Skip to main content
. 2021 Jun 25;30(22):2082–2099. doi: 10.1093/hmg/ddab159

Figure 3 .

Figure 3

Upregulated expression of DAM and neuroinflammation genes is a feature of Krabbe and SD. Spinal cord was examined as a paradigm of disease. (A) RT-qPCR of total RNA at three stages of disease was studied in twi-2J for Cst7, Ch25h, Apoe, Trem2, CatD, CatB, CatS, Mip-1α, Rantes, C3, C1qa, cIAP1 and cIAP2; (B) RT-qPCR of total RNA of Il1α, Cd4 and Gpnmb in twi-2J at HEP; (C) RT-qPCR of total RNA for the above markers in SD at HEP; (D) Immunoblot of Cst7 in twi-2J and SD at their respective HEP. Two hundred microgram protein homogenate was loaded per lane. Blots were stripped of first antibody and re-probed with anti-α-tubulin; Cst7 dimers (arrow) and monomers (arrowhead). Cystatin F (Cst7), Cholesterol 25-hydroxylase (Ch25h), Apolipoprotein E (Apoe), Triggering receptor expressed on myeloid cells 2 (Trem2), Cathepsin D (CatD), B (CatB), S (CatS), Macrophage inflammatory protein 1 alpha (Mip-1α), Regulated on activation normal T cell expressed and secreted (Rantes), Complement component 3 (C3) and component 1, q subcomponent (C1qa), Cellular Inhibitor of Apoptosis Protein 1 (cIAP1) and 2 (cIAP2), Interleukin 1 alpha (Il1α), Complement component 4B (Cd4) and Glycoprotein non-metastatic melanoma protein B (Gpnmb). mutant (mut), wild type (wt). Student’s t-test; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001.