Skeletal Stem and Progenitor cells for the Osteoblast Lineage: Origin, Regulation and Functioning
Live Webinar: 19 August 2021, 4 pm CET
Organised by ECTS
Date & Time: 19 August 2021, 4 pm CET
Featuring Christa Maes, and moderated by Katharina Jähn-Rickert
Costs: Live webinar is free for ECTS members and non-members, but a registration is required. Recordings are accessible to ECTS members only.
Format:
- 5 min welcome & introductions
- 35 min presentation on “Skeletal Stem and Progenitor cells for the Osteoblast Lineage”
- 20 min Q&A
Learning Objectives:
- Understand the use of lineage tracing and fate mapping strategies in genetically modified mice.
- Learn about the identity, heterogeneity and characteristics of skeletal stem and progenitor cells (SSPCs) with osteogenic capacity and the niches they reside in.
- Obtain insights in the molecular control of SSPC maintenance, differentiation and functioning.
The Lineage tracing of stem cells, Brussels, Belgium, 19-08-2021 has been accredited by the European Accreditation Council for Continuing Medical Education (EACCME®) with 1 European CME credits (ECMEC®s).
Each medical specialist should claim only those hours of credit that he/she
actually spent in the educational activity.”
Additional Live Coffee Shop: 15 July 2021, 5 pm CET
ECTS is pleased to invite you for an additional “Coffee Shop” informal discussion at 5 pm CET, right after the live webinar, in order to meet friends and colleagues with an interest in the bone field for a topical chat. If you are interested in this networking opportunity, please click on the button below to register for the Coffee Shop.
Featuring Prof Dr. Christa Maes, PhD
Christa Maes is Associate Professor at the KU Leuven in Belgium and Group leader of the Laboratory of Skeletal Cell Biology and Physiology (SCEBP), which is part of the Skeletal Biology and Engineering Research Center (SBE) where basic, applied and clinical research is integrated to advance repair and regeneration of cartilage, bone and joint defects.
The SCEBP lab studies the molecular control of skeletal cell functioning, with a focus on skeletal stem and progenitor cells and osteoblasts and their interplay with the vasculature. Research topics encompass the mechanisms underlying bone formation in development, adult homeostasis and fracture healing, as well as the significance of osteogenic cell biology in the broader physiological context of the organism, in particular hematopoiesis and global energy metabolism. Prime working models are genetically modified mice including in vivo lineage tracing reporters.
Christa Maes was trained at the KU Leuven (Belgium), University of Virginia (USA) and Harvard University (USA). At Harvard, working with Henry Kronenberg she started osteolineage cell tracing and visualization studies using mouse models, which led to new insights in the origin and behavior of osteogenic cells in bone development and fracture repair. During her career Christa received national and international fellowship support and several awards, including from the ECTS, ASBMR, and IBMS. She set up her own lab and independent studies at the KU Leuven in 2012 with the support of a prestigious European ERC Starting Grant. Christa is very active in the bone community: she co-chaired the IBMS Young Investigator Committee, organizing scientific and career development workshops for junior researchers, she served on the ASBMR Membership Engagement and Education Committee, she was the basic/translational program co-chair for the 2020 ECTS meeting, and is one of the lead organizers of the Herbert Fleisch workshops held since 2014 in Bruges (Belgium). Moreover, Christa serves as Associate Editor for the Journal of Bone and Mineral Research (JBMR).
Email: christa.maes@kuleuven.be
(short link: https://bit.ly/2TUXygz)
Twitter: @SCEBP_Lab
Moderated by Katharina Jähn-Rickert
Abstract
Breast cancer cells frequently disseminate to the bone marrow, where they may either enter a dormant state or colonize the bone and induce osteolysis. The mechanisms that regulate tumor cell entry and exit from dormancy in the bone are not well understood, but several factors have been identified. Previous work from our group found that leukemia inhibitory factor receptor (LIFR) promotes tumor dormancy when expressed on bone-disseminated tumor cells and that loss of LIFR enables otherwise dormant tumor cells to colonize the bone. Our lab has therefore examined how LIFR expression is regulated in breast cancer cells, with the hope that understanding its regulation might provide novel avenues to therapeutically target dormant disseminated tumor cells. Through these efforts we have found that LIFR is epigenetically regulated, and that histone deacetylase (HDAC) inhibitors, which are FDA-approved for several blood cancers, stimulate LIFR expression on breast cancer cells from all subtypes. This finding presents an interesting therapeutic opportunity to explore whether HDAC inhibitors may be used to promote a chronic state of tumor dormancy and prevent recurrence in bone. Our findings suggest that this may be feasible, but that the effects of histone deacetylase inhibitors on bone remodeling profoundly impact tumor colonization and must be combined with appropriate anti-resorptive therapies.