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Noradrenaline induces brown adipocytes cell growth via β‐receptors by a mechanism dependent on ERKs but independent of cAMP and PKA
Author(s) -
Valladares Amparo,
Porras Almudena,
Álvarez Alberto M.,
Roncero Cesar,
Benito Manuel
Publication year - 2000
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/1097-4652(200012)185:3<324::aid-jcp2>3.0.co;2-q
Subject(s) - protein kinase a , cyclic adenosine monophosphate , receptor , microbiology and biotechnology , mapk/erk pathway , signal transduction , chemistry , kinase , adenosine , endocrinology , adrenergic receptor , medicine , biology , biochemistry
It has been well established that the key role of noradrenaline is the induction of uncoupling‐protein‐1 (UCP‐1) expression, the unique marker of brown adipocytes. However, its implication on proliferation and the pathways involved are not as well characterized. By using rat fetal brown adipocytes as a model, we show that, although noradrenaline activates extracellular regulated kinases (ERKs) through β‐, α1‐, and α2‐receptors, only β‐receptors mediate cell growth by a mechanism that requires ERKs activation but is independent of cyclic‐adenosine‐monophosphate/protein kinase A (cAMP/PKA). Conversely, the cAMP/PKA cascade mediates noradrenaline‐induced UCP‐1 expression, whereas ERKs pathway attenuates thermogenic differentiation. On the other hand, α1‐ and α2‐receptors have an antiproliferative effect that is enhanced by ERK inhibition. J. Cell. Physiol. 185:324–330, 2000. © 2000 Wiley‐Liss, Inc.