MiR-29a Reduces TIMP-1 Production by Dermal Fibroblasts via Targeting TGF-β Activated Kinase 1 Binding Protein 1, Implications for Systemic Sclerosis
Figure 6
miR-29a reverses phenotype of SSc dermal fibroblasts.
The basal level of col1A1 was compared between HC and SSc fibroblasts (A). SSc dermal fibroblasts were transfected with 30 nM miR-29a, 30 nM cont-miR or stimulated with 5 ng/ml TGF-β and col1A1 mRNA level was measured (B). HC and SSc dermal fibroblasts were transfected with 30 nM miR-29a, 30 nM cont-miR or stimulated with 5 ng/ml TGF-β and secreted TIMP-1 was measured (C). Schematic representation of the role of miR-29a in ECM regulation via TAB1 and TIMP-1 suppression in HC and SSc dermal fibroblasts (D). Enhanced activation of TGF-β signaling in SSc dermal fibroblasts compared to HC fibroblasts results in downregulation of miR-29a, which leads to increased expression of miR-29a target gene - TAB1.