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Table 3 Genes associated with primary neuropathological pathways

From: Mice defective in interferon signaling help distinguish between primary and secondary pathological pathways in a mouse model of neuronal forms of Gaucher disease

Gene

WT + CBE versus WT + PBS

WT + CBE versus

MyTrMaSt + PBS

CBE + SRT

 

Fold-change

Fold-change

 

SL metabolism

Ugt8a

− 3.46

− 3.97

++

Fa2h

− 2.00

− 2.00

++

Gal3st1

− 2.42

− 1.33

n.s.

Cholesterol metabolism

Msmo1

− 2.28

− 2.27

++

Ch25h

20.3

12.8

+

Dhcr7

− 2.78

− 1.62

n.s.

Tm7sf2

− 2.05

− 1.44

n.s.

Hmgcs1

− 2.63

− 2.07

n.s.

Fdps

− 2.90

− 2.10

n.s.

Lipoprotein metabolism and lipid droplets

Apoc1

2.76

2.42

++

Plin21

5.57

2.90

++

Plin4

9.97

41.3

++

Apoe

1.85

1.56

+

Metalloproteinases

Adam8

6.20

5.20

+

Mt11

3.80

3.40

++

Mt2

6.30

4.80

++

Lysosome

Gusb1

6.08

5.88

n.s.

Hexb

3.43

3.17

+

Naglu

2.60

2.27

+

CtsD1

4.48

4.68

+

Ctsz

6.62

5.30

+

Galns

2.88

2.39

n.s.

Neuronal genes

Ccdc160

− 2.33

− 2.11

n.s.

Glra1

− 2.04

− 2.63

n.s.

Srpk1

− 2.45

− 2.05

n.s.

Inflammation (chemokines)

Ccl3

39.7

55.5

+

Ccl4

49.2

32.7

+

Cx3cr11

3.70

2.10

n.s.

Inflammation (TNF)

Tnfrsf1a

3.02

4.68

+

Tnfaip8l2

4.08

4.02

+

Slamf9

16.1

15.0

+

Ltbr

2.33

3.08

n.s.

Litaf

3.32

2.32

n.s.

Inflammation (TGF)

Tgfbr2

2.02

2.81

n.s.

Cd109

8.53

10.4

++

Inflammation (IL6)

Il6ra

5.03

3.08

n.s.

Osmr

4.73

9.70

+

Inflammation (Microglia)

Lyz2

13.2

7.80

+

Mpeg1

9.07

11.5

+

Cd68

8.08

13.9

+

Inflammation (Astrocytes)

Agt

2.10

2.80

n.s.

Gfap

9.86

9.69

+

Complement

C1qa

4.16

4.61

+

C1qb

5.55

5.11

+

C1qc

7.53

5.17

+

C4b

7.35

7.08

+

C5ar11

27. 7

14.8

+

DAMs

Trem2

6.12

8.88

+

Tyrobp1

6.65

6.55

+

Cd63

3.70

3.20

+

Clec7a

43.9

31.3

+

Csf1

3.14

2.20

-

Itgax

61.1

39.6

-

Others

St14

3.28

4.85

-

Mrpl35

− 2.33

− 2.03

n.s.

  1. Genes whose levels were changed < 2-fold in MyTrMaSt mice compared with WT mice. Fold-changes were all statistically significant (p < 0.01). The right-hand column indicates genes that reverted to control levels upon SRT (from Blumenreich et al., submitted for publication; see Discussion).
  2. n.s. not significant
  3. 1 Validated by PCR: WT + CBE versus WT + PBS, fold-change 7.9 ± 3.1 (Plin2), 1.8 ± 0.2 (Mt1), 5.9 ± 1.4 (Gusb), 5.9 ± 1.4 (CtsD), 3.1 ± 0.6 (Cx3cr1), 31.4 ± 3.8 (C5ar1), 11.4 ± 3.0 (Tyrobp). MyTrMaSt + CBE versus MyTrMaSt + PBS, fold-change 4.1 ± 1.3 (Plin2), 1.9 ± 0.2 (Mt1), 6.7 ± 0.5 (Gusb), 5.2 ± 0.5 (CtsD), 3.2 ± 0.4 (Cx3cr1), 15.9 ± 1.2 (C5ar1), 9.1 ± 0.5 (Tyrobp)
  4. + Genes whose expression were reduced upon SRT, yet remained upregulated
  5. ++ Genes that reverted to control levels upon SRT
  6. - Genes whose expression was not affected upon SRT