The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Hetty C De Boer - One of the best experts on this subject based on the ideXlab platform.
-
aspirin treatment hampers the use of plasma microrna 126 as a biomarker for the progression of vascular disease
European Heart Journal, 2013Co-Authors: Hetty C De Boer, Jacques M G J Duijs, Coen Van Solingen, Ton J Rabelink, Jurrien Prins, Menno V Huisman, Anton Jan Van ZonneveldAbstract:Aims MicroRNA-126 (Mir-126) facilitates angiogenesis and regulates endothelial cell function. Recent data suggest that Mir-126 can serve as a biomarker for vascular disease. Although endothelial cells are enriched for Mir-126, platelets also contain Mir-126. In this paper, we investigated the contribution of platelets to the pool of Mir-126 in plasma of patients with type 2 diabetes (DM2) and how this is affected by aspirin. Methods and results In vitro platelet activation resulted in the transfer of Mir-126 from the platelet to the plasma compartment, which was prevented by aspirin. In vivo platelet activation, monitored in patients with DM2 by measuring soluble P-selectin, correlated directly with circulating levels of Mir-126. The administration of aspirin resulted both in platelet inhibition and concomitantly reduced circulating levels of platelet-derived microRNAs including Mir-126. Conclusion Platelets are a major source of circulating Mir-126. Consequently, in patho-physiological conditions associated with platelet activation, such as diabetes type 2, the administration of aspirin may lead to reduced levels of circulating Mir-126. Thus, the use of platelet inhibitors should be taken into account when using plasma levels of Mir-126 as a biomarker.
-
microrna 126 modulates endothelial sdf 1 expression and mobilization of sca 1 lin progenitor cells in ischaemia
Cardiovascular Research, 2011Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Matthieu Monge, Paul H A Quax, Hetty C De Boer, Annemarie M Van Oeverenrietdijk, Margreet R De Vries, Van Der Veer Eric Peter, Ton J RabelinkAbstract:Aims MicroRNA-126 (Mir-126), which is enriched in endothelial cells, plays a role in angiogenesis. Based on the seed sequence, Mir-126 can also be predicted to regulate vasculogenesis by modulating the endothelial expression of stromal cell-derived factor-1 (SDF-1). Methods and results Using miR-reporter constructs, we first validated that Mir-126 inhibits SDF-1 expression in endothelial cells in vitro . Next, we investigated the potential relevance of this observation with respect to the mobilization of progenitor cells. For this, we studied the migration of human CD34+ progenitor cells towards chemotactic factors present in endothelial cell-conditioned medium. Antagomir-induced silencing of Mir-126 elevated SDF-1 expression by human umbilical vein endothelial cells and enhanced migration of the CD34+ cells. In a murine model of hind limb ischaemia, a striking increase in the number of circulating Sca-1+/Lin− progenitor cells in antagoMir-126-treated mice was observed when compared with scramblemir-treated controls. Immunohistochemical staining of capillaries in the post-ischaemic gastrocnemius muscle of Mir-126-silenced mice revealed elevated SDF-1 expressing CD31-positive capillaries, whereas a mobilizing effect of Mir-126 inhibition was not detected in healthy control animals. Conclusion Mir-126 can regulate the expression of SDF-1 in endothelial cells. In the context of an ischaemic event, systemic silencing of Mir-126 leads to the mobilization of Sca-1+/Lin− progenitor cells into the peripheral circulation, potentially in response to elevated SDF-1 expression by endothelial cells present in the ischaemic tissue.
-
antagomir mediated silencing of endothelial cell specific microrna 126 impairs ischemia induced angiogenesis
Journal of Cellular and Molecular Medicine, 2009Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Jacques M G J Duijs, Marko K Roeten, Annemarie M Van Oeverenrietdijk, Matthieu Monge, Hetty C De Boer, Hans J Baelde, Paul H A QuaxAbstract:MicroRNAs are negative regulators of gene expression that play a key role in cell-type specific differentiation and modulation of cell function and have been proposed to be involved in neovascularization. Previously, using an extensive cloning and sequencing approach, we identified Mir-126 to be specifically and highly expressed in human endothelial cells (EC). Here, we demonstrate EC-specific expression of Mir-126 in capillaries and the larger vessels in vivo. We therefore explored the potential role of Mir-126 in arteriogenesis and angiogenesis. Using miR-reporter constructs, we show that Mir-126 is functionally active in EC in vitro and that it could be specifically repressed using antagomirs specifically targeting Mir-126. To study the consequences of Mir-126 silencing on vascular regeneration, mice were injected with a single dose of antagoMir-126 or a control ‘scramblemir’ and exposed to ischemia of the left hindlimb by ligation of the femoral artery. Although Mir-126 was effectively silenced in mice treated with a single, high dose (HD) of antagoMir-126, laser Doppler perfusion imaging did not show effects on blood flow recovery. In contrast, quantification of the capillary density in the gastrocnemius muscle revealed that mice treated with a HD of antagoMir-126 had a markedly reduced angiogenic response. Aortic explant cultures of the mice confirmed the role of Mir-126 in angiogenesis. Our data demonstrate a facilitary function for Mir-126 in ischemia-induced angiogenesis and show the efficacy and specificity of antagomir-induced silencing of EC-specific microRNAs in vivo.
-
antagomir mediated silencing of endothelial cell specific microrna 126 impairs ischemia induced angiogenesis
Journal of Cellular and Molecular Medicine, 2009Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Jacques M G J Duijs, Marko K Roeten, Matthieu Monge, Hans J Baelde, Annemarie M Van Oeverenrietdijk, Joost B Vos, Hetty C De BoerAbstract:MicroRNAs are negative regulators of gene expression that play a key role in cell-type specific differentiation and modulation of cell function and have been proposed to be involved in neovascularization. Previously, using an extensive cloning and sequencing approach, we identified Mir-126 to be specifically and highly expressed in human endothelial cells (EC). Here, we demonstrate EC-specific expression of Mir-126 in capillaries and the larger vessels in vivo. We therefore explored the potential role of Mir-126 in arteriogenesis and angiogenesis. Using miR-reporter constructs, we show that Mir-126 is functionally active in EC in vitro and that it could be specifically repressed using antagomirs specifically targeting Mir-126. To study the consequences of Mir-126 silencing on vascular regeneration, mice were injected with a single dose of antagoMir-126 or a control 'scramblemir' and exposed to ischemia of the left hindlimb by ligation of the femoral artery. Although Mir-126 was effectively silenced in mice treated with a single, high dose (HD) of antagoMir-126, laser Doppler perfusion imaging did not show effects on blood flow recovery. In contrast, quantification of the capillary density in the gastrocnemius muscle revealed that mice treated with a HD of antagoMir-126 had a markedly reduced angiogenic response. Aortic explant cultures of the mice confirmed the role of Mir-126 in angiogenesis. Our data demonstrate a facilitary function for Mir-126 in ischemia-induced angiogenesis and show the efficacy and specificity of antagomir-induced silencing of EC-specific microRNAs in vivo. © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Shu Chien - One of the best experts on this subject based on the ideXlab platform.
-
regulation of vascular smooth muscle cell turnover by endothelial cell secreted microrna 126 role of shear stress
Circulation Research, 2013Co-Authors: Jing Zhou, Phu Nguyen, Kuei Chun Wang, Anna Weiss, Jeng Jiann Chiu, John Y J Shyy, Yichun Kuo, Shu ChienAbstract:Rationale: Endothelial microRNA-126 (Mir-126) modulates vascular development and angiogenesis. However, its role in the regulation of smooth muscle cell (SMC) function is unknown. Objective: To elucidate the role of Mir-126 secreted by endothelial cells (ECs) in regulating SMC turnover in vitro and in vivo, as well as the effects of shear stress on the regulation. Methods and Results: Coculture of SMCs with ECs or treatment of SMCs with conditioned media from static EC monoculture (EC-CM) increased SMC Mir-126 level and SMC turnover; these effects were abolished by inhibition of endothelial Mir-126 and by the application of laminar shear stress to ECs. SMC Mir-126 did not increase when treated with EC-CM from ECs subjected to inhibition of miR biogenesis, or with CM from sheared ECs. Depletion of extracellular/secreted vesicles in EC-CM did not affect the increase of SMC Mir-126 by EC-CM. Biotinylated Mir-126 or FLAG (DYKDDDDK epitope)-tagged Argonaute2 transfected into ECs was detected in the cocultured or EC-CM–treated SMCs, indicating a direct EC-to-SMC transmission of Mir-126 and Argonaute2. Endothelial Mir-126 represses forkhead box O3, B-cell lymphoma 2, and insulin receptor substrate 1 mRNAs in the cocultured SMCs, suggesting the functional roles of the transmitted Mir-126. Systemic depletion of Mir-126 in mice inhibited neointimal lesion formation of carotid arteries induced by cessation of blood flow. Administration of EC-CM or Mir-126 mitigated the inhibitory effect. Conclusions: Endothelial Mir-126 acts as a key intercellular mediator to increase SMC turnover, and its release is reduced by atheroprotective laminar shear stress.
-
regulation of vascular smooth muscle cell turnover by endothelial cell secreted microrna 126 role of shear stress
Circulation Research, 2013Co-Authors: Jing Zhou, Yi Shuan Li, Phu Nguyen, Kuei Chun Wang, Anna Weiss, Jeng Jiann Chiu, John Y J Shyy, Shu ChienAbstract:Rationale: Endothelial microRNA-126 (Mir-126) modulates vascular development and angiogenesis. However, its role in the regulation of smooth muscle cell (SMC) function is unknown. Objective: To elucidate the role of Mir-126 secreted by endothelial cells (ECs) in regulating SMC turnover in vitro and in vivo, as well as the effects of shear stress (SS) on the regulation. Methods and Results: Co-culture of SMCs with ECs or treatment of SMCs with conditioned media from static EC monoculture (EC-CM) increased SMC Mir-126 level and SMC turnover; these effects were abolished by inhibition of endothelial Mir-126 and by the application of laminar SS (LSS) to ECs. SMC Mir-126 did not increase when treated with EC-CM from ECs subjected to inhibition of miR biogenesis, nor with CM from sheared ECs. Depletion of extracellular/secreted vesicles in EC-CM did not affect the increase of SMC Mir-126 by EC-CM. Biotinylated Mir-126 or FLAG-tagged Ago2 transfected into ECs were detected in the co-cultured or EC-CM treated SMCs, indicating a direct EC-to-SMC transmission of Mir-126 and Ago2. Endothelial Mir-126 represses FOXO3, BCL2, and IRS1 mRNAs in the co-cultured SMCs, suggesting the functional roles of the transmitted Mir-126. Systemic depletion of Mir-126 in mice inhibited neointimal lesion formation of carotid arteries induced by cessation of blood flow. Administration of EC-CM or Mir-126 mitigated the inhibitory effect. Conclusions: Endothelial Mir-126 acts as a key intercellular mediator to increase SMC turnover, and its release is reduced by atheroprotective LSS.
Jacques M G J Duijs - One of the best experts on this subject based on the ideXlab platform.
-
aspirin treatment hampers the use of plasma microrna 126 as a biomarker for the progression of vascular disease
European Heart Journal, 2013Co-Authors: Hetty C De Boer, Jacques M G J Duijs, Coen Van Solingen, Ton J Rabelink, Jurrien Prins, Menno V Huisman, Anton Jan Van ZonneveldAbstract:Aims MicroRNA-126 (Mir-126) facilitates angiogenesis and regulates endothelial cell function. Recent data suggest that Mir-126 can serve as a biomarker for vascular disease. Although endothelial cells are enriched for Mir-126, platelets also contain Mir-126. In this paper, we investigated the contribution of platelets to the pool of Mir-126 in plasma of patients with type 2 diabetes (DM2) and how this is affected by aspirin. Methods and results In vitro platelet activation resulted in the transfer of Mir-126 from the platelet to the plasma compartment, which was prevented by aspirin. In vivo platelet activation, monitored in patients with DM2 by measuring soluble P-selectin, correlated directly with circulating levels of Mir-126. The administration of aspirin resulted both in platelet inhibition and concomitantly reduced circulating levels of platelet-derived microRNAs including Mir-126. Conclusion Platelets are a major source of circulating Mir-126. Consequently, in patho-physiological conditions associated with platelet activation, such as diabetes type 2, the administration of aspirin may lead to reduced levels of circulating Mir-126. Thus, the use of platelet inhibitors should be taken into account when using plasma levels of Mir-126 as a biomarker.
-
antagomir mediated silencing of endothelial cell specific microrna 126 impairs ischemia induced angiogenesis
Journal of Cellular and Molecular Medicine, 2009Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Jacques M G J Duijs, Marko K Roeten, Annemarie M Van Oeverenrietdijk, Matthieu Monge, Hetty C De Boer, Hans J Baelde, Paul H A QuaxAbstract:MicroRNAs are negative regulators of gene expression that play a key role in cell-type specific differentiation and modulation of cell function and have been proposed to be involved in neovascularization. Previously, using an extensive cloning and sequencing approach, we identified Mir-126 to be specifically and highly expressed in human endothelial cells (EC). Here, we demonstrate EC-specific expression of Mir-126 in capillaries and the larger vessels in vivo. We therefore explored the potential role of Mir-126 in arteriogenesis and angiogenesis. Using miR-reporter constructs, we show that Mir-126 is functionally active in EC in vitro and that it could be specifically repressed using antagomirs specifically targeting Mir-126. To study the consequences of Mir-126 silencing on vascular regeneration, mice were injected with a single dose of antagoMir-126 or a control ‘scramblemir’ and exposed to ischemia of the left hindlimb by ligation of the femoral artery. Although Mir-126 was effectively silenced in mice treated with a single, high dose (HD) of antagoMir-126, laser Doppler perfusion imaging did not show effects on blood flow recovery. In contrast, quantification of the capillary density in the gastrocnemius muscle revealed that mice treated with a HD of antagoMir-126 had a markedly reduced angiogenic response. Aortic explant cultures of the mice confirmed the role of Mir-126 in angiogenesis. Our data demonstrate a facilitary function for Mir-126 in ischemia-induced angiogenesis and show the efficacy and specificity of antagomir-induced silencing of EC-specific microRNAs in vivo.
-
antagomir mediated silencing of endothelial cell specific microrna 126 impairs ischemia induced angiogenesis
Journal of Cellular and Molecular Medicine, 2009Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Jacques M G J Duijs, Marko K Roeten, Matthieu Monge, Hans J Baelde, Annemarie M Van Oeverenrietdijk, Joost B Vos, Hetty C De BoerAbstract:MicroRNAs are negative regulators of gene expression that play a key role in cell-type specific differentiation and modulation of cell function and have been proposed to be involved in neovascularization. Previously, using an extensive cloning and sequencing approach, we identified Mir-126 to be specifically and highly expressed in human endothelial cells (EC). Here, we demonstrate EC-specific expression of Mir-126 in capillaries and the larger vessels in vivo. We therefore explored the potential role of Mir-126 in arteriogenesis and angiogenesis. Using miR-reporter constructs, we show that Mir-126 is functionally active in EC in vitro and that it could be specifically repressed using antagomirs specifically targeting Mir-126. To study the consequences of Mir-126 silencing on vascular regeneration, mice were injected with a single dose of antagoMir-126 or a control 'scramblemir' and exposed to ischemia of the left hindlimb by ligation of the femoral artery. Although Mir-126 was effectively silenced in mice treated with a single, high dose (HD) of antagoMir-126, laser Doppler perfusion imaging did not show effects on blood flow recovery. In contrast, quantification of the capillary density in the gastrocnemius muscle revealed that mice treated with a HD of antagoMir-126 had a markedly reduced angiogenic response. Aortic explant cultures of the mice confirmed the role of Mir-126 in angiogenesis. Our data demonstrate a facilitary function for Mir-126 in ischemia-induced angiogenesis and show the efficacy and specificity of antagomir-induced silencing of EC-specific microRNAs in vivo. © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Coen Van Solingen - One of the best experts on this subject based on the ideXlab platform.
-
aspirin treatment hampers the use of plasma microrna 126 as a biomarker for the progression of vascular disease
European Heart Journal, 2013Co-Authors: Hetty C De Boer, Jacques M G J Duijs, Coen Van Solingen, Ton J Rabelink, Jurrien Prins, Menno V Huisman, Anton Jan Van ZonneveldAbstract:Aims MicroRNA-126 (Mir-126) facilitates angiogenesis and regulates endothelial cell function. Recent data suggest that Mir-126 can serve as a biomarker for vascular disease. Although endothelial cells are enriched for Mir-126, platelets also contain Mir-126. In this paper, we investigated the contribution of platelets to the pool of Mir-126 in plasma of patients with type 2 diabetes (DM2) and how this is affected by aspirin. Methods and results In vitro platelet activation resulted in the transfer of Mir-126 from the platelet to the plasma compartment, which was prevented by aspirin. In vivo platelet activation, monitored in patients with DM2 by measuring soluble P-selectin, correlated directly with circulating levels of Mir-126. The administration of aspirin resulted both in platelet inhibition and concomitantly reduced circulating levels of platelet-derived microRNAs including Mir-126. Conclusion Platelets are a major source of circulating Mir-126. Consequently, in patho-physiological conditions associated with platelet activation, such as diabetes type 2, the administration of aspirin may lead to reduced levels of circulating Mir-126. Thus, the use of platelet inhibitors should be taken into account when using plasma levels of Mir-126 as a biomarker.
-
microrna 126 modulates endothelial sdf 1 expression and mobilization of sca 1 lin progenitor cells in ischaemia
Cardiovascular Research, 2011Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Matthieu Monge, Paul H A Quax, Hetty C De Boer, Annemarie M Van Oeverenrietdijk, Margreet R De Vries, Van Der Veer Eric Peter, Ton J RabelinkAbstract:Aims MicroRNA-126 (Mir-126), which is enriched in endothelial cells, plays a role in angiogenesis. Based on the seed sequence, Mir-126 can also be predicted to regulate vasculogenesis by modulating the endothelial expression of stromal cell-derived factor-1 (SDF-1). Methods and results Using miR-reporter constructs, we first validated that Mir-126 inhibits SDF-1 expression in endothelial cells in vitro . Next, we investigated the potential relevance of this observation with respect to the mobilization of progenitor cells. For this, we studied the migration of human CD34+ progenitor cells towards chemotactic factors present in endothelial cell-conditioned medium. Antagomir-induced silencing of Mir-126 elevated SDF-1 expression by human umbilical vein endothelial cells and enhanced migration of the CD34+ cells. In a murine model of hind limb ischaemia, a striking increase in the number of circulating Sca-1+/Lin− progenitor cells in antagoMir-126-treated mice was observed when compared with scramblemir-treated controls. Immunohistochemical staining of capillaries in the post-ischaemic gastrocnemius muscle of Mir-126-silenced mice revealed elevated SDF-1 expressing CD31-positive capillaries, whereas a mobilizing effect of Mir-126 inhibition was not detected in healthy control animals. Conclusion Mir-126 can regulate the expression of SDF-1 in endothelial cells. In the context of an ischaemic event, systemic silencing of Mir-126 leads to the mobilization of Sca-1+/Lin− progenitor cells into the peripheral circulation, potentially in response to elevated SDF-1 expression by endothelial cells present in the ischaemic tissue.
-
antagomir mediated silencing of endothelial cell specific microrna 126 impairs ischemia induced angiogenesis
Journal of Cellular and Molecular Medicine, 2009Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Jacques M G J Duijs, Marko K Roeten, Matthieu Monge, Hans J Baelde, Annemarie M Van Oeverenrietdijk, Joost B Vos, Hetty C De BoerAbstract:MicroRNAs are negative regulators of gene expression that play a key role in cell-type specific differentiation and modulation of cell function and have been proposed to be involved in neovascularization. Previously, using an extensive cloning and sequencing approach, we identified Mir-126 to be specifically and highly expressed in human endothelial cells (EC). Here, we demonstrate EC-specific expression of Mir-126 in capillaries and the larger vessels in vivo. We therefore explored the potential role of Mir-126 in arteriogenesis and angiogenesis. Using miR-reporter constructs, we show that Mir-126 is functionally active in EC in vitro and that it could be specifically repressed using antagomirs specifically targeting Mir-126. To study the consequences of Mir-126 silencing on vascular regeneration, mice were injected with a single dose of antagoMir-126 or a control 'scramblemir' and exposed to ischemia of the left hindlimb by ligation of the femoral artery. Although Mir-126 was effectively silenced in mice treated with a single, high dose (HD) of antagoMir-126, laser Doppler perfusion imaging did not show effects on blood flow recovery. In contrast, quantification of the capillary density in the gastrocnemius muscle revealed that mice treated with a HD of antagoMir-126 had a markedly reduced angiogenic response. Aortic explant cultures of the mice confirmed the role of Mir-126 in angiogenesis. Our data demonstrate a facilitary function for Mir-126 in ischemia-induced angiogenesis and show the efficacy and specificity of antagomir-induced silencing of EC-specific microRNAs in vivo. © 2009 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
Paul H A Quax - One of the best experts on this subject based on the ideXlab platform.
-
microrna 126 modulates endothelial sdf 1 expression and mobilization of sca 1 lin progenitor cells in ischaemia
Cardiovascular Research, 2011Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Matthieu Monge, Paul H A Quax, Hetty C De Boer, Annemarie M Van Oeverenrietdijk, Margreet R De Vries, Van Der Veer Eric Peter, Ton J RabelinkAbstract:Aims MicroRNA-126 (Mir-126), which is enriched in endothelial cells, plays a role in angiogenesis. Based on the seed sequence, Mir-126 can also be predicted to regulate vasculogenesis by modulating the endothelial expression of stromal cell-derived factor-1 (SDF-1). Methods and results Using miR-reporter constructs, we first validated that Mir-126 inhibits SDF-1 expression in endothelial cells in vitro . Next, we investigated the potential relevance of this observation with respect to the mobilization of progenitor cells. For this, we studied the migration of human CD34+ progenitor cells towards chemotactic factors present in endothelial cell-conditioned medium. Antagomir-induced silencing of Mir-126 elevated SDF-1 expression by human umbilical vein endothelial cells and enhanced migration of the CD34+ cells. In a murine model of hind limb ischaemia, a striking increase in the number of circulating Sca-1+/Lin− progenitor cells in antagoMir-126-treated mice was observed when compared with scramblemir-treated controls. Immunohistochemical staining of capillaries in the post-ischaemic gastrocnemius muscle of Mir-126-silenced mice revealed elevated SDF-1 expressing CD31-positive capillaries, whereas a mobilizing effect of Mir-126 inhibition was not detected in healthy control animals. Conclusion Mir-126 can regulate the expression of SDF-1 in endothelial cells. In the context of an ischaemic event, systemic silencing of Mir-126 leads to the mobilization of Sca-1+/Lin− progenitor cells into the peripheral circulation, potentially in response to elevated SDF-1 expression by endothelial cells present in the ischaemic tissue.
-
antagomir mediated silencing of endothelial cell specific microrna 126 impairs ischemia induced angiogenesis
Journal of Cellular and Molecular Medicine, 2009Co-Authors: Coen Van Solingen, Roel Bijkerk, Leonard Seghers, Jacques M G J Duijs, Marko K Roeten, Annemarie M Van Oeverenrietdijk, Matthieu Monge, Hetty C De Boer, Hans J Baelde, Paul H A QuaxAbstract:MicroRNAs are negative regulators of gene expression that play a key role in cell-type specific differentiation and modulation of cell function and have been proposed to be involved in neovascularization. Previously, using an extensive cloning and sequencing approach, we identified Mir-126 to be specifically and highly expressed in human endothelial cells (EC). Here, we demonstrate EC-specific expression of Mir-126 in capillaries and the larger vessels in vivo. We therefore explored the potential role of Mir-126 in arteriogenesis and angiogenesis. Using miR-reporter constructs, we show that Mir-126 is functionally active in EC in vitro and that it could be specifically repressed using antagomirs specifically targeting Mir-126. To study the consequences of Mir-126 silencing on vascular regeneration, mice were injected with a single dose of antagoMir-126 or a control ‘scramblemir’ and exposed to ischemia of the left hindlimb by ligation of the femoral artery. Although Mir-126 was effectively silenced in mice treated with a single, high dose (HD) of antagoMir-126, laser Doppler perfusion imaging did not show effects on blood flow recovery. In contrast, quantification of the capillary density in the gastrocnemius muscle revealed that mice treated with a HD of antagoMir-126 had a markedly reduced angiogenic response. Aortic explant cultures of the mice confirmed the role of Mir-126 in angiogenesis. Our data demonstrate a facilitary function for Mir-126 in ischemia-induced angiogenesis and show the efficacy and specificity of antagomir-induced silencing of EC-specific microRNAs in vivo.