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Additional Supporting Information may be found in the online version of this article.

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sc-12-0297_sm_SupplFigure1.tif706KFigure S1. MSCs were recruited to the neointimal tissue in femoral artery injured mice. Left two columns in (A): H&E staining of mouse femoral artery sections prepared from uninjured control, 1 wk (1W) or 2 wks (2W) after wire injury. Scale bars of 1st column: 100μm. Scale bars of 2nd column: 50μm. Right three columns in (A): Triple-immunofluorescence staining for nestin (green), αSMA (red), and DAPI (blue) in mouse femoral artery sections prepared from uninjured control, 1W or 2W after injury. Scale bars: 50μm. I, intima layer; M, media smooth muscle layer; A, adventitia layer. (B) The ratio of intima/media thickness (I/M Ratio). Values are the calculations for 4 mice at each time point. *P<0.001 vs uninjured control group.
sc-12-0297_sm_SupplFigure2.tif57KFigure S2. A schematic diagram illustrating the nestin-Cre;ROSA26-EYFP mouse model. The gene encoding a Cre Recombinase is “knocked into” the endogenous nestin locus. When crossed with the uniform Cre-reporter mouse ROSA26-loxP-stop-loxP-EYFP (ROSA26-EYFP), the Cre enzyme can excise a transcriptional roadblock in front of the EYFP gene, leading to irreversible genetic marking of the Cre-expressing cell and its offspring.
sc-12-0297_sm_SupplFigure3.tif449KFigure S3. TGFβ1 was activated in the arteries following injury. (A) Immunohistochemical staining of active TGFβ1 (brown) in rat carotid arteries at 3 days, 1 wks and 3 wks post injury. 0 hr sample was uninjured control. Scale bars: 50μm. (B) Immunohistochemical staining of active TGFβ1 (brown) in mouse femoral arteries at 3 days, 1 wks and 3 wks post injury. 0 hr sample was uninjured control. Scale bars: 50μm. I, intima layer; M, media smooth muscle layer; A, adventitia layer.
sc-12-0297_sm_SupplFigure4.tif101KFigure S4. Smad- and JNK-signaling pathways were involved in TGFβ- stimulated MSCs migration. Transwell assay for MSCs migration using injured Aorta-CM with addition of various inhibitors and vehicle as indicated. Numbers of migrated cells were counted per FV (magnification 20X). Results means±SD, n=4 per group, *p<0.01 vs. vehicle control.
sc-12-0297_sm_SupplFigure5.tif449KFigure S5. Biotinylated TGFβ1-bound nestin+ cells were not detected in adipose, lung, liver and femoral arteries. Triple-immunofluorescence staining for biotyinylated TGFβ (green), nestin (red), and DAPI (blue) in different tissue sections of mice following biotyinylated TGFβ injection. Scale bar: 50μm.
sc-12-0297_sm_SupplFigure6.tif212KFigure S6. Hypothetical model of the involvement of TGFβ in vascular remodeling following injury. High level of active TGFβ in peripheral blood after vascular injury mobilizes MSCs from bone marrow to peripheral blood (a). TGFβ activation in injured vasculature stimulates the expression of MCP1, leading to the migration and homing of MSCs from the blood circulation to the injured sites (b). MSCs differentiate into either myofibroblasts (c) for neointima formation or endothelial cells (d) for repair.

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