Table 4 ALK5 TGFβ inhibitors downregulate the expression of fibrotic markers following fibrotic nodule formation assay in human primary MPCs.

From: Preclinical validation of TGFβ inhibitors as a novel therapeutic strategy for post-traumatic heterotopic ossification

Treatment Conditions

Relative Gene Expression Levels [Gene/GAPDH]

ACTA2

COL1A1

COL3A1

VIM

Control

1.02 ± 0.15

1.10 ± 0.18

1.15 ± 0.37

1.06 ± 0.18

TGFβ1 10 ng/mL

1.64 ± 0.92

4.62 ± 2.36

2.76 ± 0.96

0.72 ± 0.19

SB431542 1 µM ± TGFβ1

1.18 ± 0.17, p = 0.18

0.95 ± 0.33, p = 0.03

1.21 ± 0.57, p = 0.04

1.18 ± 0.10, p = 0.08

SB431542 3 µM + TGFβ1

0.92 ± 0.24, p = 0.10

0.65 ± 0.27, p = 0.03

0.71 ± 0.26, p = 0.04

1.37 ± 0.22, p = 0.08

LY2157299 1 µM + TGFβ1

1.02 ± 0.18, p = 0.12

1.30 ± 0.37, p = 0.04

1.43 ± 0.86, p = 0.06

1.09 ± 0.26, p = 0.21

LY2157299 3 µM + TGFβ1

1.03 ± 0.16, p = 0.12

0.73 ± 0.19, p = 0.04

0.85 ± 0.11, p = 0.06

1.12 ± 0.28, p = 0.21

Halofuginone 10 nM + TGFβ1

1.42 ± 0.76, p = 0.14

4.80 ± 2.27, p = 0.34

2.47 ± 1.00, p = 0.49

0.84 ± 0.27, p = 0.21

Halofuginone 30 nM + TGFβ1

0.86 ± 0.30, p = 0.06

3.14 ± 1.42, p = 0.04

2.42 ± 1.30, p = 0.48

0.83 ± 0.31, p = 0.32

SIS3 10 µM + TGFβ1

1.43 ± 0.74, p = 0.10

4.46 ± 1.78, p = 0.44

3.27 ± 1.18, p = 0.21

0.82 ± 0.27, p = 0.19

SIS3 20 µM + TGFβ1

2.01 ± 1.24, p = 0.14

5.29 ± 1.56, p = 0.21

3.85 ± 2.46, p = 0.23

0.96 ± 0.10, p = 0.20

  1. Primary MPCs were treated with ALK5 inhibitors (SB431542 or Galunisertib/LY2157299) and SMAD3 inhibitors (Halofuginone or SIS3) and TGFβ [10 ng/mL] for 4 days following fibrotic nodule formation assay conditions. Relative expression levels were analyzed by qRT-PCR for the fibrotic markers ACTA2, COL1A1, COL3A1, and VIM. GAPDH was used as a housekeeping control gene. Non-treated control was used as a reference to calculate relative gene expression levels. DMSO treatment was used as vehicle control. Average ± SE from three to seven independent donors. Adjusted p-value was calculated by 1-tail student’s T-test in comparison with TGFβ treatment alone.
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