growth hormone-releasing hormone (GHRH) and their mechanism of action were investigated in

85 Growth hormone-releasing hormone (GHRH) antagonist MIA-690 and GHRH agonist MR-409, previo

86 ggest that growth hormone-releasing hormone (GHRH) antagonists effectively shrink experimentally enla

87 ivities of growth hormone-releasing hormone (GHRH) antagonists have been demonstrated in different ex

88 effects of growth hormone-releasing hormone (GHRH) antagonists, JV-1-65 and JV-1-63, and bombesin/gas

89 ected that growth hormone-releasing hormone (GHRH) antagonists, such as MIA602, kill H295R cells in a

90 gonists of growth hormone-releasing hormone (GHRH) are being developed for the treatment of various c

91 pothalamic growth hormone-releasing hormone (GHRH) controls the release of growth hormone and acts as

92 hesis that growth hormone-releasing hormone (GHRH) directly activates cellular reparative mechanisms

93 2, contains a modified GH-releasing hormone (GHRH) domain and the endopeptidase domain of botulinum t

94 peptides, growth hormone-releasing hormone (GHRH) for GHRH-neurons and somatostatin (Sst) for Sst-ne

95 Growth hormone-releasing hormone (GHRH) has been previously shown to have cognition-enhanc

96 eptors for growth hormone-releasing hormone (GHRH) have been found in primary human prostate cancers

97 gonists of growth hormone-releasing hormone (GHRH) have been previously reported to promote growth, f

98 ruption of growth hormone-releasing hormone (GHRH) in mice on longevity and the putative mechanisms o

99 pothalamic growth hormone-releasing hormone (GHRH) inhibit growth of various malignancies, including

100 gonists of growth hormone-releasing hormone (GHRH) inhibit the growth of various human cancers by mul

101 Growth hormone-releasing hormone (GHRH) is a hypothalamic neuropeptide that has been shown

102 n of human growth hormone-releasing hormone (GHRH) is significantly diminished in the Cdk4+/- genetic

103 agonist of growth hormone-releasing hormone (GHRH) JV-1-38 were evaluated in nude mice bearing s.c. x

104 gonists of growth hormone-releasing hormone (GHRH) MZ-J-7-138 and JV-1-92 on H460 human non-small cel

105 GH-releasing hormone (GHRH) neurons express estrogen receptor alpha (ERalpha)

106 pothalamic growth hormone-releasing hormone (GHRH) neurons orchestrate body growth/maturation and hav

107 (NPY) and growth hormone releasing hormone (GHRH) neurons, regulates feeding, energy balance and bod

108 Growth hormone-releasing hormone (GHRH) promotes non-rapid eye movement sleep (NREMS), in

109 of treatment with the GH-releasing hormone (GHRH) receptor antagonist MZ-5-156 on aging in SAMP8 mic

110 shown that growth hormone-releasing hormone (GHRH) reduces cardiomyocyte (CM) apoptosis, prevents isc

111 pothalamic growth hormone-releasing hormone (GHRH) regulates the release of GH by the pituitary but a

112 lamic growth hormone (GH)-releasing hormone (GHRH) stimulates the synthesis and release of GH from th

113 a greater response to GH releasing hormone (GHRH) stimulation along with lower weight gain, and decr

114 gonists of growth hormone-releasing hormone (GHRH) synthesized previously inhibit proliferation of va

115 agonist of growth-hormone-releasing hormone (GHRH) to promote islet viability and function, and we ex

116 gonists of growth hormone-releasing hormone (GHRH) were shown to inhibit the growth of various cancer

117 Growth hormone-releasing hormone (GHRH), a hypothalamic polypeptide, acts as a potent auto

118 eceptor of growth hormone releasing hormone (GHRH), activation of which improves injury responses aft

119 olypeptide growth hormone-releasing hormone (GHRH), as well as for GHRH itself, in human lung microva

120 (CRF) and growth hormone-releasing hormone (GHRH), suggesting novel interactions of BRS-3 with stres

121 ivities of growth hormone-releasing hormone (GHRH), we hypothesized that pretreatment with a GHRH ago

122 back loops mediated by GH-releasing hormone (GHRH)- or somatostatin-expressing neurons.

123 herapeutic growth hormone releasing hormone (GHRH).

124 However, GHRH may also act in the cortex to influence sleep.

125 ologies Inc), a stabilized analogue of human GHRH (1 mg/d), or placebo 30 minutes before bedtime for

126 Kcnq1 is expressed in hypothalamic GHRH neurons and pituitary somatotropes.

127 ired for the proper function of hypothalamic GHRH neurons.

128 Overall, these results identify GHRH as an antihypertrophic regulator, underlying its th

129 ssues contain SV1 protein and immunoreactive GHRH.

130 Thus, direct estrogen action in GHRH/Kiss1 dual-phenotype neurons modulates growth and p

131 Lack of AR in GHRH cells (GHRH(DeltaAR) mice) induced no changes in bo

132 roups, but puberty completion was delayed in GHRH(DeltaERalpha) females.

133 e generated mice with deletion of ERalpha in GHRH cells (GHRH(DeltaERalpha)), which displayed reduced

134 Lack of ERalpha in GHRH neurons disrupts growth in both sexes and causes pu

135 Deletion of androgen receptor in GHRH neurons only delayed female puberty.

136 f/MEK/ERK pathways and from the reduction in GHRH produced by cancer cells.

137 e that direct actions of gonadal steroids in GHRH neurons modulate growth and puberty and indicate th

138 ponectin decreased GH-release, and inhibited GHRH-, but not ghrelin-stimulated GH-secretion.

139 46 and MZ-J-7-30, more effectively inhibited GHRH-induced GH release in vitro in a superfused rat pit

140 (siRNA)-mediated knockdown of Cdk4 inhibits GHRH-induced proliferation of GH3 somato/lactotroph cell

141 rats (STZ-rats) were treated with 15 mug/kg GHRH agonist, MR-409, or GHRH antagonist, MIA-602.

142 dioligand binding assays with (125)I-labeled GHRH antagonist JV-1-42 detected high affinity (K(d) = 0

143 igand competition assays with (125)I-labeled GHRH antagonist JV-1-42.

144 They lack mature GHRH, have low pituitary growth hormone (GH) and hepatic

145 pically the "little" mouse that has a mutant GHRH receptor.

146 th Kiss1(hrGFP) in prepubertal mice, ~30% of GHRH neurons coexpressed both reporter genes in adult fe

147 s induced by the direct inhibitory action of GHRH and of LHRH antagonists exerted through prostatic r

148 dy sheds light on the mechanism of action of GHRH antagonists in BPH and suggests that GHRH antagonis

149 umor activity and the mechanism of action of GHRH antagonists in human non-Hodgkin's lymphomas (NHL).

150 sponse is mediated entirely by activation of GHRH receptor (GHRHR), as demonstrated by the use of a h

151 Addition of GHRH-R agonists to porcine CSCs induced activation of ER

152 ave demonstrated that s.c. administration of GHRH antagonist (JV-1-36) inhibited growth of s.c. U-87M

153 Potent antagonistic analogues of GHRH have been synthesized that strongly suppress the gr

154 state cancer and suggest that antagonists of GHRH should be considered for further development as the

155 showed that potent synthetic antagonists of GHRH strongly inhibit the growth of diverse experimental

156 ental models of BPH, in which antagonists of GHRH suppressed the levels of proinflammatory cytokines

157 We synthesized a series of antagonists of GHRH(1-29)NH(2) acylated at the N terminus with monocarb

158 implications for therapeutic application of GHRH agonists to ischemic disorders.

159 Application of GHRH to the surface of the cortex changes electroencepha

160 previous results suggest that this class of GHRH antagonists might be effective in the treatment of

161 se in integrin alpha3) of the combination of GHRH agonist and DOX.

162 recombinant GH, MIA-602, or a combination of GHRH-A and MIA-602, for a 4-wk period.

163 The content of GHRH protein in PC-3 xenografts was lowered markedly, by

164 suggest a neurovascular protective effect of GHRH analogs during the early stage of diabetic retinopa

165 T pathways completely reversed the effect of GHRH-R agonists on CSC proliferation.

166 CSCs of different species and the effect of GHRH-R agonists on their cell proliferation and survival

167 he presence of GHRH-R in CSCs, the effect of GHRH-R agonists on their proliferation and survival, and

168 The receptor-dependent effects of GHRH also involved activation of Galphas and cAMP/PKA, a

169 nxiolytic and antidepressant-like effects of GHRH analogs that could involve modulatory effects on mo

170 l antinflammatory and antioxidant effects of GHRH antagonist MIA-690 and GHRH agonist MR-409, on isol

171 We investigated the effects of GHRH antagonist on prostatic enlargement induced by infl

172 s caused by the direct inhibitory effects of GHRH antagonists exerted through prostatic GHRH receptor

173 gs suggest that antiproliferative effects of GHRH antagonists in H460 NSCLC are associated with down-

174 er investigation to elucidate the effects of GHRH antagonists in prostatitis and BPH.

175 Expression of GHRH and splice variant 1 of the GHRH receptor in both c

176 lactotroph cells with restored expression of GHRH receptors.

177 The expression of GHRH, GHRH receptors, and their main splice variant, SV1

178 extend the observations of the expression of GHRH-R by CSCs and demonstrate that GHRH-R agonists have

179 We investigated the expression of GHRH-R in CSCs of different species and the effect of GH

180 The influence of GHRH antagonists on animal models of BPH has not been in

181 However, the influence of GHRH antagonists on the redox (reduction/oxidation) stat

182 ne fashion in prostate cancer, inhibition of GHRH-R represents a compelling approach to treatment.

183 The expression levels of GHRH and its receptor (GHRH-R) measured by qPCR and West

184 aP and VCaP cells expressed higher levels of GHRH-R protein compared with castration-resistant 22Rv1

185 GHRH mutation are additive, with lifespan of GHRH-KO mutants further increased by CR.

186 sted the myocardial therapeutic potential of GHRH stimulation in vitro and in vivo, using GHRH or its

187 esent study was to determine the presence of GHRH-R in CSCs, the effect of GHRH-R agonists on their p

188 uilding blocks involved in the regulation of GHRH release and its downstream sexual specific function

189 Our findings support the role of GHRH as an autocrine growth factor in prostate cancer an

190 ypothesis that antagonizing the signaling of GHRH in T1D may improve GLP-1 function in the small inte

191 In adult females, not males, a subset of GHRH neurons shift phenotype to start producing Kiss1.

192 ion could be mediated in part through SVs of GHRH receptors.

193 Recently, four splice variants (SVs) of GHRH-R have been described, of which SV1 has the highest

194 improved approach to the therapeutic use of GHRH agonists in the treatment of diabetes mellitus.

195 Use of GHRH may potentially be a beneficial treatment strategy

196 These results support the therapeutic use of GHRH-R agonists for stimulating endogenous mechanisms fo

197 ated by Western blot the effects in vitro of GHRH and its antagonist JMR-132 on proliferating cell nu

198 Twenty weeks of GHRH administration increased GABA levels in all 3 brain

199 After 20 weeks of GHRH administration, GABA levels were increased in all b

200 ce of a potential signaling pathway based on GHRH in the heart.

201 he GH axis, we examined its acute effects on GHRH neurons in brain slices from male and female GHRH-G

202 stimulatory responses to GHRH(1-29)NH(2) or GHRH agonist JI-38 and inhibitory responses to GHRH anta

203 ated with 15 mug/kg GHRH agonist, MR-409, or GHRH antagonist, MIA-602.

204 hat depend on insulin-like growth factors or GHRH.

205 Similar results were observed with other GHRH-R agonists, MR-356 and MR-409.

206 t also exerts separate actions on peripheral GHRH receptors, the functional role of which remains elu

207 s, mRNA, and protein expression of pituitary GHRH receptors and its splice variant (SV) 1 were found

208 ncreased binding affinities to rat pituitary GHRH receptors, but they showed weaker inhibition of GH

209 ding affinities of the peptides to pituitary GHRH receptors were also determined.

210 were randomly assigned to receive: placebo, GHRH-A (JI-38), rat recombinant GH, MIA-602, or a combin

211 enotypic profile of the response to a potent GHRH agonist has therapeutic implications.

212 I-38 (n = 8; 50 microg/kg per day), a potent GHRH agonist.

213 the latest series of improved, highly potent GHRH antagonists--MIA-602, MIA-606, and MIA-690--on the

214 In the present study, the most potent GHRH agonist MR403 was tested on insulinoma cells, isola

215 f GHRH antagonists exerted through prostatic GHRH receptors.

216 Participants were assigned to receive GHRH (1 mg subcutaneously twice daily) or placebo for 12

217 levels were diminished in animals receiving GHRH antagonists.

218 -releasing hormone (GHRH) and GHRH receptor (GHRH-R) are regulated in an autocrine fashion in prostat

219 f growth hormone-releasing hormone receptor (GHRH-R) in heart failure models are associated with an i

220 expression levels of GHRH and its receptor (GHRH-R) measured by qPCR and Western blotting were signi

221 gs, together with results from M(3) receptor/GHRH colocalization studies and hypothalamic hormone mea

222 f the ligand mifepristone (MFP) up-regulated GHRH expression, as shown by elevations of IGF-I levels,

223 emonstrated by the use of a highly selective GHRH antagonist (MIA-602).

224 e cellular level, SST irregularly suppressed GHRH neuron electrical activity, leading to slow oscilla

225 Here we evaluated recently synthesized GHRH agonists on the proliferation and biological functi

226 t model of streptozotocin (STZ)-induced T1D, GHRH receptor expression was found to be up-regulated in

227 In all these tests, GHRH antagonists exerted strong antioxidant activity.

228 tive site for islet transplantation and that GHRH analogs might allow reduction of the islet mass nee

229 findings confirm and extend the concept that GHRH and its receptors play an important role in the pat

230 We conclude that GHRH antagonists can lower prostate weight in experiment

231 We conclude that GHRH-KO mice feature perturbations in a network of signa

232 Our results demonstrate that GHRH antagonists inhibit androgen-independent prostate c

233 Our results demonstrate that GHRH antagonists might provide a therapy for breast canc

234 ssion of GHRH-R by CSCs and demonstrate that GHRH-R agonists have a direct effect on proliferation an

235 einforce previous experimental evidence that GHRH antagonists could be useful for cancer therapy.

236 This study provides evidence that GHRH plays important roles in prostatic inflammation and

237 are also consistent with the hypothesis that GHRH contributes to local network state regulation.

238 odulate growth and puberty and indicate that GHRH/Kiss1 dual-phenotype neurons play a sex-specific ro

239 This study indicates that GHRH antagonists and BN/GRP antagonist inhibit the growt

240 This finding indicates that GHRH antagonists could provide a potential treatment for

241 Preclinical studies revealed that GHRH and LHRH antagonists both can cause a reduction in

242 Various studies show that GHRH antagonists have antiproliferative effects in many

243 Our findings suggest that GHRH antagonists inhibit the growth of RL and HT lymphom

244 tor splice variants 1 and 2, suggesting that GHRH could be an autocrine growth factor.

245 ate, lung, and other tumors, suggesting that GHRH is also a tumor growth factor.

246 of GHRH antagonists in BPH and suggests that GHRH antagonists should be considered for further develo

247 The GHRH agonist also reduced the release of humoral regulat

248 effects of caloric restriction (CR) and the GHRH mutation are additive, with lifespan of GHRH-KO mut

249 f the mRNA for the pGHRH-R, its SVs, and the GHRH peptide.

250 GHRH and the GHRH receptor (GHRHR) mRNAs are detectable in the rat co

251 ted from an initial inhibitory action at the GHRH neuron level via K(+) channel activation, followed

252 neous fat improved significantly more in the GHRH group (-0.19 [0.28] vs 0.07 [0.27], P =.02).

253 ean body mass significantly increased in the GHRH group vs the placebo group (0.9 [1.3] kg vs -0.3 [1

254 oncentrations increased significantly in the GHRH group vs the placebo group (104 [110] ng/mL vs 6 [4

255 erefore, we have evaluated the effect of the GHRH agonist JI-34 on PLY-induced barrier and ALC dysfun

256 in vivo, showing that the combination of the GHRH agonist, JI-34, and DOX inhibited the growth of GBM

257 The unilateral application of the GHRH antagonist ipsilaterally decreased EEG delta wave p

258 demonstrates the preclinical efficacy of the GHRH antagonist MIA-602 for treatment of both androgen-d

259 We evaluated the effects of the GHRH antagonist, JMR-132, on PC-3 human androgen-indepen

260 We evaluated the effects of the GHRH antagonists JMR-132 given at doses of 40 mug/d, MIA

261 We assessed the effects of the GHRH antagonists MIA-602 and MIA-690 in vitro in MPM cel

262 red sufficient in pacing the activity of the GHRH neuronal population.

263 pression of GHRH and splice variant 1 of the GHRH receptor in both cell lines was examined by RT-PCR.

264 ponds to the estimated molecular mass of the GHRH receptor isoform encoded by SV1.

265 ells through the splice variants (SV) of the GHRH receptor.

266 nd mRNA for GHRH and splice variant-1 of the GHRH receptors were found on RL and HT tumors.

267 ndings point toward a protective role of the GHRH signaling pathway in PLY-induced permeability edema

268 y, our findings reveal the importance of the GHRH signaling pathway within the heart.

269 Approximately 18% of the GHRH-responsive cells were GABAergic as illustrated by g

270 ormation in GSNOR(-/-) MSCs by L-NAME or the GHRH agonists JI-38, MR-409, and MR-356.

271 In vitro, SXN101742 targeted the GHRH receptor and depleted a SNARE protein involved in G

272 These findings indicate that the GHRH agonists can potentiate the anticancer activity of

273 The reverse, using the GHRH antagonist, MIA-602, resulted in worsening of retin

274 Treatment of STZ-rats with the GHRH agonist, MR-409, prevented retinal morphological al

275 Treatment of porcine CSCs with the GHRH-R agonist JI-38 significantly increased the rate of

276 nM, indicating a high affinity of JMR-132 to GHRH receptors.

277 Exposure of INS-1 cells to GHRH agonists, MR-356 and MR-409, induced activation of

278 hnique, cultured cortical cells responded to GHRH by increasing intracellular calcium.

279 nal body composition improved in response to GHRH, with increased lean mass and reduced truncal and v

280 t overall change in GH levels in response to GHRH.

281 RH agonist JI-38 and inhibitory responses to GHRH antagonist JV-1-38 as compared with pcDNA3 controls

282 of SV1 augments the stimulatory responses to GHRH(1-29)NH(2) or GHRH agonist JI-38 and inhibitory res

283 ls expressing SV1 are much more sensitive to GHRH analogs than the pcDNA3 controls.

284 e antiserum developed recognizes the tumoral GHRH receptor protein encoded by SV1, it should be of va

285 ene and protein expression of pituitary-type GHRH-receptor in prefrontal cortex of mice after 4 weeks

286 GHRH stimulation in vitro and in vivo, using GHRH or its agonistic analog MR-409.

287 We show that in vitro, GHRH(1-44)NH2 attenuates phenylephrine-induced hypertrop

288 However, it is still not known whether GHRH would be beneficial for life-threatening pathologic

289 two reporter genes, we observed that, while GHRH(tdTom) neurons minimally colocalize with Kiss1(hrGF

290 In vitro treatment of INS-1 cells with GHRH agonists increased cell proliferation, the expressi

291 mone-releasing hormone receptor (GHRHR) with GHRH agonists augmented VEGF-A production and normalized

292 Daily treatment for 1 mo with GHRH antagonist MIA-690 caused a 30% reduction in prosta

293 splanted with rat islets preconditioned with GHRH agonist, MR-409, and received additional treatment

294 further revealed that the pretreatment with GHRH agonist evoked differentiation decreasing the expre

295 Thus, the therapy with GHRH antagonist could be considered for the management o

296 Therapy with GHRH antagonists also significantly reduced tumoral bFGF

297 Therapy with GHRH-A although initiated 1 mo after MI substantially im

298 fts of RL and HT human NHL were treated with GHRH antagonists MZ-5-156 and MZ-J-7-138 at a dose of 40

299 The group treated with GHRH-expressing plasmid at 14 days of age demonstrated g

300 stigated the effectiveness of treatment with GHRH antagonist JMR-132 alone and in combination with do

301 l, these results suggest that treatment with GHRH antagonists, alone or in association with chemother

302 ts was observed after 6 wk of treatment with GHRH antagonists: a 17.8% decrease with JMR-132 treatmen