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Endogenous α-calcitonin-gene-related peptide promotes exercise-induced, physiological heart hypertrophy in mice

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dc.contributor.author Schuler, B.
dc.contributor.author Rieger, G.
dc.contributor.author Gubser, M.
dc.contributor.author Arras, M.
dc.contributor.author Gianella, M.
dc.contributor.author Vogel, O.
dc.contributor.author Jirkof, P.
dc.contributor.author Cesarovic, N.
dc.contributor.author Klohs, J.
dc.contributor.author Jakob, P.
dc.contributor.author Brock, M.
dc.contributor.author Gorr, T.A.
dc.contributor.author Baum, O.
dc.contributor.author Hoppeler, H.
dc.contributor.author Samillan-Soto, V.
dc.contributor.author Gassmann, M.
dc.contributor.author Fischer, J.A.
dc.contributor.author Born, W.
dc.contributor.author Vogel, J.
dc.date.accessioned 2020-06-10T18:11:36Z
dc.date.available 2020-06-10T18:11:36Z
dc.date.issued 2014
dc.identifier.uri https://hdl.handle.net/20.500.12866/8022
dc.description.abstract Aim: It is unknown how the heart distinguishes various overloads, such as exercise or hypertension, causing either physiological or pathological hypertrophy. We hypothesize that alpha-calcitonin-gene-related peptide (αCGRP), known to be released from contracting skeletal muscles, is key at this remodelling. Methods: The hypertrophic effect of αCGRP was measured in vitro (cultured cardiac myocytes) and in vivo (magnetic resonance imaging) in mice. Exercise performance was assessed by determination of maximum oxygen consumption and time to exhaustion. Cardiac phenotype was defined by transcriptional analysis, cardiac histology and morphometry. Finally, we measured spontaneous activity, body fat content, blood volume, haemoglobin mass and skeletal muscle capillarization and fibre composition. Results: While αCGRP exposure yielded larger cultured cardiac myocytes, exercise-induced heart hypertrophy was completely abrogated by treatment with the peptide antagonist CGRP(8-37). Exercise performance was attenuated in αCGRP-/- mice or CGRP(8-37) treated wild-type mice but improved in animals with higher density of cardiac CGRP receptors (CLR-tg). Spontaneous activity, body fat content, blood volume, haemoglobin mass, muscle capillarization and fibre composition were unaffected, whereas heart index and ventricular myocyte volume were reduced in αCGRP-/- mice and elevated in CLR-tg. Transcriptional changes seen in αCGRP-/- (but not CLR-tg) hearts resembled maladaptive cardiac phenotype. Conclusions: Alpha-calcitonin-gene-related peptide released by skeletal muscles during exercise is a hitherto unrecognized effector directing the strained heart into physiological instead of pathological adaptation. Thus, αCGRP agonists might be beneficial in heart failure patients. en_US
dc.language.iso eng
dc.publisher Wiley
dc.relation.ispartof urn:issn:1748-1716
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject hemoglobin en_US
dc.subject Animals en_US
dc.subject histology en_US
dc.subject adult en_US
dc.subject male en_US
dc.subject priority journal en_US
dc.subject Mice en_US
dc.subject controlled study en_US
dc.subject oxygen consumption en_US
dc.subject article en_US
dc.subject phenotype en_US
dc.subject genetics en_US
dc.subject metabolism en_US
dc.subject animal experiment en_US
dc.subject animal model en_US
dc.subject animal tissue en_US
dc.subject nonhuman en_US
dc.subject animal en_US
dc.subject mouse en_US
dc.subject Mice, Knockout en_US
dc.subject Motor Activity en_US
dc.subject exercise en_US
dc.subject drug effects en_US
dc.subject physiology en_US
dc.subject animal cell en_US
dc.subject protein expression en_US
dc.subject nuclear magnetic resonance imaging en_US
dc.subject in vitro study en_US
dc.subject mean arterial pressure en_US
dc.subject skeletal muscle en_US
dc.subject in vivo study en_US
dc.subject knockout mouse en_US
dc.subject morphometrics en_US
dc.subject motor activity en_US
dc.subject exhaustion en_US
dc.subject exercise test en_US
dc.subject endurance training en_US
dc.subject Oxygen Consumption en_US
dc.subject collagen type 1 en_US
dc.subject body fat en_US
dc.subject alpha calcitonin gene related peptide en_US
dc.subject Athlete's heart en_US
dc.subject basal metabolic rate en_US
dc.subject blood volume en_US
dc.subject calcitonin gene related peptide en_US
dc.subject Calcitonin Gene-Related Peptide en_US
dc.subject Cardiomegaly, Exercise-Induced en_US
dc.subject collagen type 3 en_US
dc.subject Doping en_US
dc.subject Endurance capacity en_US
dc.subject exercise induced cardiomegaly en_US
dc.subject exercise induced heart hypertrophy en_US
dc.subject Exercise performance en_US
dc.subject heart hypertrophy en_US
dc.subject heart index en_US
dc.subject heart muscle cell en_US
dc.subject heart ventricle hypertrophy en_US
dc.subject muscle cell en_US
dc.subject Muscle metaboreflex en_US
dc.subject Myocytes, Cardiac en_US
dc.subject Physical Conditioning, Animal en_US
dc.subject Sport en_US
dc.title Endogenous α-calcitonin-gene-related peptide promotes exercise-induced, physiological heart hypertrophy in mice en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1111/apha.12244
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.02.00 es_PE
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#3.01.08


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