Deletion of the Basement Membrane Heparan Sulfate Proteoglycan Type XVIII Collagen Causes Hypertriglyceridemia in Mice and Humans
Figure 6
Normal vascular distribution of Gpihbp1 in Col18a1−/− mice.
(A) mRNA expression was determined in RNA samples isolated from gonadal fat pad, heart and soleus muscle from wild-type and Col18a1−/− mice (n = 4, for each strain). Results were verified in two independent assays. (B) Primary cardiac endothelial cells were isolated from control (solid line) and Col18a1−/− mice (dashed line) by collagenase digestion and magnetic beads separations using anti-CD31 antibodies. Gpihbp1 was detected with a specific polyclonal antibody and Alexa-488 labeled anti-rabbit secondary antibodies followed by FACS analysis. The curve to the left represents cells incubated with a control IgG and secondary antibodies. Data are representative of 3 separate experiments. (C) Cardiac tissue sections from wild-type, Col18a1−/− and Gpihbp1−/− mice were analyzed by confocal microscopy and compared for differences in the distributions of Lpl (red), Col18 (blue) and the Gpihbp1 (green). The distributions of Lpl and Gpihbp1 overlap with Col18 staining in wild-type heart tissues and are not altered in the Col18a1−/− mutant. The patterns of Lpl and Gpihbp1 staining were unaffected in skeletal muscle and fat (data not shown).