Cell-cell bond modulates vascular smooth muscle cell responsiveness to Angiotensin II.

Chiara Barisione, Marzia Mura, Silvano Garibaldi, Patrizia Fabbi, Paola Altieri, Mario Passalacqua, Barbara Salani, Giorgio Ghigliotti, Concetta Aloi, Paolo Spallarossa, Claudio Brunelli

Division of Cardiology, Department of Internal Medicine, Research Center of Cardiovascular Biology, University of Genova, Viale Benedetto XV, 6, Genova 16132, Italy. cbari@libero.it

Biochemical and biophysical research communications 2009 Oct 23

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Cell attachment is provided by cell-matrix and cell-cell bonds, and acts as a regulator of vascular smooth muscle cell (VSMC) survival, activity and homeostasis, as well as of VSMCs response to pathogenic stimuli. In this work we elicited an exclusive cell-cell contact by culturing A7r5 VSMCs on agarose-coated wells to form floating cell clusters, and we demonstrated that a steady state with a reduced response to the vasoactive peptide Angiotensin II (ATII) was induced. We found that clustered VSMCs showed subcortical stabilization of beta-catenin and Caveolin 1 (Cav1), unlike adherent confluent counterparts. We demonstrated that beta-catenin and Cav1 stabilization at the membrane level hampers the molecular cross-talk induced by ATII-activated AT1 receptor (AT1R), thereby impeding the phosphorylation of Cav1 and IGF1R, the NADPH oxidase activity, and counteracting ATII-dependent hypertrophy. Thus, elective cell-cell bond might modulate the proatherogenic activity of ATII, reducing the adverse vascular remodelling associated with AT1R activation.

Citation

Chiara Barisione, Marzia Mura, Silvano Garibaldi, Patrizia Fabbi, Paola Altieri, Mario Passalacqua, Barbara Salani, Giorgio Ghigliotti, Concetta Aloi, Paolo Spallarossa, Claudio Brunelli. Cell-cell bond modulates vascular smooth muscle cell responsiveness to Angiotensin II. Biochemical and biophysical research communications. 2009 Oct 23;388(3):523-8