Publications by authors named "C Urbich"
The contribution of myeloid cells to tumour microenvironments is a decisive factor in cancer progression. Tumour-associated macrophages (TAMs) mediate tumour invasion and angiogenesis through matrix remodelling, immune modulation and release of pro-angiogenic cytokines. Nothing is known about how pathogenic bacteria affect myeloid cells in these processes.
View Article and Find Full Text PDFObjective: Histone deacetylases (HDACs) modulate gene expression by deacetylation of histone and nonhistone proteins. Several HDACs control angiogenesis, but the role of HDAC9 is unclear.
Methods And Results: Here, we analyzed the function of HDAC9 in angiogenesis and its involvement in regulating microRNAs.
The shear-responsive transcription factor Krüppel-like factor 2 (KLF2) is a critical regulator of endothelial gene expression patterns induced by atheroprotective flow. As microRNAs (miRNAs) post-transcriptionally control gene expression in many pathogenic and physiological processes, we investigated the regulation of miRNAs by KLF2 in endothelial cells. KLF2 binds to the promoter and induces a significant upregulation of the miR-143/145 cluster.
View Article and Find Full Text PDFArticle Synopsis
- MicroRNAs (miRs), specifically miR-27a and miR-27b, play crucial roles in regulating endothelial cell behaviour, enhancing cell sprouting and angiogenesis.
- Inhibition of these miRs leads to decreased sprout formation and increased cell repulsion in vitro and reduced vessel formation in vivo, indicating their importance in blood vessel development.
- The study identifies semaphorin 6A (SEMA6A) as a target of miR-27, showing that miR-27's effect on endothelial cells involves regulating SEMA6A, which inhibits their repulsion.
Rationale: Proangiogenic hematopoietic and endothelial progenitor cells (EPCs) contribute to postnatal neovascularization, but the mechanisms regulating differentiation to the endothelial lineage are unclear.
Objective: To elucidate the epigenetic control of endothelial gene expression in proangiogenic cells and EPCs.
Methods And Results: Here we demonstrate that the endothelial nitric oxide synthase (eNOS) promoter is epigenetically silenced in proangiogenic cells (early EPCs), CD34(+) cells, and mesoangioblasts by DNA methylation and prominent repressive histone H3K27me3 marks.