Fig 1: Angiogenic capacity and FSP27 mRNA expression of subcutaneous fat after weight‐loss. A, Longitudinally, paired fat tissue explants demonstrated increased angiogenic growth in subcutaneous depots after weight‐loss (B) mRNA expression of FSP27 increased following weight loss and (C) positively correlated with angiogenic sprouting (n=7, P<0.05). au indicates arbitrary units; FSP27, fat‐specific protein 27. *indicates statistical significance, such as P < 0.05.
Fig 2: Insulin‐mediated activation of eNOS (endothelial NO synthase) and AKT (protein Kinase B) in response to recombinant FSP27 in visceral depot. A, Representative visceral adipose tissue immunoblot demonstrating severe impairment in insulin‐mediated activation of eNOS and AKT in visceral fat. After 24 hours of rFSP27 (recombinant FSP27) exposure, insulin‐mediated activation is restored. B, Quantification of percent change in insulin‐mediated activation of eNOS at baseline and after 24 hours of treatment with rFSP27 in the visceral depot. C, Quantification of percent change in insulin‐mediated activation of AKT at baseline and after 24 hours of treatment with rFSP27 in the visceral depot (n=10, P<0.05). Data are presented as arbitrary units (au) and as mean±SEM. rFSP27 indicates recombinant fat‐specific protein 27. *indicates statistical significance, such as P < 0.05.
Fig 3: Comparison of FSP27 (fat‐specific protein 27) protein in primary endothelial cells from subcutaneous vs visceral fat of obese subjects. A, Representative immunofluorescence image of isolated endothelial cells demonstrating significantly reduced expression of FSP27 protein (red=FSP27, green=CD31, endothelial cell marker, blue=DAPI, a nuclear stain) in endothelial cells isolated from visceral compared with subcutaneous depots from obese subjects. B, Quantification of FSP27 protein expression in endothelial cells isolated from subcutaneous and visceral fat (n=14, P<0.01). Data are presented as arbitrary units and as mean±SEM, indexed to 1 for the subcutaneous depot. *indicates statistical significance, such as P < 0.05.
Fig 4: Insulin‐mediated activation of eNOS (endothelial NO synthase) and AKT (protein Kinase B) in response to siRNA‐mediated knockdown of FSP27 in the subcutaneous depot. A, Representative immunoblot demonstrating insulin‐mediated activation of eNOS and AKT in subcutaneous fat under scrambled siRNA (small interfering RNA) conditions and after knockdown of FSP27 by siRNA. B, Quantification of percent change in insulin‐mediated activation of eNOS at baseline and after siRNA‐mediated knockdown of FSP27 in the subcutaneous fat depot. C, Quantification of percent change in insulin‐mediated activation of AKT at baseline and after siRNA‐mediated knockdown of FSP27 in subcutaneous fat depot (n=10, P<0.05). Data are presented as arbitrary units and as mean±SEM. FSP27 indicates fat‐specific protein 27. *indicates statistical significance, such as P < 0.05.
Fig 5: Endothelium‐dependent, insulin‐mediated vasodilation of adipose arterioles from visceral fat. Endothelium‐dependent, insulin‐mediated vasodilation was severely impaired in arterioles from visceral depot (circle). Within an hour of treatment with human recombinant FSP27 (5‐nmol/L) endothelium‐dependent, insulin‐mediated vasodilation of arterioles from the visceral depot improved significantly (square). The improvement in vasodilation with recombinant FSP27 was completely blocked by N(ω)‐nitro‐L‐arginine methyl ester (L‐NAME) (triangle). (n=10 vessels, by repeated measures ANOVA P<0.01). Data are presented as mean±SEM. ET indicates endothelin; pap, papaverine. *indicates statistical significance, such as P < 0.05.
Supplier Page from Abcam for Recombinant Human FSP27 protein