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Progenitor cell fate: fine tuning by blood vessels and oxygen (342.2)
Author(s) -
Hankenson Kurt
Publication year - 2014
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.28.1_supplement.342.2
Subject(s) - mesenchymal stem cell , progenitor cell , regeneration (biology) , microbiology and biotechnology , angiogenesis , cell fate determination , biology , matricellular protein , bone healing , stem cell , anatomy , cancer research , extracellular matrix , biochemistry , gene , transcription factor
Bone regeneration is a complex physiological process that progresses rapidly through distinct cellular and tissue types before ultimately restoring normal bone structure and function. Recent work has begun to demonstrate the essential mechanistic role of the vasculature ‐ and in turn tissue oxygenation ‐ in regulating multiple aspects of bone healing, including influencing progenitor cell differentiation. Dr. Hankenson is a mesenchymal progenitor cell biologist, whom also studies bone regeneration. His most recent work has shown that when expression of the matricellular protein thrombospondin‐2 (TSP2) is disrupted, enhanced vascularization of the early regenerate tissue (soft callus) during the fracture healing process results in differential mesenchymal progenitor cell fate through the regulation of tissue oxygenation. TSP2 is a potent angiogenesis inhibitor highly expressed during tissue regeneration. Under ischemic conditions, enhanced callus vascularization expedites healing. Computational models that consider alterations in TSP2 levels, vascularization, and oxygen gradients in the callus are highly predictive of observed experimental outcomes. These studies will be used as a starting point to discuss the role of tissue oxygenation in regulating mesenchymal cell fate and how these fate decisions impact bone regeneration.