In brown adipocytes, adrenergically induced beta(1)-/beta(3)-(G(s))-, alpha(2)-(G(i))- and alpha(1)-(G(q))-signalling to Erk1/2 activation is not mediated via EGF receptor transactivation

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Wang, YanlingStockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut (author)

In brown adipocytes, adrenergically induced beta(1)-/beta(3)-(G(s))-, alpha(2)-(G(i))- and alpha(1)-(G(q))-signalling to Erk1/2 activation is not mediated via EGF receptor transactivation

Article/chapterEnglish2013

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Elsevier BV,2013
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LIBRIS-ID:oai:DiVA.org:su-96647
https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-96647URI
https://doi.org/10.1016/j.yexcr.2013.08.007DOI

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Language:English
Summary in:English

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Brown adipose tissue is unusual in that the neurotransmitter norepinephrine influences cell destiny in ways generally associated with effects of classical growth factors: regulation of cell proliferation, of apoptosis, and progression of differentiation. The norepinephrine effects are mediated through G-protein-coupled receptors; further mediation of such stimulation to e.g. Erk1/2 activation is in cell biology in general accepted to occur through transactivation of the EGF receptor (by external or internal pathways). We have examined here the significance of such transactivation in brown adipocytes. Stimulation of mature brown adipocytes with cirazoline (alpha(1)-adrenoceptor coupled via G(q)), clonidine (alpha(2) via G(i)) or CL316243 (beta(3) via G(s)) or via beta(1)-receptors significantly activated Erk1/2. Pretreatment with the EGF receptor kinase inhibitor AG1478 had, remarkably, no significant effect on Erk1/2 activation induced by any of these adrenergic agonists (although it fully abolished EGF-induced Erk1/2 activation), demonstrating absence of EGF receptor-mediated transactivation. Results with brown preadipocytes (cells in more proliferative states) were not qualitatively different. Joint stimulation of all adrenoceptors with norepinephrine did not result in synergism on Erk1/2 activation. AG1478 action on EGF-stimulated Erk1/2 phosphorylation showed a sharp concentration response relationship (IC50 0.3 mu M); a minor apparent effect of AG1478 on norepinephrine-stimulated Erk1/2 phosphorylation showed nonspecific kinetics, implying caution in interpretation of partial effects of AG1478 as reported in other systems. Transactivation of the EGF receptor is clearly not a universal prerequisite for coupling of G-protein coupled receptors to Erk1/2 signalling cascades.

Subject headings and genre

NATURVETENSKAP Biologi Cellbiologi hsv//swe
NATURAL SCIENCES Biological Sciences Cell Biology hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Cancer och onkologi hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Cancer and Oncology hsv//eng
Transactivation
G-protein-coupled receptors
Erk1/2 activation
Brown adipocytes
Norepinephrine

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Fälting, Johanna M.Stockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut (author)
Mattsson, Charlotte L.Stockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut (author)
Holmström, Therese E.Stockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut (author)
Nedergaard, JanStockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut(Swepub:su)neder (author)
Stockholms universitetInstitutionen för molekylär biovetenskap, Wenner-Grens institut (creator_code:org_t)

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In:Experimental Cell Research: Elsevier BV319:17, s. 2718-27270014-48271090-2422

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