Contact information

Email	angus.wann@kennedy.ox.ac.uk
Tel	+44 (0)1865 612670

My connections

Wann Group | Primary Cilia in Inflammatory Signalling Research Group, Kennedy Institute
Wann Group | Primary Cilia in Inflammatory Signalling Research Group

Molecular pathogenesis of OA Research Group

Angus Wann

PhD

KTRR/ARUK Research Fellow

I was an undergraduate student of Physiology at Cardiff. I received my PhD from St Georges University Medical School in 2009, where I worked on the mechanobiology of the synovial joint under Professor J.R Levick. From 2009 until 2014 I worked with Professor Martin Knight in a bioengineering group at Queen Mary University of London, studying the role of the primary cilium in a range of contexts but primarily the cellular response to mechanical cues.

During the latter part of my time at Queen Mary I began to study how the cilium is altered by and regulates the cellular response to inflammatory cytokines. I am now keen to understand how this role is important in disease pathogenesis and whether we can learn enough about ciliary regulation of signalling as such to exploit this contexts where signalling is ‘miss-tuned’. This involves working from the molecular level, including high resolution microscopy, all the way through to models of human disease. I’m keen to understand how ciliary regulation of signalling affects homeostasis and the workings of the adult body as well as the cell. I’m very keen to employ microscopy to answer these questions but also translate the work up to physiology and pathology.

I’m a new principal investigator in the Kennedy Institute of Rheumatology at Oxford. I have a Kennedy fellowship within the ARUK Centre for Osteoarthritis Pathogenesis, which is enabling the translation of cilia biology to disease.

THE REGULATION OF PATHOLOGICAL SIGNALLING BY THE CHONDROCYTE CILIUM
McFie M. et al, (2016), OSTEOARTHRITIS AND CARTILAGE, 24, S177 - S178
CHONDROCYTE DEDIFFERENTIATION DOWN REGULATES MECHANO-RESPONSIVENESS AND HEDGEHOG SIGNALLING ASSOCIATED WITH CHANGES IN PRIMARY CILIA STRUCTURE
Kelly T-AN. et al, (2016), OSTEOARTHRITIS AND CARTILAGE, 24, S342 - S343
IFT88 influences chondrocyte actin organization and biomechanics.
Wang Z. et al, (2016), Osteoarthritis Cartilage, 24, 544 - 554
Hedgehog signalling does not stimulate cartilage catabolism and is inhibited by Interleukin-1β.
Thompson CL. et al, (2015), Arthritis Res Ther, 17
The primary cilium influences interleukin-1β-induced NFκB signalling by regulating IKK activity.
Wann AK. et al, (2014), Cell Signal, 26, 1735 - 1742
Are cellular mechanosensors potential therapeutic targets in osteoarthritis?
Drexler S. et al, (2014), International Journal of Clinical Rheumatology, 9, 155 - 167
Surface topography regulates wnt signaling through control of primary cilia structure in mesenchymal stem cells.
McMurray RJ. et al, (2013), Sci Rep, 3
Interleukin-1β sequesters hypoxia inducible factor 2α to the primary cilium.
Wann AK. et al, (2013), Cilia, 2
Primary cilia elongation in response to interleukin-1 mediates the inflammatory response.
Wann AK. and Knight MM., (2012), Cell Mol Life Sci, 69, 2967 - 2977
Primary cilia mediate mechanotransduction through control of ATP-induced Ca2+ signaling in compressed chondrocytes.
Wann AK. et al, (2012), FASEB J, 26, 1663 - 1671
Primary cilia are essential for chondrocyte mechanotransduction
Wann AK. et al, (2010), European Cells and Materials, 20
Eicosapenaenoic acid (EPA) and docasahexaenoic acid (DHA) reduce IL-1β mediated cartilage degradation
Wann AK. et al, (2010), European Cells and Materials, 20
Eicosapentaenoic acid and docosahexaenoic acid reduce interleukin-1β-mediated cartilage degradation.
Wann AK. et al, (2010), Arthritis Res Ther, 12
Signal pathways regulating hyaluronan secretion into static and cycled synovial joints of rabbits.
Ingram KR. et al, (2009), J Physiol, 587, 4361 - 4376
Mechanosensitive hyaluronan secretion: stimulus-response curves and role of transcription-translation-translocation in rabbit joints.
Wann AK. et al, (2009), Exp Physiol, 94, 350 - 361
Cyclic movement stimulates hyaluronan secretion into the synovial cavity of rabbit joints.
Ingram KR. et al, (2008), J Physiol, 586, 1715 - 1729
The role of the primary cilium in chondrocyte response to mechanical loading.
Wann AKT. et al, Mechanically gated channels and their regulation, mechanosensitivity in cells no.6

Key publications

The primary cilium influences interleukin-1β-induced NFκB signalling by regulating IKK activity.
Wann AK. et al, (2014), Cell Signal, 26, 1735 - 1742
Interleukin-1β sequesters hypoxia inducible factor 2α to the primary cilium.
Wann AK. et al, (2013), Cilia, 2
Surface topography regulates wnt signaling through control of primary cilia structure in mesenchymal stem cells.
McMurray RJ. et al, (2013), Sci Rep, 3
Primary cilia mediate mechanotransduction through control of ATP-induced Ca2+ signaling in compressed chondrocytes.
Wann AK. et al, (2012), FASEB J, 26, 1663 - 1671
Primary cilia elongation in response to interleukin-1 mediates the inflammatory response.
Wann AK. and Knight MM., (2012), Cell Mol Life Sci, 69, 2967 - 2977

Recent Publications

THE REGULATION OF PATHOLOGICAL SIGNALLING BY THE CHONDROCYTE CILIUM
McFie M. et al, (2016), OSTEOARTHRITIS AND CARTILAGE, 24, S177 - S178
CHONDROCYTE DEDIFFERENTIATION DOWN REGULATES MECHANO-RESPONSIVENESS AND HEDGEHOG SIGNALLING ASSOCIATED WITH CHANGES IN PRIMARY CILIA STRUCTURE
Kelly T-AN. et al, (2016), OSTEOARTHRITIS AND CARTILAGE, 24, S342 - S343
IFT88 influences chondrocyte actin organization and biomechanics.
Wang Z. et al, (2016), Osteoarthritis Cartilage, 24, 544 - 554
Hedgehog signalling does not stimulate cartilage catabolism and is inhibited by Interleukin-1β.
Thompson CL. et al, (2015), Arthritis Res Ther, 17
The primary cilium influences interleukin-1β-induced NFκB signalling by regulating IKK activity.
Wann AK. et al, (2014), Cell Signal, 26, 1735 - 1742

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