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-A markedly improved cardiac function as shown by ec

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

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

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

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

21 SV(2) may encode a GHRH-R isoform truncated after the second transmembrane

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

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

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

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

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

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

34 tuitary cells and various tumors to GHRH and GHRH antagonists.

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

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

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

38 lowed by an increase in cAMP production, and GHRH antagonist JV-1-38 competitively inhibited this eff

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

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

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

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

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

44 These receptors bind GHRH antagonists preferentially and display a lower affi

45 mRNA for both GHRH and SV(1) isoform of GHRH receptors was expressed i

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

47 The stimulation of SV1-expressing cells by GHRH or JI-38 is followed by an increase in cAMP product

48 some gastroenteropancreatic cancer cells by GHRH was followed by an increase in cAMP production, and

49 nonmyocyte mitosis was markedly increased by GHRH-A.

50 imulated by GHRH(1-29)NH(2) and inhibited by GHRH antagonist JV-1-38.

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

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

53 , and gastric cancer cells was stimulated by GHRH(1-29)NH(2) and inhibited by GHRH antagonist JV-1-38

54 ration of SV1-expressing cells stimulated by GHRH.

55 In conclusion, GHRH antagonists in combination with docetaxel synergist

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

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

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

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

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

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

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

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

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

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

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

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

68 study we examined the expression of mRNA for GHRH and for SVs of its receptors in tumors of human pan

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

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

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

72 ct effects mediated by tumoral receptors for GHRH.

73 s splice variants (SVs) of the receptors for GHRH.

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

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

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

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

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

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

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

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

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

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

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

85 effects of growth hormone-releasing hormone (GHRH) and the antiproliferative action of GHRH antagonis

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

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

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

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

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

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

92 2, contains a modified GH-releasing hormone (GHRH) domain and the endopeptidase domain of botulinum t

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

94 inducible growth hormone releasing hormone (GHRH) gene, into the tibialis anterior muscles of adult

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 gonists of growth hormone-releasing hormone (GHRH) inhibit the proliferation of various human cancers

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

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

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

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

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 pothalamic growth hormone-releasing hormone (GHRH), pituitary proopiomelanocortin to adrenocorticotro

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

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

123 herapeutic growth hormone releasing hormone (GHRH).

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

125 ajor splice variants (SVs) of mRNA for human GHRH receptor (GHRH-R) in human cancer cell lines, inclu

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

127 tumors and that differ from pituitary human GHRH (hGHRH) receptors.

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

129 ired for the proper function of hypothalamic GHRH neurons.

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

131 ssues contain SV1 protein and immunoreactive GHRH.

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

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

134 46 and MZ-J-7-30, more effectively inhibited GHRH-induced GH release in vitro in a superfused rat pit

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

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

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

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

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

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

141 stimulatory loop based on GHRH and SV(1) of GHRH receptors in human pancreatic, colorectal, and gast

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

143 e (GHRH) and the antiproliferative action of GHRH antagonists have been demonstrated in various cance

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 lactotroph cells with restored expression of GHRH receptors.

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

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

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

174 based gene therapy, and chronic induction of GHRH expression in adult animals led to improvements in

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

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

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

178 mRNA for both GHRH and SV(1) isoform of GHRH receptors was expressed in tumors of pancreatic (SW

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

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

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

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

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

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

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

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

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

188 Thus SVs of GHRH-Rs have now been identified in human extrapituitary

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

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

191 Use of GHRH may potentially be a beneficial treatment strategy

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

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

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

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

196 utocrine/paracrine stimulatory loop based on GHRH and SV(1) of GHRH receptors in human pancreatic, co

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

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

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

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

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

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

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

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

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

206 its the greatest similarity to the pituitary GHRH receptor and is most likely to be functional.

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

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

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

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

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

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

213 f GHRH antagonists exerted through prostatic GHRH receptors.

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

215 levels were diminished in animals receiving GHRH antagonists.

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

217 iants (SVs) of mRNA for human GHRH receptor (GHRH-R) in human cancer cell lines, including LNCaP pros

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

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

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

221 In summary, long-term drug-regulated GHRH expression was achieved following plasmid-based gen

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 on the blockade of this receptor by specific GHRH antagonists.

225 on the blockade of this receptor by specific GHRH antagonists.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 The GHRH agonist also reduced the release of humoral regulat

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

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

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

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

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

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

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

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

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

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

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

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

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

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 of nonpituitary cells and various tumors to GHRH and GHRH antagonists.

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

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

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

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

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

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

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

295 Therapy with GHRH antagonists also significantly reduced tumoral bFGF

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

297 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

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

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

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