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  Newsletter Issue 9, 13 November 2013

Gold Sponsors

 

STEM CELL SOCIETY SYMPOSIUM 2013

"Early Human Development & Fetal-Maternal Medicine"

18 - 19 November

Matrix Building Level 2 & 2M
30 Biopolis Street, Singapore 138671

Silver Sponsors

 

Bronze Sponsors

Dear Members, Delegates, Friends, and Colleagues,

The Symposium 2013 Newsletter, Issue 9 (the last before the symposium!) brings to you abstracts and bios of Kazutoshi Takahashi from CIRA, Japan, Minitori Saitou from Kyoto University, Japan, Sheila Vasoo, from NUHS, Singapore, and last but not least Xinyian FU, from NUS, Singapore.

It's time to get excited! The symposium starts in only 5 days.

We also would like to highlight the most recent publication of Jacob Hanna, one of our pleanry speakers:

Gafni O, Weinberger L, Mansour AA, Manor YS, Chomsky E, Ben-Yosef D, Kalma Y, Viukov S, Maza I, Zviran A, Rais Y, Shipony Z, Mukamel Z, Krupalnik V, Zerbib M, Geula S, Caspi I, Schneir D, Shwartz T, Gilad S, Amann-Zalcenstein D, Benjamin S, Amit I, Tanay A, Massarwa R, Novershtern N, Hanna JH. Derivation of novel human ground state naive pluripotent stem cells. Nature. 2013 Oct 30. doi: 10.1038/nature12745. [Epub ahead of print]

Updates:

Programme: The programme can be viewed here.

Delegate Networking Event: A networking event open to all delegates of the symposium will take place on the first evening (18th November). Venue will be the Epicentre at Biopolis. Drinks and food should help stimulating interactions and communications among delegates.

 

For enquiries contact us HERE.

We look forward to welcoming you very soon.

The Organizing Committee Stem Cell Society Singapore Symposium 2013

 

 

 

 

 

Featured Speakers  

Kazutoshi TAKAHASHI

CIRA, Japan

 
Abstract  
Dissecting the molecular mechanisms of human cellular reprogramming toward pluripotency

 

Abstract text (max. 300 Words): Pluripotency can be reacquired in committed somatic cells using a combination of handful transcription factors, such as OCT3/4 (also known as POU5F1), SOX2, KLF4 and c-MYC (OSKM), albeit with low efficiency. Therefore, large numbers of non-reprogrammed cells during the generation of iPSCs inhibit accurate analyses of the reprogramming process. To overcome this issue, we used a pluripotent cell-specific surface antigen, Tumor-related Antigen (TRA)-1-60 to capture cells being reprogrammed. By

using this technology, we found that the limiting step toward pluripotency is the maturation of TRA-1-60 positive (+) intermediate reprogrammed cells but not initiation of reprogramming. In addition, we focused on the transient changes of gene expression and epigenetic modification in TRA-1-60 (+) cells. In my talk, I would like to introduce the recent progress of understanding the molecular mechanisms of human cellular reprogramming.

Biography

 

Kazutoshi Takahashi, PhD, is a principal investigator in Center for iPS cell Research and Application in Kyoto University, Japan

 

 

Mitinori SAITOU

Kyoto University , Japan

 

 
Abstract  
Mechanism and Reconstitution in vitro of Germ Cell Development in Mice  

The germ cell lineage ensures the creation of new individuals, thereby perpetuating and diversifying the genetic and epigenetic information across the generations. We have been investigating signaling, global transcription and epigenetic dynamics associated with germ cell specification and development in mice at a single-cell resolution, and have proposed that germ cell specification integrates repression of the somatic program, re-acquisition of potential pluripotency, and an ensuing genome-wide epigenetic reprogramming. Recently, using pluripotent stem cells [embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs)], we have succeeded in precisely reconstituting the specification and subsequent development of germ cells in culture both in males and

females: ESCs/iPSCs are induced into epiblast-like cells (EpiLCs) and then into primordial germ cell-like cells (PGCLCs), which contribute to spermatogenesis and oogenesis and to fertile offspring. Our work will serve as a foundation for systems analysis of germ cell development, including the elucidation of key transcriptional network for germ cell specification, the mechanism of genome-wide epigenetic reprogramming, and the mechanism for meiosis, as well as for the reconstitution of the entire germ-cell development process in vitro, not only in mice but also in other mammals, including humans.

Biography PubMed  

Mitinori Saitou received his M.D. from the Kyoto University Faculty of Medicine in 1995, and received his Ph.D. in 1999 for his study of the structure and function of tight junctions under Shoichiro Tsukita in the Kyoto University Graduate School of Medicine. He then moved to the Wellcome Trust/Cancer Research Campaign Institute (present name: Wellcome Trust/Cancer Research UK Gurdon Institute), where he worked as a postdoctoral research associate in Azim Surani’s laboratory, focusing on the origin of the germ line in the mouse. He was appointed team leader at the RIKEN Center for Developmental Biology in 2003. He continued to work on the origin, properties and regulation of the germ line in the mouse. He was appointed Professor at the Kyoto University Graduate School of Medicine in 2009. He was appointed Director of the JST ERATO program in 2011.

His work now focuses on the mechanism and reconstitution in vitro of germ cell development in mammals.He was appointed team leader at the RIKEN Center for Developmental Biology in 2003. He continued to work on the origin, properties and regulation of the germ line in the mouse. He was appointed Professor at the Kyoto University Graduate School of Medicine in 2009. He was appointed Director of the JST ERATO program in 2011. His work now focuses on the mechanism and reconstitution in vitro of germ cell development in mammals.

 

Sheila VASOO

NUHS, Singapore

 

 

 

 
Abstract  
Recurrent Miscarriages: Maternofetal Interface, Microvesicles and More  

Recurrent miscarriage (RM) is a perplexing clinical problem that affects up to 5% of pregnancies and not only has a significant psychological impact on couples but also societal implications, particularly in Singapore with its declining birthrate. Although multiple etiologies have been described, over one-half of the cases remain unexplained. Immunopathologic studies of the placental bed in RM have demonstrated decidual inflammation, perivillous and decidual fibrin deposition and thrombosis in decidual vessels. While it is clear that inflammatory and thrombotic processes at the maternofetal interface are the final pathologic assault in most cases, the exact immunopathogenic mechanisms preceding this remain unclear. There is mounting evidence to suggest that fetus-derived syncytiotrophoblast microvesicles (STBMs), shed into maternal circulation as normal turnover of the placental surface, are potential contributors to altered systemic inflammatory responsiveness in normal and adverse pregnancies. However, to date, few studies have compared the inflammatory potential of purified STBMs generated from placentas in normal and adverse pregnancy outcomes.

Our findings showed that STBM in RM showed increased immunostimulatory activity as evidenced by their induction of significantly increased release of proinflammatory cytokines such as IL-6 and TNF-α from monocyte-derived dendritic cells and macrophages as well as their phenotypic maturation. In addition, mass-spectrometry showed these STBM differentially express proteins and lipids related to cell apoptosis, inflammation, coagulation and oxidative stress compared to healthy controls.Finally, we hope to characterize decidual immune cell populations such as dendritic cells (DCs) and Natural Killer (NK) cells as well as extravillous trophoblasts (EVTs) and decidual stromal cells (DSCs) to further elucidate important pathways involved in RM and thus provide insights into the mechanisms of immune-dysregulation underlying RM by delineating changes in their morphological phenotypes, gene expression and functions in women with RM compared to normal pregnancy.

Biography  
Dr Sheila Vasoo is a Visiting Senior Consultant in the Division of Rheumatology, University Medicine Cluster, National University Health System and Assistant Professor at the Yong Loo Lin School of Medicine, National University of Singapore. She obtained her Membership from the Royal College of Physicians (UK) in 1998 and has been a Fellow of the Royal College of Physicians since 2011. She received her specialist accreditation in Rheumatology and has been a Fellow of the Academy of Medicine (Singapore) since 2005. Her subspecialty training was in Antiphospholipid syndrome and Recurrent pregnancy loss at St Thomas’ Hospital, London, UK under Dr GRV Hughes. Dr Vasoo is the Programme Director of the Pregnancy Loss Clinic @NUH, which she runs with Prof Mahesh Choolani and his team. Her research interests are in the field of reproductive immunology with a focus on adverse pregnancy outcomes such as recurrent pregnancy loss and the antiphospholipid syndrome. In 2009, she was awarded the NMRC EDG/NIG grant award for the study on the role of microvesicles in adverse pregnancy outcomes. The research team headed by her was first in Singapore to embark on this challenging research. In 2012, the group was awarded the John Gusdon New Investigator Award at the joint American and European Society of Reproductive Immunology Annual Scientific Meeting for their novel findings on the role of microvesicles in this setting
 

Xinyian FU

NUS, Singapore

 
Abstract  
STAT3 Regulates a Novel Epigenetic Pathway for ESC Pluripotency and Early Embryogenesis  
Recently STAT3-dependent regulation of the OCT4-NANOG circuitry has been shown to be necessary to maintain the pluripotent inner cell mass (ICM), the source of in vitro-derived ESCs. STAT3 directly binds to the Oct4 and Nanog distal enhancers, modulating their expression to maintain pluripotency of mouse embryonic and induced pluripotent stem cells. However, it is not known if STAT3 may also regulate any epigenetic event for transition from pluripotency to diffentiated cells.  We report here that STAT3 may be involved in regulation of a novel epigenetic factor, which affects epigenetic dynamics of ESCs. Interestingly, we found that ESC pluripotency is not dependent on common pluripotent genes but through suppressing the expression of lineage specific genes. Through microarray analysis, RNA-seq and real-time-PCR, we identified a set of lineage genesthat wereinduced when this epigenetic factor is down-regulated in ESCs. Finally, we show that this newly identified factor plays important roles for blastocyst formation in early embryonic development in vivo. Our data thus reveal a novel pathway from STAT3 to an epigenetic statue that controls pluripotency of ESC through the regulation of lineage specific genes.
Biography  
Xin-Yuan Fu, PhD, is currently Professor and Senior Principle Investigator since 2008 in Biochemistry Department, NUS, and Cancer Science Institute of Singapore. He is also a professor of Immunology at Indiana University School of Medicine USA.  He received his PhD in molecular biology at Columbia University in 1988 (Mentor: James Manley); postdoctoral training in Rockefeller University with James Darnell (1988-1991) where he purified and cloned first STAT genes (Stat1 and Stat2). He was an Assistant Professor in Mt Sinai School of Medicine NY (1992-1994); an Associate Professor at Yale University (1994-2003), a Full Professor at Indiana University (2004-present). In the past 5 years his work has focused on STAT3’s role in regulation of inflammation and development. Currently, one of Dr Fu’s research interests is to reveal roles of the STAT gene family in epigenetic regulation of stem cell differentiation and development.