Angus Wann

PhD

KTRR/VersusArthritis 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 mechanotransduction. 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’m a principal investigator in the Kennedy Institute of Rheumatology at Oxford. I have a Kennedy Trust fellowship within the Versus Arthritis Centre for Osteoarthritis Pathogenesis, which is enabling this translation of cilia biology to disease.

I am now involved in trying to understand how cells and tissue use cilia to make appropriate decisions and adaptations to physiological and pathophysiologically relevant cues such as mechanical force, inflammatory cytokines and growth factors. Ultimately the aim is to learn enough about ciliary regulation of signalling such as to exploit this contexts where signalling is ‘miss-tuned’ in disease. This involves working from the molecular level all the way through to models of human disease. This includes genomic and proteomic approaches, imaging with high resolution microscopy and the Diamond Light synchrotron to study the architecture of the peri-ciliary region and genetic and pre-clinical models to study tissue-level biology. We are starting to employ developmental engineering approaches, humanised organoid and organ on a chip models and have recently begun to screen clinical samples for changes in cilia and the ciliome.

Key publications

Ciliary IFT88 protects coordinated adolescent growth plate ossification from disruptive physiological mechanical forces.
Journal article

Coveney CR. et al, (2022), J Bone Miner Res
The ciliary protein IFT88 controls post-natal cartilage thickness and influences development of osteoarthritis
Journal article

Coveney CR. et al, (2020)
Age-dependent changes in protein incorporation into collagen-rich tissues of mice by in vivo pulsed SILAC labelling.
Journal article

Ariosa-Morejon Y. et al, (2021), Elife, 10
Ciliary proteins specify the cell inflammatory response by tuning NFκB signalling, independently of primary cilia.
Journal article

Mc Fie M. et al, (2020), J Cell Sci, 133
Cilia protein IFT88 regulates extracellular protease activity by optimizing LRP-1-mediated endocytosis.
Journal article

Coveney CR. et al, (2018), FASEB J
Primary cilia mediate mechanotransduction through control of ATP-induced Ca2+ signaling in compressed chondrocytes.
Journal article

Wann AKT. et al, (2012), FASEB J, 26, 1663 - 1671

Recent publications

Ciliary IFT88 protects coordinated adolescent growth plate ossification from disruptive physiological mechanical forces.
Journal article

Coveney CR. et al, (2022), J Bone Miner Res
Age-dependent changes in protein incorporation into collagen-rich tissues of mice by in vivo pulsed SILAC labelling.
Journal article

Ariosa-Morejon Y. et al, (2021), Elife, 10
The ciliary protein IFT88 controls post-natal cartilage thickness and influences development of osteoarthritis.
Journal article

Coveney CR. et al, (2021), Arthritis Rheumatol
IDENTIFICATION OF A NOVEL REGULATOR OF ADAMTS-5-MEDIATED AGGRECAN DEGRADATION IN CHONDROCYTES
Conference paper

Collins I. et al, (2021), OSTEOARTHRITIS AND CARTILAGE, 29, S100 - S100
Identification of a novel regulator of ADAMTS-5-mediated aggrecan degradation in chondrocytes
Conference paper

Collins I. et al, (2021), INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 102, 120 - 121
IS THE CILIARY PROTEIN INTRAFLAGELLAR TRANSPORT 88 A DAMPENER OF MECHANICAL CUES IN ADOLESCENT EPIPHYSEAL PLATE CLOSURE?
Conference paper

Coveney CR. et al, (2021), OSTEOARTHRITIS AND CARTILAGE, 29, S107 - S107
THE CILIARY PROTEIN INTRAFLAGELLAR TRANSPORT 88 IS REQUIRED FOR THE MATURATION, HOMEOSTASIS AND MECHANOADAPTATION OF ARTICULAR CARTILAGE
Conference paper

Coveney CR. et al, (2021), OSTEOARTHRITIS AND CARTILAGE, 29, S26 - S27
The ciliary protein IFT88 controls post-natal cartilage thickness and influences development of osteoarthritis
Journal article

Coveney CR. et al, (2020)
Ciliary proteins specify the cell inflammatory response by tuning NFκB signalling, independently of primary cilia.
Journal article

Mc Fie M. et al, (2020), J Cell Sci, 133
THE CILIARY PROTEIN INTRAFLAGELLAR TRANSPORT 88 IS REQUIRED FOR THE MATURATION, HOMEOSTASIS AND MECHANOADAPTATION OF ARTICULAR CARTILAGE
Conference paper

Coveney CR. et al, (2020), OSTEOARTHRITIS AND CARTILAGE, 28, S75 - S75

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