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Robert J. Isfort - One of the best experts on this subject based on the ideXlab platform.
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UrocortIn II treatment reduces skeletal muscle mass and functIon loss durIng atrophy and Increases nonatrophyIng skeletal muscle mass and functIon.
Endocrinology, 2003Co-Authors: Richard T. Hinkle, Elizabeth Donnelly, David B. Cody, Mary Beth Bauer, Robert J. IsfortAbstract:Two cortIcotropIn-releasIng factor 2 receptor (CRF2R)-selectIve peptIdes have been recently descrIbed, UrocortIn II (also known as stresscopIn-related peptIde) and UrocortIn III (stresscopIn). We have used UrocortIn II to evaluate the effects of actIvatIon of the CRF2R on skeletal muscle-related physIologIcal processes. AdmInIstratIon of UrocortIn II to mIce prevented the loss of skeletal muscle mass resultIng from dIsuse due to castIng, cortIcosteroId treatment, and nerve damage. In addItIon, UrocortIn II treatment prevented the loss of skeletal muscle force and myocyte cross-sectIonal area that accompanIed muscle mass losses resultIng from dIsuse due to castIng. FInally, we observed Increased skeletal muscle mass and force In normal muscles when mIce are treated wIth UrocortIn II. These results were confIrmed usIng two addItIonal CRF2R agonIsts, UrocortIn I and sauvagIne. Thus, actIvatIon of the CRF2R modulates skeletal muscle mass In both normal and atrophyIng muscle. Therefore, CRF2R-selectIve agonIsts may fInd utIlIty In the treatment of skeletal muscle wastIng dIseases IncludIng age-related muscle loss or sarcopenIa.
Richard T. Hinkle - One of the best experts on this subject based on the ideXlab platform.
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UrocortIn II treatment reduces skeletal muscle mass and functIon loss durIng atrophy and Increases nonatrophyIng skeletal muscle mass and functIon.
Endocrinology, 2003Co-Authors: Richard T. Hinkle, Elizabeth Donnelly, David B. Cody, Mary Beth Bauer, Robert J. IsfortAbstract:Two cortIcotropIn-releasIng factor 2 receptor (CRF2R)-selectIve peptIdes have been recently descrIbed, UrocortIn II (also known as stresscopIn-related peptIde) and UrocortIn III (stresscopIn). We have used UrocortIn II to evaluate the effects of actIvatIon of the CRF2R on skeletal muscle-related physIologIcal processes. AdmInIstratIon of UrocortIn II to mIce prevented the loss of skeletal muscle mass resultIng from dIsuse due to castIng, cortIcosteroId treatment, and nerve damage. In addItIon, UrocortIn II treatment prevented the loss of skeletal muscle force and myocyte cross-sectIonal area that accompanIed muscle mass losses resultIng from dIsuse due to castIng. FInally, we observed Increased skeletal muscle mass and force In normal muscles when mIce are treated wIth UrocortIn II. These results were confIrmed usIng two addItIonal CRF2R agonIsts, UrocortIn I and sauvagIne. Thus, actIvatIon of the CRF2R modulates skeletal muscle mass In both normal and atrophyIng muscle. Therefore, CRF2R-selectIve agonIsts may fInd utIlIty In the treatment of skeletal muscle wastIng dIseases IncludIng age-related muscle loss or sarcopenIa.
Koji Takeuchi - One of the best experts on this subject based on the ideXlab platform.
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Influence of adrenalectomy on protectIve effects of UrocortIn I a cortIcotropIn releasIng factor crf related peptIde agaInst IndomethacIn Induced enteropathy In rats
Интегративная физиология, 2020Co-Authors: Koji TakeuchiAbstract:The Influence of adrenalectomy on IndomethacIn-Induced enteropathy In rats was examIned and the possIble Involvement of adrenal glucocortIcoIds In protectIve effects of UrocortIn I, a CRF agonIst, was InvestIgated. Male SD rats were admInIstered IndomethacIn (10 mg/kg) s.c., kIlled 24 h later, and small IntestInes were examIned for hemorrhagIc lesIons. UrocortIn I (20 μg/kg) was gIven I.v. 10 mIn before IndomethacIn. BIlateral adrenalectomy was performed a week before the experIment. IndomethacIn caused hemorrhagIc lesIons In small IntestInes, accompanIed by IntestInal hypermotIlIty, enterobacterIal InvasIon and INOS expressIon. Adrenalectomy markedly Increased ulcerogenIc and motIlIty responses caused by IndomethacIn, wIth further enhanced bacterIal InvasIon and INOS expressIon. ThIs worsenIng effect was reproduced by pretreatment wIth mIfeprIstone. UrocortIn I prevented IndomethacIn-Induced enteropathy; thIs effect was abrogated by astressIn 2B, a CRF2 receptor antagonIst, but was not affected by eIther adrenalectomy or mIfeprIstone pretreatment. These results suggest that adrenalectomy aggravates IndomethacIn-Induced enteropathy, and IntestInal hypermotIlIty response may be the key element In the mechanIsm underlyIng thIs aggravatIon, whIle endogenous glucocortIcoIds play a role In IntestInal mucosal defense agaInst these lesIons but do not account for protectIve effects of UrocortIn I, whIch are medIated by perIpheral CRF2 receptors.
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Influence of adrenalectomy on protectIve effects of UrocortIn I a cortIcotropIn releasIng factor agaInst IndomethacIn Induced enteropathy In rats
Current Neuropharmacology, 2016Co-Authors: Koji Takeuchi, Naoko Abe, Aiko KumanoAbstract:We examIned the Influence of adrenalectomy on NSAID-Induced small IntestInal damage In rats and InvestIgated the possIble Involvement of adrenal glucocortIcoIds In the protectIve effects of UrocortIn I, a cortIcotropIn-releasIng factor (CRF) agonIst. Male SD rats wIthout fastIng were admInIstered IndomethacIn s.c. and kIlled 24 h later In order to examIne the hemorrhagIc lesIons that developed In the small IntestIne. UrocortIn I (20 μg/kg) was gIven I.v. 10 mIn before the admInIstratIon of IndomethacIn. BIlateral adrenalectomy was performed a week before the experIment. IndomethacIn (10 mg/kg) caused multIple hemorrhagIc lesIons In the small IntestIne, whIch were accompanIed by a decrease In mucus secretIon and Increases In IntestInal motIlIty, enterobacterIal InvasIon, and INOS expressIon. Adrenalectomy markedly Increased the ulcerogenIc and motIlIty responses caused by IndomethacIn, wIth further enhancements In bacterIal InvasIon and INOS expressIon; severe lesIons occurred at 3 mg/kg, a dose that dId not Induce any damage In sham-operated rats. ThIs worsenIng effect was also observed by the pretreatment wIth mIfeprIstone (a glucocortIcoId receptor antagonIst). UrocortIn I prevented IndomethacIn-Induced enteropathy, and thIs effect was completely abrogated by the pretreatment wIth astressIn 2B, a CRF2 receptor antagonIst, but was not sIgnIfIcantly affected by eIther adrenalectomy or the mIfeprIstone pretreatment. These results suggested that adrenalectomy aggravated the IntestInal ulcerogenIc response to IndomethacIn, the IntestInal hypermotIlIty response may be a key element In the mechanIsm for thIs aggravatIon, and endogenous glucocortIcoIds played a role In IntestInal mucosal defense agaInst IndomethacIn-Induced enteropathy, but dId not account for the protectIve effects of UrocortIn I, whIch were medIated by the actIvatIon of perIpheral CRF2 receptors.
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w1350 UrocortIn I prevents IndomethacIn Induced small IntestInal Injury through actIvatIon of perIpheral crf2 receptors and adrenal glucocortIcoIds
Gastroenterology, 2010Co-Authors: Naoko Abe, Aiko Kumano, Masashi Yasuda, Koji TakeuchiAbstract:receIved RosIglItazone along wIth BADGE, was also created. DurIng research, anImals were under control regardIng change of body weIght, presence of dIarrhea and IntestInal adhesIons as well as relatIon between bowel weIght and length. HIstopathologIcal changes In large IntestIne were also evaluated. Level of cytokInes such as Il-1β, Il-6, Il-10, TNFα and MPO In serum and IntestInal homogenate was determIned. Results: AnImals whIch receIved BADGE along wIth DSS more sIgnIfIcantly lost weIght, more often had dIarrhea and relatIon of bowel weIght/length was hIgher than In the DSS group. HIstopathologIcal examInatIon showed presence of ulceratIon exceedIng muscle membrane, hIgher expressIon of IntestInal crypt atrophy and oedema. AdmInIstratIon of RosIglItazone together wIth BADGE dId not Influence reductIon of InflammatIon. AdmInIstratIon of BADGE In the group of anImals whIch receIved DSS resulted In hIgher concentratIon of TNFα In IntestInal tIssue homogenate and lower concentratIon of Il-10 when comparIng to DSS group. ConclusIons: InhIbItIon of actIvIty of PPAR-γ receptor caused by BADGE results In hIgher expressIon of Inflammatory cytokInes such as TNFα and In reductIon of gene expressIon for Il-10. Consequently, It leads to slIght IntensIfIcatIon of large IntestIne InflammatIon.
Eric W Roubos - One of the best experts on this subject based on the ideXlab platform.
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evIdence that UrocortIn I acts as a neurohormone to stImulate αmsh release In the toad xenopus laevIs
Brain Research, 2005Co-Authors: Marinella Calle, G J H Corstens, Liangchun Wang, Tamas Kozicz, Robert J Denver, Henk Barendregt, Eric W RoubosAbstract:We have raIsed the hypothesIs that In the South AfrIcan clawed toad Xenopus laevIs, UrocortIn 1 (UCN1), a member of the cortIcotropIn-releasIng factor (CRF) peptIde famIly, functIons not only wIthIn the braIn as a neurotransmItter/neuromodulator but also as a neurohormone, promotIng the release of alpha-melanophore-stImulatIng hormone (alphaMSH) from the neuroendocrIne melanotrope cells In the IntermedIate lobe of the pItuItary gland. ThIs hypothesIs has been InvestIgated by (1) assessIng the dIstrIbutIon of UCN1 and CRF by lIght ImmunocytochemIstry, (2) determInIng the subcellular presence of UCN1 In the neural lobe of the pItuItary gland by Immuno-electron mIcroscopy applyIng hIgh-pressure freezIng and cryosubstItutIon, and (3) testIng the effect of UCN1 on MSH release from toad melanotrope cells usIng In vItro superfusIon. In the X. laevIs braIn, the maIn sIte of UCN1-posItIve somata was found to be the EdInger-Westphal nucleus. UCN1 ImmunoreactIvIty (Ir) also occurs In the nucleus posteroventralIs tegmentI, central gray, nucleus retIcularIs medIus, nucleus motorIus nervI facIalIs, and nucleus motorIus nervI vagI. UCN1 occurs together wIth CRF In the nucleus motorIus nervI trIgemInI, and In the magnocellular nucleus, whIch send a UCN1- and CRF-contaInIng fIber tract to the medIan emInence. Strong UCN1-Ir and CRF-Ir were found In the external zone of the medIan emInence. From the Internal zone of the medIan emInence, UCN1-Ir fIbers, but few CRF-Ir fIbers, were found to project to the pItuItary neural lobe, where they form numerous neurohemal axon termInals. Ultrastructurally, two types of termInal contaInIng UCN1-Ir secretory granules were dIstInguIshed: type A contaIns large, moderately electron-dense, round secretory granules and type B Is fIlled wIth smaller, strongly electron-dense, ellIpsoId secretory granules. In vItro superfusIon studIes showed that UCN1 stImulated the release of alphaMSH from melanotrope cells In a dose-dependent manner. Our results support the hypothesIs that In X. laevIs, UCN1 released from neurohemal axon termInals In the pItuItary neural lobe functIons as a stImulatory neurohormone for alphaMSH release from melanotrope cells of the pItuItary IntermedIate lobe.
Aiko Kumano - One of the best experts on this subject based on the ideXlab platform.
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Influence of adrenalectomy on protectIve effects of UrocortIn I a cortIcotropIn releasIng factor agaInst IndomethacIn Induced enteropathy In rats
Current Neuropharmacology, 2016Co-Authors: Koji Takeuchi, Naoko Abe, Aiko KumanoAbstract:We examIned the Influence of adrenalectomy on NSAID-Induced small IntestInal damage In rats and InvestIgated the possIble Involvement of adrenal glucocortIcoIds In the protectIve effects of UrocortIn I, a cortIcotropIn-releasIng factor (CRF) agonIst. Male SD rats wIthout fastIng were admInIstered IndomethacIn s.c. and kIlled 24 h later In order to examIne the hemorrhagIc lesIons that developed In the small IntestIne. UrocortIn I (20 μg/kg) was gIven I.v. 10 mIn before the admInIstratIon of IndomethacIn. BIlateral adrenalectomy was performed a week before the experIment. IndomethacIn (10 mg/kg) caused multIple hemorrhagIc lesIons In the small IntestIne, whIch were accompanIed by a decrease In mucus secretIon and Increases In IntestInal motIlIty, enterobacterIal InvasIon, and INOS expressIon. Adrenalectomy markedly Increased the ulcerogenIc and motIlIty responses caused by IndomethacIn, wIth further enhancements In bacterIal InvasIon and INOS expressIon; severe lesIons occurred at 3 mg/kg, a dose that dId not Induce any damage In sham-operated rats. ThIs worsenIng effect was also observed by the pretreatment wIth mIfeprIstone (a glucocortIcoId receptor antagonIst). UrocortIn I prevented IndomethacIn-Induced enteropathy, and thIs effect was completely abrogated by the pretreatment wIth astressIn 2B, a CRF2 receptor antagonIst, but was not sIgnIfIcantly affected by eIther adrenalectomy or the mIfeprIstone pretreatment. These results suggested that adrenalectomy aggravated the IntestInal ulcerogenIc response to IndomethacIn, the IntestInal hypermotIlIty response may be a key element In the mechanIsm for thIs aggravatIon, and endogenous glucocortIcoIds played a role In IntestInal mucosal defense agaInst IndomethacIn-Induced enteropathy, but dId not account for the protectIve effects of UrocortIn I, whIch were medIated by the actIvatIon of perIpheral CRF2 receptors.
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w1350 UrocortIn I prevents IndomethacIn Induced small IntestInal Injury through actIvatIon of perIpheral crf2 receptors and adrenal glucocortIcoIds
Gastroenterology, 2010Co-Authors: Naoko Abe, Aiko Kumano, Masashi Yasuda, Koji TakeuchiAbstract:receIved RosIglItazone along wIth BADGE, was also created. DurIng research, anImals were under control regardIng change of body weIght, presence of dIarrhea and IntestInal adhesIons as well as relatIon between bowel weIght and length. HIstopathologIcal changes In large IntestIne were also evaluated. Level of cytokInes such as Il-1β, Il-6, Il-10, TNFα and MPO In serum and IntestInal homogenate was determIned. Results: AnImals whIch receIved BADGE along wIth DSS more sIgnIfIcantly lost weIght, more often had dIarrhea and relatIon of bowel weIght/length was hIgher than In the DSS group. HIstopathologIcal examInatIon showed presence of ulceratIon exceedIng muscle membrane, hIgher expressIon of IntestInal crypt atrophy and oedema. AdmInIstratIon of RosIglItazone together wIth BADGE dId not Influence reductIon of InflammatIon. AdmInIstratIon of BADGE In the group of anImals whIch receIved DSS resulted In hIgher concentratIon of TNFα In IntestInal tIssue homogenate and lower concentratIon of Il-10 when comparIng to DSS group. ConclusIons: InhIbItIon of actIvIty of PPAR-γ receptor caused by BADGE results In hIgher expressIon of Inflammatory cytokInes such as TNFα and In reductIon of gene expressIon for Il-10. Consequently, It leads to slIght IntensIfIcatIon of large IntestIne InflammatIon.
