Tom Nightingale completed his undergraduate studies at the University of Bath (M.biochem) and obtained his Phd at the University of Oxford. Subsequently Tom worked with Prof Daniel Cutler at the Laboratory for Molecular and Cellular Biology at University College London and joined the Centre for Microvascular Research at the WHRI in 2013. Tom is establishing his own research group to investigate the effect of intracellular trafficking of endothelial cell adhesion molecules on leukocyte extravasation.
Fellowships and awards
- Early Career Research Fellowship (2013)
- MRC New Investigator grant (2015)
Summary of Research
Leukocyte recruitment from the blood vascular to infected tissues is a crucial part of the normal inflammatory response and allows clearance of pathogens from the affected area. However in some situations inappropriate and excessive recruitment of leukocytes can result in chronically inflamed tissues. The control of this process is therefore central to a normal resolution of an inflammatory situation.
The blood vascular endothelium plays a key part in this process as a number of endothelial cell surface receptors such as P- and E-selectin, CD31 and the Junctional Adhesion Molecules (JAMs) have important roles in the recruitment and transmigration of leukocytes through blood-vessel walls. Some of these adhesion receptors such as Jam-C are known to undergo intracellular trafficking and are found on intracellular vesicles and non-junctional plasma membrane following certain stimuli. My research centres on the mechanisms and machinery required for this intracellular trafficking and the subsequent impact on transmigration of leukocytes through the endothelial cell layer.
Figure 1: An activated endothelial cell. Von Willebrands factor (Red) Phalloidin (Green) and pan non-muscle myosin II (Blue)
Members of the Group
Researchers staff: Dr Amy Barker
For a full list of publist publications click here
Nightingale T, Cutler DF. (2013) The secretion of Von Willebrand Factor from endothelial cells; an increasingly complicated story. J.Thromb. Haemostasis.Jun;11 Suppl 1:192-201
Nightingale TD, Cutler DF, Cramer LP. (2012) Actin coats and rings promote regulated exocytosis.Trends Cell Biol. 22(6) p329-37.
Nightingale TD, White IJ, Doyle EL, Turmaine M, Harrison-Lavoie KJ, Webb KF, Cramer LP, Cutler DF. (2011) Actomyosin II contractility expels von Willebrand factor from Weibel-Palade bodies during exocytosis. J Cell Biol.194(4) p613-29.
Rojo Pulido I, Nightingale TD, Darchen F, Seabra MC, Cutler DF, Gerke V. (2011) Myosin Va acts in concert with Rab27a and MyRIP to regulate acute von-Willebrand factor release from endothelial cells. Traffic 12 (10) p1371-82
Michaux G, Dyer CE, Nightingale TD, Gallaud E, Nurrish S, Cutler DF. (2011) A role for Rab10 in von Willebrand factor release discovered by an AP-1 interactor screen in C. elegans.J.Thromb. Haemostasis 9 (2) p392-401
Nightingale TD, Pattni K, Hume AN, Seabra MC, Cutler DF. (2009) Rab27a and MyRIP regulate the amount and multimeric state of VWF released from endothelial cells. Blood113(20), p5010-18.
Nightingale TD, Frayne ME, Clasper S, Banerji S, Jackson DG. (2009) A mechanism of sialylation functionally silences the hyaluronan receptor LYVE-1 in lymphatic endothelium. J. Biol. Chem. 284(6), p3935-45.
Lui-Roberts WW, Ferraro F, Nightingale TD, Cutler DF.(2008) Aftiphilin and gamma-synergin are required for secretagogue sensitivity of Weibel-Palade bodies in endothelial cells. (2008) Mol. Biol. Cell. 19(12): p5072-81.
Metcalf DJ, Nightingale TD, Zenner HL, Lui-Roberts WW, Cutler DF. Formation and function of Weibel-Palade bodies. (2008) J. Cell. Sci. 121(Pt 1): p19-27.