KLF4 Promotes Angiogenesis by Activating VEGF Signaling in Human Retinal Microvascular Endothelial Cells
Copyright policy )KLF4 Promotes Angiogenesis by Activating VEGF Signaling in Human Retinal Microvascular Endothelial Cells
The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in regulating cell proliferation, migration and differentiation in a variety of human cells and is one of four factors required for the induction of pluripotent stem cell reprogramming. However, its role has not been addressed in ocular neovascular diseases. This study investigated the role of KLF4 in angiogenesis and underlying molecular mechanisms in human retinal microvascular endothelial cells (HRMECs). The functional role of KLF4 in HRMECs was determined following lentiviral vector mediated inducible expression and shRNA knockdown of KLF4. Inducible expression of KLF4 promotes cell proliferation, migration and tube formation. In contrast, silencing KLF4 inhibits cell proliferation, migration, tube formation and induces apoptosis in HRMECs. KLF4 promotes angiogenesis by transcriptionally activating VEGF expression, thus activating the VEGF signaling pathway in HRMECs.
- Center for Cancer Research United States
- University of Tennessee Health Science Center United States
- University of Chicago United States
- National Cancer Institute United States
- University of Illinois at Chicago United States
Transcriptional Activation, Vascular Endothelial Growth Factor A, Science, Q, R, Kruppel-Like Transcription Factors, Endothelial Cells, Neovascularization, Physiologic, Retinal Vessels, Apoptosis, Retina, Kruppel-Like Factor 4, Cell Movement, Medicine, Humans, RNA Interference, RNA, Small Interfering, Cells, Cultured, Research Article, Cell Proliferation, Signal Transduction
Transcriptional Activation, Vascular Endothelial Growth Factor A, Science, Q, R, Kruppel-Like Transcription Factors, Endothelial Cells, Neovascularization, Physiologic, Retinal Vessels, Apoptosis, Retina, Kruppel-Like Factor 4, Cell Movement, Medicine, Humans, RNA Interference, RNA, Small Interfering, Cells, Cultured, Research Article, Cell Proliferation, Signal Transduction
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