Ashwin Woodhoo
Ashwin Woodhoo
Ikerbasque Research Associate
Address: Bizkaia Science and Technology Park,
building 801A, Derio (Bizkaia)
Nerve Disorders Lab

Dr Ashwin Woodhoo started his research career in the group of his mentors Profs. Kristján R. Jessen and Rhona Mirsky at Univeristy College London, first as a PhD student (Dec 2001- Dec 2006), followed by a short post-doctoral period (Jan 2007- Dec 2008). There, he learnt and developed several projects related to Schwann cell biology. He then joined the group of Dr Malu Martínez-Chantar and Prof. José M. Mato at the CIC bioGUNE to start his independent research lines on the control of gene expression changes during Schwann cell development and in pathological conditions by epigenetic and post-transcriptional mechanisms. Since 2015, he is directing his own laboratory at the CIC bioGUNE.

He has received different fellowships, including the Juan de la Cierva (2009), AECC fellowship (2010), Ramón y Cajal (2010 – 2015) and Ikerbasque Research Fellowship (2014 – 2019), and his work has received funding from the Instituto Carlos III, Fundación Científica AECC, Spanish Ministry of Economy (Plan Nacional i+D+i and Europa Excelencia), Basque Department of Education, Fundación BBVA and the Royal Society.

Axon myelination is essential for rapid saltatory conduction of nerve impulses in the vertebrate nervous system. A central feature of several of these pathological conditions in the peripheral nervous system (PNS) is the destruction of myelin and the reprogramming of myelinating Schwann cells to a 'progenitor-like' state, a highly unusual feature in mammals.  This rests on the surprising plasticity of Schwann cells that allows them to switch between differentiation states. The work of in the laboratory addresses a set of interlocking issues in Schwann cell biology that deal with Schwann cell myelination, and the response of Schwann cells to pathological conditions. More specifically, we are focused on identifying the key mechanisms that drive Schwann cell reprogramming in different pathological conditions, including nerve injury, genetic disorders, immune cell attack and microbial infections. For these, we have been examining the role of autophagy, and the role of DNA methylation, histone modifications and non-coding RNAs in this process using high-throughput techniques. Another related ongoing project in the lab on is focused on the identification of therapeutical targets for neurofibromatosis type 1 and malignant peripheral nerve sheath tumours (MPNST)