Deficient angiogenesis in redox-dead Cys17Ser PKARIα knock-in mice

Joseph R. Burgoyne (), Olena Rudyk, Hyun-ju Cho, Oleksandra Prysyazhna, Natasha Hathaway, Amanda Weeks, Rachel Evans, Tony Ng, Katrin Schröder, Ralf P. Brandes, Ajay M. Shah and Philip Eaton ()
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Joseph R. Burgoyne: King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, Saint Thomas’ Hospital
Olena Rudyk: King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, Saint Thomas’ Hospital
Hyun-ju Cho: King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, Saint Thomas’ Hospital
Oleksandra Prysyazhna: King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, Saint Thomas’ Hospital
Natasha Hathaway: King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, Saint Thomas’ Hospital
Amanda Weeks: King’s College London, The Rayne Institute, Saint Thomas’ Hospital
Rachel Evans: King’s College London, 2nd Floor, New Hunt's House, Guy’s Medical School Campus
Tony Ng: King’s College London, 2nd Floor, New Hunt's House, Guy’s Medical School Campus
Katrin Schröder: Institut für Kardiovaskuläre Physiologie, Goethe-Universität
Ralf P. Brandes: Institut für Kardiovaskuläre Physiologie, Goethe-Universität
Ajay M. Shah: King’s College London, The British Heart Foundation Centre of Excellence, The James Black Centre, Denmark Hill Campus
Philip Eaton: King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, Saint Thomas’ Hospital

Nature Communications, 2015, vol. 6, issue 1, 1-8

Abstract: Abstract Angiogenesis is essential for tissue development, wound healing and tissue perfusion, with its dysregulation linked to tumorigenesis, rheumatoid arthritis and heart disease. Here we show that pro-angiogenic stimuli couple to NADPH oxidase-dependent generation of oxidants that catalyse an activating intermolecular-disulphide between regulatory-RIα subunits of protein kinase A (PKA), which stimulates PKA-dependent ERK signalling. This is crucial to blood vessel growth as ‘redox-dead’ Cys17Ser RIα knock-in mice fully resistant to PKA disulphide-activation have deficient angiogenesis in models of hind limb ischaemia and tumour-implant growth. Disulphide-activation of PKA represents a new therapeutic target in diseases with aberrant angiogenesis.

Date: 2015
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DOI: 10.1038/ncomms8920

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