Matteo Vecellio

PhD

Versus Arthritis Career Development Fellow

Ankylosing Spondylitis (AS) is an inflammatory arthritis with numerous robust genetic associations.

My research goal is to investigate the epigenetic mechanisms by which RUNX3 gene contribute to AS, deciphering how RUNX3 genetic variants (SNPs) alter transcriptional regulation and affect CD8+ T-cell compartment. I'm trying to assess the impact of disrupted transcriptional regulation for AS patients and gain new insight into disease pathogenesis.

I joined the Lab of Professor Wordsworth at NDORMS, in June 2013. Previously, I received my PhD degree in Translational and Molecular Medicine in 2012 from the University of Milan – Bicocca (Italy). Soon after my Ph.D I spent one year at the Goethe University in Frankfurt-am-Main (Germany), carrying on the work started during the Ph.D period focused on the epigenetic regulation of human cardiac mesenchymal stromal cells.

I've been recently awarded with a 5 years Arthritis Research UK Career Development Fellowship to decipher the RUNX3 role in AS.

Key publications

The histone acetylase activator pentadecylidenemalonate 1b rescues proliferation and differentiation in the human cardiac mesenchymal cells of type 2 diabetic patients.
Journal article

Vecellio M. et al, (2014), Diabetes, 63, 2132 - 2147
CBP30, a selective CBP/p300 bromodomain inhibitor, suppresses human Th17 responses.
Journal article

Hammitzsch A. et al, (2015), Proceedings of the National Academy of Sciences of the United States of America, 112, 10768 - 10773
In vitro epigenetic reprogramming of human cardiac mesenchymal stromal cells into functionally competent cardiovascular precursors.
Journal article

Vecellio M. et al, (2012), PloS one, 7
Detrimental effect of class-selective histone deacetylase inhibitors during tissue regeneration following hindlimb ischemia.
Journal article

Spallotta F. et al, (2013), The Journal of biological chemistry, 288, 22915 - 22929
The genetic association of RUNX3 with ankylosing spondylitis can be explained by allele-specific effects on IRF4 recruitment that alter gene expression.
Journal article

Vecellio M. et al, (2016), Annals of the rheumatic diseases, 75, 1534 - 1540

Recent publications

The severity of ankylosing spondylitis and responses to anti-tumour necrosis factor biologics are not influenced by the tumour necrosis factor receptor polymorphism incriminated in multiple sclerosis.
Journal article

Watts L. et al, (2019), Genes immun, 20, 167 - 171
Quantifying the genetic risk for the development of axial spondyloarthropathy: could this become a diagnostic tool?
Journal article

Wordsworth BP. et al, (2018), Current opinion in rheumatology, 30, 319 - 323
Evidence for a second ankylosing spondylitis-associated RUNX3 regulatory polymorphism.
Journal article

Vecellio M. et al, (2018), Rmd open, 4
Investigation of a possible extended risk haplotype in the IL23R region associated with ankylosing spondylitis.
Journal article

Roberts AR. et al, (2017), Genes immun, 18, 105 - 108
Reply to Reeves et al.: No evidence for rare ERAP1 haplotypes and haplotype combinations in ankylosing spondylitis.
Journal article

Wordsworth BP. et al, (2017), Proceedings of the National Academy of Sciences of the United States of America, 114

More publications