Skip to main content
Figure 5 | BMC Developmental Biology

Figure 5

From: Selective reconstitution of liver cholesterol biosynthesis promotes lung maturation but does not prevent neonatal lethality in Dhcr7 null mice

Figure 5

Sterol analyses of lung tissues from wild-type, knockout and knockout- transgenic pups. Panel A shows that cholesterol level in lung tissues was restored to normal by the liver transgene expression (to 2.51 ± 0.71 mg/g tissue) in Dhcr7-/-Tg+ lungs and was not statistically different from WT lungs (of 3.06 ± 0.40 mg/g tissue), while the non-transgenic-KO lungs exhibited significant cholesterol deficiency (1.25 ± 0.44 mg/g tissue). Cholesterol level in lungs from Dhcr7+/+Tg+ littermates was 3.18 ± 0.54 mg/g tissue (data not shown). Panel B shows that this also led to a fall in precursor sterols (0.88 ± 0.30 mg/g tissue in Dhcr7-/-Tg+ cf 1.39 ± 0.22 mg/g tissue in Dhcr7-/-Tg-), with a significant fall in the percentage of precursor sterol in the lung tissues of the transgenic-KO mice (25 ± 8 %, compared to 53 ± 5 % in Dhcr7-/-Tg- mice, p < 0.001, Panel C). There was no significant difference (p > 0.05) in total sterols among the three groups (lung total sterols mg/g tissue: 3.10 ± 0.40 in WT, 2.64 ± 0.62 in Dhcr7-/-Tg- and 3.59 ± 1.08 in Dhcr7-/-Tg+, data not shown). Error bars represent mean ± SD.

Back to article page