Figure 7.

SPARC and ASC migration. (A): Activation of ASC motility by recombinant human SPARC and hPep, compared with untreated cells (mock) and cont peptide, assayed by quantification of cell transmigration through 5-µm-pore membranes. Shown are numbers (±SEM) of migrated cells within 24 hours from quadruplicate wells. *, statistically significant (p < .03) increase in cell migration over levels observed for cont peptide. (B): A model for SPARC function in white adipose tissue (WAT). ASC reside in the perivascular niche via firm adhesion to the ECM/BM through α5β1 integrin. SPARC (SPARC+) maintains balance among ASC quiescence, proliferation, and differentiation: nutrients supplied through systemic circulation result in ASC lipogenesis and their differentiation into adipocytes that secrete SPARC, leading to deadhesion and proliferation/migration of other uncommitted ASC. Thus, upon continuous nutrient input, adipogenesis is accompanied by concomitant proliferation and migration of ASC for their incorporation into WAT neovasculature, resulting in tissue growth. In the absence of SPARC (SPARC−), ASC differentiate into adipocytes that do not secrete SPARC, which promotes ECM/BM attachment of ASC, hence shifting the balance toward extended lipogenesis, resulting in adipocyte hypertrophy. Arrows, cell fates; red line, point at which SPARC interferes with the interaction between α5β1 and ECM. Abbreviations: ASC, adipose stem cells; BM, basement membrane; cont, control; ECM, extracellular matrix.