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Translating insights from development into regenerative medicine with a focus on Wnt Biology
Author(s) -
Helms Jill Ann
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.202.2
Subject(s) - wnt signaling pathway , bone remodeling , osteoclast , microbiology and biotechnology , osteoblast , regeneration (biology) , bone remodeling period , biology , chondrogenesis , regenerative medicine , osteoporosis , bone healing , cartilage , bioinformatics , neuroscience , stem cell , medicine , signal transduction , anatomy , endocrinology , genetics , in vitro
Substantial progress has been made towards understanding the molecular machinery governing skeletal tissue development, repair, and remodeling. The next challenge is to determine how these findings can be translated into therapeutic strategies to enhance skeletal tissue regeneration. Such therapeutic strategies are oftentimes built upon the basic principles underlying bone development, because it has become increasingly evident that the mechanisms controlling fetal bone formation are similar to the mechanisms regulating adult bone repair and bone remodeling. Only the time scale and the extent/distribution of bone‐forming activity are different. For example, bone remodeling is a life‐long process that occurs within every skeletal element. Conversely, injury‐induced bone repair occurs within a compressed time frame and in a precise location. The cellular and molecular machinery governing osteoblast and osteoclast function, however, are indistinguishable. Consequently, studies that investigate how undifferentiated cells choose a chondrogenic or an osteogenic fate during fetal development provide a “window” into that same decision that occurs as part of adult repair and remodeling. Likewise, high bone mass diseases and osteoporosis are part of a continuum of bone remodeling, representing the extremes of too little or too much bone mass. With this perspective in mind, I will discuss a new perspective we have developed regarding skeletogenesis, viewing it as a cellular program that extends from the fetal period through to the end of life. I will focus on the roles of one pathway in particular, the Wnt family of secreted proteins, and how we have developed a therapeutic strategy to stimulate skeletal healing that is built on the well‐established role for Wnt signaling in stem cell self‐renewal, proliferation, and osteogenic differentiation.