细胞凋亡除了在发育和体内平衡是具有重要性之外，它还牵涉到许多疾病，其中包括动脉粥样硬化。 凋亡的内皮细胞，在粥样硬化板块处的，会将被称作凋亡小体的微泡释放到循环之中，而其量的丰富程度与疾病的负指征相关。
在2009年12月8日的期刊中，Zernecke 等人研究发现，来自内皮细胞的凋亡小体中含有微RNA-126（miR-126），它们会被邻近的血管细胞摄取。 MiR-26增加了来自趋化因子受体CXCR4的信号，而这又触发了自动调节反馈环路，从而导致了CXCL12产生的增加。CXCL12是CXCR4的配基。 CXCL12可限制动脉粥样硬化，而从动脉粥样硬化病人身上分离出的凋亡小体可缩小不同的小鼠动脉粥样硬化模型的粥样斑块的大小。 因此，垂死的内皮细胞会以包裹的微RNA形式向邻近的细胞发出警示信号以触发一个能减少动脉粥样硬化的复原反应。（生物谷Bioon.com）
生物谷推荐原始出处：
Sci. Signal. , 8 December 2009 DOI: 10.1126/scisignal.2000610
Delivery of MicroRNA-126 by Apoptotic Bodies Induces CXCL12-Dependent Vascular Protection
Alma Zernecke1,2*, Kiril Bidzhekov1*, Heidi Noels1*, Erdenechimeg Shagdarsuren1, Lin Gan3, Bernd Denecke3, Mihail Hristov1, Thomas K?ppel4, Maliheh Nazari Jahantigh1, Esther Lutgens1,5, Shusheng Wang6, Eric N. Olson6, Andreas Schober1, and Christian Weber1,5
1 Institute of Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, 52074 Aachen, Germany.
2 Rudolf-Virchow-Center–DFG Research Center for Experimental Biomedicine, University of Würzburg, 97080 Würzburg, Germany.
3 Interdisciplinary Centre for Clinical Research BIOMAT, Department of Vascular Surgery, RWTH Aachen University, 52074 Aachen, Germany.
4 Department of Vascular Surgery, RWTH Aachen University, 52074 Aachen, Germany.
5 Cardiovascular Research Institute Maastricht (CARIM), University of Maastricht, 6200 MD Maastricht, the Netherlands.
6 Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390–9148, USA.
Apoptosis is a pivotal process in embryogenesis and postnatal cell homeostasis and involves the shedding of membranous microvesicles termed apoptotic bodies. In response to tissue damage, the CXC chemokine CXCL12 and its receptor CXCR4 counteract apoptosis and recruit progenitor cells. Here, we show that endothelial cell–derived apoptotic bodies are generated during atherosclerosis and convey paracrine alarm signals to recipient vascular cells that trigger the production of CXCL12. CXCL12 production was mediated by microRNA-126 (miR-126), which was enriched in apoptotic bodies and repressed the function of regulator of G protein (heterotrimeric guanosine triphosphate–binding protein) signaling 16, an inhibitor of G protein–coupled receptor (GPCR) signaling. This enabled CXCR4, a GPCR, to trigger an autoregulatory feedback loop that increased the production of CXCL12. Administration of apoptotic bodies or miR-126 limited atherosclerosis, promoted the incorporation of Sca-1+ progenitor cells, and conferred features of plaque stability on different mouse models of atherosclerosis. This study highlights functions of microRNAs in health and disease that may extend to the recruitment of progenitor cells during other forms of tissue repair or homeostasis.
