Delivery of MicroRNA-126 by Apoptotic Bodies Induces CXCL12-Dependent Vascular Protection

Alma Zernecke,* Kiril Bidzhekov, Heidi Noels, Erdenechimeg Shagdarsuren, Lin Gan, Bernd Denecke, Mihail Hristov, Thomas Köppel, Maliheh Nazari Jahantigh, Esther Lutgens, Shusheng Wang, Eric N. Olson, Andreas Schober, Christian Weber*

*To whom correspondence should be addressed. E-mail: cweber{at}ukaachen.de (C.W.) and alma.zernecke{at}virchow.uni-wuerzburg.de. (A.Z.)

This PDF file includes:

• Fig. S1. Identification of the targets of miR-126.
• Fig. S2. Repression of luciferase reporter activity by RGS16, CXCL12, and mutated controls.
• Fig. S3. Comparative analysis of the abundance of RGS3 and RGS16.
• Fig. S4. Increased abundance of RGS16 in transfected HUVECs.
• Fig. S5. CXCL12-mediated phosphorylation of ERK1/2 in HUVECs.
• Fig. S6. Generation of apoptotic bodies by apoptotic HUVECs.
• Fig. S7. Apoptotic bodies do not mobilize monocytes or neutrophils to peripheral blood.
• Fig. S8. Sparse colocalization of Sca-1 with macrophages in atherosclerotic lesions of mice treated with apoptotic bodies.
• Fig. S9. Apoptotic bodies isolated from human plaques and from mouse blood contain miR-126.
• Fig. S10. Apoptotic bodies specifically inhibit apoptosis and induce the proliferation of HUVECs.
• Table S1. The expression of miRNAs in SMCs.

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© 2009 American Association for the Advancement of Science