NDLI: Laminin acts via focal adhesion kinase/phosphatidylinositol-3′ kinase/protein kinase B to down-regulate β1-adrenergic receptor signalling in cat atrial myocytes

Content Provider	PubMed Central
Author	Wang, Y. G. Pabbidi, M. Samarel, A. M. Lipsius, S. L. Ji, X.
Copyright Year	2009
Abstract	We previously reported that short-term (2 h) plating of cat atrial myocytes on the extracellular matrix protein, laminin (LMN) decreases adenylate cyclase activity and β1-adrenergic receptor (β1-AR) stimulation of L-type Ca2+ current (I Ca,L). The present study sought to determine whether LMN-mediated down-regulation of β1 signalling is due to down-regulation of adenylate cyclase and to gain insight into the signalling mechanisms responsible. β1-AR stimulation was achieved by 0.01 μm isoproterenol (isoprenaline) plus 0.1 μm ICI 118551, a selective β2-AR antagonist. Atrial myocytes were plated for at least 2 h on uncoated cover-slips (−LMN) or cover-slips coated with LMN (+LMN). As previously reported, β1-AR stimulation of I Ca,L was significantly smaller in +LMN compared to −LMN atrial myocytes. In −LMN myocytes, 10 μm LY294002 (LY), a specific inhibitor of PI-(3)K, had no effect on β1-AR stimulation of I Ca,L. In +LMN myocytes, however, LY significantly increased β1-AR stimulation of I Ca,L. Western blots revealed that compared with −LMN myocytes, +LMN myocytes showed a significant increase in Akt phosphorylation at Ser-473, which was prevented by LY. In another approach, +LMN myocytes were infected (multiplicity of infection (MOI), 100; 24 h) with replication-defective adenoviruses (Adv) expressing dominant-negative inhibitors of focal adhesion kinase (FAK) (Adv-FRNK or Adv-Y397F-FAK) or Akt (Adv-dnAkt). Compared with control cells infected with Adv-β-galactosidase, cells infected with Adv-FRNK, Adv-Y397F-FAK or Adv-dnAkt each exhibited a significantly greater β1-AR stimulation of I Ca,L. In −LMN myocytes LY had no effect on forskolin (FSK)-stimulated I Ca,L. However, in +LMN myocytes LY significantly increased FSK-stimulated I Ca,L. Similar results were obtained in +LMN atrial myocytes infected with Adv-FRNK. We conclude that LMN binding to β1-integrin receptors acts via FAK/PI-(3)K/Akt to inhibit adenylate cyclase activity and thereby down-regulates β1-AR-mediated stimulation of I Ca,L. These findings provide new insight into the cellular mechanisms by which the extracellular matrix can modulate atrial β-AR signalling.
Related Links	http://dx.doi.org/10.1113/jphysiol.2008.163824
Ending Page	550
Page Count	10
Starting Page	541
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 3
Volume Number	587
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2009-02-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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