Non-transactivational, dual pathways for LPA-induced Erk1/2 activation in primary cultures of brown pre-adipocytes

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Holmström, Therese E.Stockholms universitet,Wenner-Grens institut (author)

Non-transactivational, dual pathways for LPA-induced Erk1/2 activation in primary cultures of brown pre-adipocytes

Article/chapterEnglish2010

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Elsevier BV,2010
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LIBRIS-ID:oai:DiVA.org:su-37122
https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-37122URI
https://doi.org/10.1016/j.yexcr.2010.05.029DOI

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Language:English
Summary in:English

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Subject category:art swepub-publicationtype

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In many cell types, G-protein-coupled receptor (GPCR)-induced Erk1/2 MAP kinase activation is mediated via receptor tyrosine kinase (RTK) transactivation, in particular via the epidermal growth factor (EGF) receptor. Lysophosphatidic acid (LPA), acting via GPCRs, is a mitogen and MAP kinase activator in many systems, and LPA can regulate adipocyte proliferation. The mechanism by which LPA activates the Erk1/2 MAP kinase is generally accepted to be via EGF receptor transactivation. In primary cultures of brown pre-adipocytes, EGF can induce Erk1/2 activation, which is obligatory and determinant for EGF-induced proliferation of these cells. Therefore, we have here examined whether LPA, via EGF transactivation, can activate Erk1/2 in brown pre-adipocytes. We found that LPA could induce Erk1/2 activation. However, the LPA-induced Erk1/2 activation was independent of transactivation of EGF receptors (or PDGF receptors) in these cells (whereas in transformed HIB-1B brown adipocytes, the LPA-induced Erk1/2 activation indeed proceeded via EGF receptor transactivation). In the brown pre-adipocytes, LPA instead induced Erk1/2 activation via two distinct non-transactivational pathways, one G(i)-protein dependent, involving PKC and Src activation, the other, a PTX-insensitive pathway, involving PI3K (but not Akt) activation. Earlier studies showing LPA-induced Erk1/2 activation being fully dependent on RTK transactivation have all been performed in cell lines and transfected cells. The present study implies that in non-transformed systems, RTK transactivation may not be involved in the mediation of GPCR-induced Erk1/2 MAP kinase activation

Subject headings and genre

NATURVETENSKAP Biologi Annan biologi hsv//swe
NATURAL SCIENCES Biological Sciences Other Biological Topics hsv//eng
Lysophosphatidic acid
Transactivation
Brown adipocytes
Erk1/2
EGF receptor
PI3K
fysiologi
Physiology

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Mattsson, Charlotte L.Stockholms universitet,Wenner-Grens institut(Swepub:su)chma1180 (author)
Wang, Yanling,1982-Stockholms universitet,Wenner-Grens institut(Swepub:su)yawa0699 (author)
Iakovleva, IrinaStockholms universitet,Wenner-Grens institut (author)
Petrovic, NatasaStockholms universitet,Wenner-Grens institut(Swepub:su)npetr (author)
Nedergaard, JanStockholms universitet,Wenner-Grens institut(Swepub:su)neder (author)
Stockholms universitetWenner-Grens institut (creator_code:org_t)

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In:Experimental Cell Research: Elsevier BV316:16, s. 2664-750014-48271090-2422

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