Academic Journal

Role of ERK1/2 activation in microtubule stabilization and glucose transport in cardiomyocytes

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Role of ERK1/2 activation in microtubule stabilization and glucose transport in cardiomyocytes
Συγγραφείς: Mohamed Asrih, Irène Papageorgiou, René Lerch, Corinne Pellieux, Christophe Albert Montessuit
Πηγή: American Journal of Physiology. Endocrinology and Metabolism, Vol. 301, No 5 (2011) pp. E836-43
American journal of physiology. Endocrinology and metabolism
Στοιχεία εκδότη: American Physiological Society, 2011.
Έτος έκδοσης: 2011
Θεματικοί όροι: Male, 0301 basic medicine, Insulin/pharmacology, MAP Kinase Signaling System, Primary Cell Culture, Tretinoin, Microtubules, Rats, Sprague-Dawley, 03 medical and health sciences, Stress, Physiological/physiology, Stress, Physiological, Protein Stability/drug effects, Glucose/metabolism, Animals, Insulin, Myocytes, Cardiac, Enzyme Activation/drug effects/physiology, Alitretinoin, Cells, Cultured, ddc:616, 0303 health sciences, Mitogen-Activated Protein Kinase 3, Tretinoin/pharmacology, Microtubules/drug effects/metabolism, Protein Stability, Biological Transport, Mitogen-Activated Protein Kinase 3/metabolism, Protein Multimerization/drug effects, Rats, Myocytes, Cardiac/drug effects/metabolism/physiology, Enzyme Activation, Biological Transport/drug effects/physiology, Glucose, MAP Kinase Signaling System/drug effects/physiology, Protein Multimerization
Περιγραφή: We previously demonstrated that microtubule disruption impairs stimulation of glucose uptake in cardiomyocytes and that 9-cis retinoic acid (9cRA) treatment preserved both microtubule integrity and stimulated glucose transport. Herein we investigated whether 1) activation of the extracellular signal-regulated kinases (ERK1/2) is responsible for microtubule destabilization and 2) ERK1/2 inactivation may explain the positive effects of 9cRA on glucose uptake and microtubule stabilization. Adult rat cardiomyocytes in primary culture showed increased basal ERK1/2 phosphorylation. Cardiomyocytes exposed to inhibitors of the ERK1/2 kinase mitogen/extracellular signal-regulated kinase (MEK) 1/2 had preserved microtubular scaffold, including microtubule-organizing centers (MTOC), together with increased insulin and metabolic stress-stimulated glucose transport as well as signaling, thus replicating the effects of 9cRA treatment. Although 9cRA treatment did not significantly reduce global ERK1/2 activation, it markedly reduced perinuclear-activated ERK1/2 at the location of MTOC. 9cRA also triggered relocation of the ERK1/2 phosphatase mitogen-activated protein kinase phosphatase-3 from the cytosol to the nucleus. These results indicate that, in cardiomyocytes, microtubule destabilization, leading to impaired stimulation of glucose transport, is mediated by ERK1/2 activation, impacting on the MTOC. 9cRA acid restores stimulated glucose transport indirectly through compartmentalized inactivation of ERK1/2.
Τύπος εγγράφου: Article
Περιγραφή αρχείου: application/pdf
Γλώσσα: English
ISSN: 1522-1555
0193-1849
DOI: 10.1152/ajpendo.00160.2011
Σύνδεσμος πρόσβασης: https://pubmed.ncbi.nlm.nih.gov/21771966
https://journals.physiology.org/doi/full/10.1152/ajpendo.00160.2011
https://www.physiology.org/doi/10.1152/ajpendo.00160.2011
https://core.ac.uk/display/60997633
https://ajpendo.physiology.org/content/ajpendo/301/5/E836.full.pdf
https://archive-ouverte.unige.ch/unige:88465
https://www.physiology.org/doi/pdf/10.1152/ajpendo.00160.2011
https://archive-ouverte.unige.ch/unige:88465
Αριθμός Καταχώρησης: edsair.doi.dedup.....f0f4ffcc3443c0d1cdb59659732d946b
Βάση Δεδομένων: OpenAIRE
Περιγραφή
ISSN:15221555
01931849
DOI:10.1152/ajpendo.00160.2011