Download Biochemical Society Conference Report

Biochemical Society Conference Report
Timothy Bowen
Institute of Nephrology, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN
Hyaluronan 2010, held in early June in Kyoto, Japan, was the eighth global hyaluronan conference
organised by the International Society for Hyaluronan Sciences (ISHAS). Together with the biennial
Gordon Research Conference on Proteoglycans, the ISHAS meetings represent the premier global
forum at which hyaluronan biologists congregate. This symposium was therefore an ideal environment
for networking and generating collaborations, as well as to hear the latest findings from leading groups
in hyaluronan research. Indeed, the focused nature of the meeting meant that many of the talks were
directly relevant to our work at the Institute of Nephrology at Cardiff University School of Medicine.
Regulation of gene expression is the basis of much of my group’s research, forming part of an
ongoing series of studies at the Institute that aims to determine the pathogenic mechanisms
underlying renal fibrosis and the progression of chronic kidney disease. Fibrosis is associated with
increased synthesis in the renal cortex of hyaluronan (HA), a ubiquitous extracellular matrix
glycosaminoglycan (GAG). Also known as hyaluronic acid, HA is a non-sulphated GAG comprised of
alternating D-glucuronic acid and D-N-acetylglucosamine residues linked via alternating -1,4 and 1,3 glycosidic bonds. HA is synthesised at the cell membrane by the HA synthase (HAS) enzymes,
encoded by the corresponding multigene family HAS1-3.
Previous analyses of renal biopsy samples from diabetic nephropathy patients carried out at
the Institute have shown that HA is a correlate of interstitial fibrosis in vivo. Our in vitro findings have
suggested that transcriptional induction of the HAS2 gene and subsequent HAS2-driven HA synthesis
may impact on fibrosis via the modulation of renal proximal tubular epithelial cell (PTC) phenotype and
fibroblast-to-myofibroblast differentiation.
In a range of cell types, including PTC and fibroblasts, we have identified transcription of
HAS2AS, a natural antisense RNA to HAS2, and are evaluating its role in the post-transcriptional
regulation of HAS2 expression in these cells. I’m pleased to say that both of the abstracts that I
submitted were accepted for poster presentation and that one, Coordinated expression of the human
hyaluronan synthase 2 gene and its natural antisense in the renal proximal tubular epithelial cell, was
also selected for a short oral presentation on the conference’s final day. In contrast to the originally
described role of HAS2AS in osteosarcoma cells, our data show that HAS2AS and HAS2 transcription
are coordinated in PTC, and that the presence of the antisense RNA appears to stabilise and/or
augment HAS2 mRNA synthesis.
My talk attracted a number of questions from the conference floor and further comments
immediately afterwards, in addition to those discussed during the poster sessions throughout the
preceding week.
These poster sessions led to two particularly strong leads on international
collaboration that I am now following up via escalating email traffic.
Many thanks to the Biochemical Society for covering my registration fee and thereby helping
me to attend Hyaluronan 2010.