Tuesday 7 October 2014

Osteoblasts and Osteoarthritis, Myofibroblasts and Renal Fibrosis





Institute Research Student Seminars

Speakers:  Dimitra Tsompani & Lotfia Nawafa


Venue: Seminar room L2.6, 2nd floor, William Leech Building, Medical School

Date and time:  Wednesday 8th October 2014 at 12.30


Dimitra Tsompani will present:


"The Role of Histone Deacetylase 3 in Chondrogenesis and Osteoarthritis"


Histone deacetylases (HDACs) regulate the acetylation pattern of chromatin to control gene expression and determine cell differentiation and mammalian development. Our aim is to examine the ability of a broad-spectrum of HDAC inhibitors and a HDAC3- targeting small interfering RNA (siRNA) to protect against cartilage degeneration in vivo and in vitro and to investigate the role of HDAC3 loss in chondrogenesis differentiation using human mesenchymal stem cells. In this way we hope to achieve a better understanding of the potential role of HDAC3 in the development and/or progression of osteoarthritis (OA).


Key words: HDAC3, Osteoarthritis, Chondrogenesis


Lotfia Nawafa will speak on:


"The Contribution of Methyltransferase SET9 in Renal Fibrosis"


The essential role of TGF β-1/SMAD signalling in stimulating fibrogenic cells to produce ECM proteins and promoting proliferation of  Myofibroblasts is widely recognised. SMAD3 is known as a mediator in TGF β- 1-induced fibrosis in the kidney.


SET9, a methyltransferase enzyme that specifically methylates histone 3 at lysine 4 position, is shown to play a central role in regulating SMAD3 activity, as shown by SET9 knockdown. The overexpression of wild type SET9 results in increased SMAD3 activity, specifically in the presence of TGF β-1. Conversely, expression of a mutant SET9, which lacks methyltransferase activity, failed to increase SMAD3 activity, even in the presence of TGF β-1.



Keywords: TGFB-1 pathway,SMAD3,SET9


Chair:  Cecilia Jimenez Moreno







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