Meyerhoff Graduate Fellows Program

Student Profiles

Atum Buo
Molecular Medicine

Area of Doctoral Study: Orthopaedics; Molecular Medicine Cell Physiology and Pharmacology

Undergraduate Institute: Haverford College

Research Advisor: Joseph Stains, Ph.D.

Description of Research

Our laboratory research generally focuses on intercellular communication among bone cells. The coupling of bone-forming osteoblast cells via gap junctions is critical in maximizing bone formation induced by anabolic growth factors. Of the gap junctional proteins present in human osteoblasts, connexin43 is the most abundantly expressed and is directly responsible for the functional coupling and transfer of information between neighboring osteoblasts. This suggests that connexin43 plays an integral role in enabling osteoblasts to communicate cooperatively and transmit locally generated anabolic signals throughout the skeletal tissue, resulting in optimal bone growth. The work in our lab has been primarily devoted to the study of connexin43 and the signaling mechanisms associated with the connexin43-dependent increase in bone-forming processes. We have extensively shown that signaling pathways involving ERK and protein kinase C delta act as downstream mediators of the connexin43-dependent increase in gene expression of osteogenic factors induced by treating osteoblasts with FGF2. However, whether this effect requires the transmission of second messengers through connexin43 gap junction channels remains unclear as the identity of the upstream signaling cascades involved in this response have not been fully established. Therefore, the focus of my research is to further elucidate the signaling cascades upstream of connexin43 that are activated by anabolic factors such as FGF2. Specifically, I am interested in the contribution of the membrane-associated phospholipase Cgamma1/inositolpolyphosphate signaling cascade to the connexin43-dependent transcriptional response induced by FGF2 in mouse MC3T3 osteoblast cells. By use of various in vitro cell biology techniques, as well as transgenic mouse models, I wish to identify which members of this signaling pathway are essential in propagating the osteogenic gene transcriptional changes mediated by connexin43, as well as establish the physiological relevance of these signaling proteins in vivo. Insight gained from these research endeavors will hopefully shed light on the second messengers that travel through connexin43 channels and ultimately result in enhanced bone growth, thereby identifying novel molecular targets in the battle against debilitating bone disorders.

 

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