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. Author manuscript; available in PMC: 2023 Jan 1.
Published in final edited form as: Lipids. 2021 Oct 7;57(1):3–16. doi: 10.1002/lipd.12325

Fig. 5.

Fig. 5.

Relative mRNA levels for multiple genes involved in the regulation of cholesterol homeostasis (a), or that serve as markers of inflammation (b) in the brains of 141-day old Lal+/+ and Lal−/− mice. The details of these analyses are given in Materials and Methods. For each genotype brains were obtained from 2 male and 2 female mice, all of the FVB/N strain. The expression level for each gene in the Lal+/+ mice was arbitrarily set at 1.0 (dashed line) so bars reflect fold-change observed in the Lal−/− mice. Values represent the mean ± SEM. *Significantly different from the value for the Lal+/+ controls (p<0.05). The full name of each gene in the order as it appears in the figure is: Lipa, gene that encodes LAL; Npc2, Niemann-Pick type C2; Npc1, Niemann-Pick type C1; Srebp2, sterol regulatory element-binding protein 2; Hmgcs, 3-hydroxy-3-methylglutaryl coenzyme A synthase; Hmgcr, 3-hydroxy-3-methylglutaryl-coenzyme A reductase; Cyp46a1, cholesterol 24-hydroxylase; Apoe, apolipoprotein E; Ldlr, low-density lipoprotein receptor; Soat1, sterol O-acyltransferase 1 (previously called Acat1); Lcat, lecithin:cholesterol acyltransferase; Abca1, ATP-binding cassette transporter A1; Abca2, ATP-binding cassette transporter A2; Abcg1, ATP-binding cassette transporter G1; Ccl3, chemokine (C-C motif) ligand 3 (also known as Mip1α); TNFα, tumor necrosis factor alpha; ltgax, integrin subunit alpha X (also known as CD11c); Cd14 (Cluster of differentiation 14 antigen).