Date: Friday, 15 March 2019

Venue: Seminar Room 1, G/F
Laboratory Block, Faculty of Medicine Building
21 Sassoon Road, Hong Kong

Time: 5:00 p.m.

Title: The Role of β‑catenin and IRX3/5 in Hypertrophic Chondrocyte Descendant Cell Fate
Speaker: Mr. KONG Mingpeng (PhD candidate)

Summary:
Bone marrow adipose tissue (BMAT), whose volume increases with age, has been found to have different endocrine and metabolic functions. Studies suggest that BMAT is highly related to skeletal health conditions, especially skeletal diseases in the aged population like osteoporosis and osteopenia. Our group recently demonstrated the transition of hypertrophic chondrocyte (HC) to osteoblast (Ob) during endochondral bone formation and the potential adipogenic fate of HC descendants. These findings indicate that HC descendants may play critical roles in regulating bone-fat balance. However, the molecular control of the fate decision of HC descendants has not been revealed. Therefore, my research focuses on the role of β catenin mediated Wnt signaling, and Iroquois homeobox genes Irx3 and Irx5 and the effect of their interactions on HC descendant fate decision. Understanding of bone-fat balance in this research can ultimately suggest innovative approaches in the treatment of skeletal disorders and fat-related metabolic syndromes.

Title: The role and regulation of miR-128 in Alzheimer’s disease
Speaker: Miss LI Siwen (PhD candidate)

Summary:
Alzheimer’s disease (AD) is a neurodegenerative disorder, characterized by a progressive loss of cognitive, language, and behavioural functions. Recently, growing evidence has indicated that microRNAs (miRNAs) play an important role in AD progression. Our results discovered that miR-128 expression significantly downregulated in plasma samples of AD patients, and brain tissues of transgenic APP mice (TgCRND8). Gain-of-function studies of in vitro models revealed that miR-128 not only suppressed the secretion of Aβ but also repressed the phosphorylation of tau protein. Subsequent investigations disclosed that miR-128 directly inhibited the expression of amyloid beta precursor protein binding protein 2 (APPBP2) and glycogen synthase kinase 3 beta (GSK3-β) by binding to their 3’-untranslated regions (UTRs). In the future, we will further explore the suppressive role of miR-128 in AD pathogenesis and clarify its underlying mechanism through in vitro cell models and in vivo TgCRND8 mice. Furthermore, we will also investigate the mechanisms underlying the transcriptional regulation and expression deregulation of miR-128 in AD.

ALL ARE WELCOME