human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: The endothelial cell-specific microRNA ( miRNA ) , miR-126 , is considered a master regulator of physiological angiogenesis . Transplanted mesenchymal stem cells ( MSCs ) release soluble factors contributing to neoangiogenesis and cardiac repair . Therefore , we hypothesized that the over-expression of miR-126 may prolong MSC survival and enhance the cell secretome , thereby improving post-infarction angiogenesis and cardiac function . In this study , MSCs harvested from male C57BL/6 mouse bone marrow were infected in vitro with miR-126 ( MSC(miR-126) ) by using recombinant lentiviral vectors ; the control cells were either non-transfected or transduced with mock vectors ( MSC(null) ) . The results showed an increased secretion of angiogenic factors and a higher resistance against hypoxia in MSC(miR-126) compared with the control cells . The expression of the Notch ligand Delta-like ( Dll)-4 in the MSC(miR-126) group was also increased . For in vivo experiments , MSC(miR-126) cultures were intramyocardially injected into the infarct region of the hearts of female C57BL/6 mice ( an acute myocardial infarction model ) who had undergone ligation of the left anterior descending coronary artery . The survival of MSC(miR-126) cultures , determined by Sry expression , was increased at 7 days after transplantation . MSC(miR-126)-treated animals showed significantly improved cardiac function as assessed by echocardiography 2 weeks later . The expression levels of angiogenic factors and Dll-4 in the infarcted myocardium were further increased by MSC(miR-126) compared with MSCs or MSC(null) cultures . Furthermore , fluorescent microsphere and histological studies revealed that myocardial blood flow and microvessel density were significantly increased in the MSC(miR-126)-transplanted animals . In addition , we found increased immature vessel proliferation following the transplantation of MSC(miR-126) cultures in which the expression of Dll-4 had been knocked down . However , blood vessels with lumen were barely detected , which indicated that Dll-4 plays a key role in tubulogenesis . We conclude that the transplantation of MSCs overexpressing miR-126 can further enhance functional angiogenesis in the ischemic myocardium possibly by the secretion of angiogenic factors and the activation of Dll-4 , thus increasing MSC survival . Therefore , MSCs modified with miR-126 may represent a novel and efficient therapeutic approach for ischemic angiogenesis and the improvement of cardiac function .
    OUTPUT:

agent
inducing angiogenesis
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: The endothelial cell-specific microRNA ( miRNA ) , miR-126 , is considered a master regulator of physiological angiogenesis . Transplanted mesenchymal stem cells ( MSCs ) release soluble factors contributing to neoangiogenesis and cardiac repair . Therefore , we hypothesized that the over-expression of miR-126 may prolong MSC survival and enhance the cell secretome , thereby improving post-infarction angiogenesis and cardiac function . In this study , MSCs harvested from male C57BL/6 mouse bone marrow were infected in vitro with miR-126 ( MSC(miR-126) ) by using recombinant lentiviral vectors ; the control cells were either non-transfected or transduced with mock vectors ( MSC(null) ) . The results showed an increased secretion of angiogenic factors and a higher resistance against hypoxia in MSC(miR-126) compared with the control cells . The expression of the Notch ligand Delta-like ( Dll)-4 in the MSC(miR-126) group was also increased . For in vivo experiments , MSC(miR-126) cultures were intramyocardially injected into the infarct region of the hearts of female C57BL/6 mice ( an acute myocardial infarction model ) who had undergone ligation of the left anterior descending coronary artery . The survival of MSC(miR-126) cultures , determined by Sry expression , was increased at 7 days after transplantation . MSC(miR-126)-treated animals showed significantly improved cardiac function as assessed by echocardiography 2 weeks later . The expression levels of angiogenic factors and Dll-4 in the infarcted myocardium were further increased by MSC(miR-126) compared with MSCs or MSC(null) cultures . Furthermore , fluorescent microsphere and histological studies revealed that myocardial blood flow and microvessel density were significantly increased in the MSC(miR-126)-transplanted animals . In addition , we found increased immature vessel proliferation following the transplantation of MSC(miR-126) cultures in which the expression of Dll-4 had been knocked down . However , blood vessels with lumen were barely detected , which indicated that Dll-4 plays a key role in tubulogenesis . We conclude that the transplantation of MSCs overexpressing miR-126 can further enhance functional angiogenesis in the ischemic myocardium possibly by the secretion of angiogenic factors and the activation of Dll-4 , thus increasing MSC survival . Therefore , MSCs modified with miR-126 may represent a novel and efficient therapeutic approach for ischemic angiogenesis and the improvement of cardiac function .
    OUTPUT:
