Divergent modulation of adipose-derived stromal cell differentiation by TGF-beta1 based on species of derivation.
BACKGROUND
Adipose-derived stromal cells hold promise for skeletal tissue engineering. However, various studies have observed that adipose-derived stromal cells differ significantly in their biology depending on species of derivation. In the following study, the authors sought to determine the species-specific response of adipose-derived stromal cells to recombinant TGF-beta1 (rTGF-beta1).


METHODS
Adipose-derived stromal cells were derived from mouse and human sources. Recombinant TGF-beta1 was added to culture medium (2.5 to 10 ng/ml); proliferation and osteogenic and adipogenic differentiation were assessed by standardized parameters, including cell counting, alkaline phosphatase, alizarin red, oil red O staining, and quantitative real-time polymerase chain reaction.


RESULTS
Recombinant TGF-beta1 was found to significantly repress cellular proliferation in both mouse and human adipose-derived stromal cells (p < 0.01). Recombinant TGF-beta1 was found to significantly repress osteogenic differentiation in mouse adipose-derived stromal cells. In contrast, osteogenic differentiation of human adipose-derived stromal cells proceeded unimpeded in either the presence or the absence of rTGF-beta1. Interestingly, rTGF-beta1 induced expression of a number of osteogenic genes in human adipose-derived stromal cells, including BMP2 and BMP4.


CONCLUSIONS
The authors' results further detail an important facet in which mouse and human adipose-derived stromal cells differ. Mouse adipose-derived stromal cell osteogenesis is completely inhibited by rTGF-beta1, whereas human adipose-derived stromal cell osteogenesis progresses in the presence of rTGF-beta1. These data highlight the importance of species of derivation in basic adipose-derived stromal cell biology. Future studies will examine in more detail the species-specific differences among adipose-derived stromal cell populations.
Levi
Benjamin
B
Stanford and San Francisco, Calif.; and Ann Arbor, Mich. From the Hagey Pediatric Regenerative Research Laboratory, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine; the School of Medicine, University of California, San Francisco; and the Division of Plastic Surgery, Department of General Surgery, University of Michigan.
James
Aaron W
AW
Xu
Yue
Y
Commons
George W
GW
Longaker
Michael T
MT
D000273:Adipose Tissue / Q000166:cytology* / Q000187:drug effects; D000818:Animals; D019485:Bone Morphogenetic Proteins / Q000032:analysis / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology*; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D017077:Culture Media, Conditioned; D005260:Female; D006801:Humans; D051379:Mice; D008815:Mice, Inbred Strains; D010012:Osteogenesis / Q000187:drug effects / Q000502:physiology; D016133:Polymerase Chain Reaction; D011336:Probability; D012313:RNA / Q000032:analysis; D012038:Regeneration / Q000502:physiology; D013045:Species Specificity; D017154:Stromal Cells / Q000187:drug effects / Q000502:physiology*; D020858:Tissue and Organ Harvesting; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology*; D014182:Transplantation, Autologous
D019485:Bone Morphogenetic Proteins; D017077:Culture Media, Conditioned; D053773:Transforming Growth Factor beta1; D012313:RNA