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Cardiovasc Res. 2017 May 1;113(6):681-691. doi: 10.1093/cvr/cvx032.

Shear stress-regulated miR-27b controls pericyte recruitment by repressing SEMA6A and SEMA6D.

Author information

Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany.
Institute for Neurology (Edinger Institute), Goethe University, 60528 Frankfurt, Germany.
Medizinische Klinik und Poliklinik I, Ludwig-Maximilians-University Munich, 81377 Munich, Germany.
ZIM III, Department of Cardiology, Goethe University, 60590 Frankfurt am Main, Germany.
Institute of Physiology and Pathophysiology, Division of Cardiovascular Physiology, 69120 Heidelberg, Germany.
German Center of Cardiovascular Research (DZHK), Partnersite Heidelberg, Mannheim, Germany.
German Center of Cardiovascular Research (DZHK), Partnersite Munich, Germany.
German Center of Cardiovascular Research (DZHK), Partnersite RheinMain, Germany.



Vessel maturation involves the recruitment of mural cells such as pericytes and smooth muscle cells. Laminar shear stress is a major trigger for vessel maturation, but the molecular mechanisms by which shear stress affects recruitment of pericytes are unclear. MicroRNAs (miRs) are small non-coding RNAs, which post-transcriptionally control gene expression. The aim of the present study was to unveil the mechanism by which shear stress-regulated microRNAs contribute to vessel maturation.

Methods and results:

Here, we show that laminar shear stress increased miR-27a and miR-27b expression in vitro and in ex vivo in mouse femoral artery explants. Overexpression of miR-27b in endothelial cells increased pericyte adhesion and pericyte recruitment in vitro. In vitro barrier function of endothelial-pericyte co-cultures was augmented by miR-27b overexpression, whereas inhibition of miR-27a/b reduced adhesion and pericyte coverage and decreased barrier functions. In vivo, pharmacological inhibition of miR-27a/b by locked nucleic acid antisense oligonucleotides significantly reduced pericyte coverage and increased water content in the murine uterus. MiR-27b overexpression repressed semaphorins (SEMA), which mediate repulsive signals, and the vessel destabilizing human but not mouse Angiopoietin-2 (Ang-2). Silencing of SEMA6A and SEMA6D rescued the reduced pericyte adhesion by miR-27 inhibition. Furthermore, inhibition of SEMA6D increased barrier function of an endothelial-pericyte co-culture in vitro.


The present study demonstrates for the first time that shear stress-regulated miR-27b promotes the interaction of endothelial cells with pericytes, partly by repressing SEMA6A and SEMA6D.


Endothelial cell; Laminar shear stress; MicroRNA; Pericyte; Semaphorins

[Indexed for MEDLINE]

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