FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022023305> ?p ?o ?g. }

• W2022023305 endingPage "6315" @default.
• W2022023305 startingPage "6303" @default.
• W2022023305 abstract "Angiogenesis is a dynamic process required for embryonic development. However, postnatal vascular growth is characteristic of multiple disease states. Despite insights into the multistep process in which adhesion molecules, extracellular matrix proteins, growth factors, and their receptors work in concert to form new vessels from the preexisting vasculature, there remains a lack of insight of the nuclear transcriptional mechanisms that occur within endothelial cells (ECs) in response to VEGF. Iroquois homeobox gene 3 (Irx3) is a transcription factor of the Iroquois family of homeobox genes. Irx homeodomain transcription factors are involved in the patterning and development of several tissues. Irx3 is known for its role during embryogenesis in multiple organisms. However, the expression and function of Irx3 in human postnatal vasculature remains to be investigated. Here we show that Irx3 is expressed in human microvascular endothelial cells, and expression is elevated by VEGF stimulation. Genetic Irx3 gain and loss of function studies in human microvascular endothelial cells resulted in the modulation of EC migration during wound healing, chemotaxis and invasion, and tubulogenesis. Additionally, we observed increased delta-like ligand 4 (Dll4) expression, which suggests an increase in EC tip cell population. Finally, siRNA screening studies revealed that transient knockdown of Hey1, a downstream Notch signaling mediator, resulted in increased Irx3 expression in response to VEGF treatment. Strategies to pharmacologically regulate Irx3 function in adult endothelial cells may provide new therapies for angiogenesis. Angiogenesis is a dynamic process required for embryonic development. However, postnatal vascular growth is characteristic of multiple disease states. Despite insights into the multistep process in which adhesion molecules, extracellular matrix proteins, growth factors, and their receptors work in concert to form new vessels from the preexisting vasculature, there remains a lack of insight of the nuclear transcriptional mechanisms that occur within endothelial cells (ECs) in response to VEGF. Iroquois homeobox gene 3 (Irx3) is a transcription factor of the Iroquois family of homeobox genes. Irx homeodomain transcription factors are involved in the patterning and development of several tissues. Irx3 is known for its role during embryogenesis in multiple organisms. However, the expression and function of Irx3 in human postnatal vasculature remains to be investigated. Here we show that Irx3 is expressed in human microvascular endothelial cells, and expression is elevated by VEGF stimulation. Genetic Irx3 gain and loss of function studies in human microvascular endothelial cells resulted in the modulation of EC migration during wound healing, chemotaxis and invasion, and tubulogenesis. Additionally, we observed increased delta-like ligand 4 (Dll4) expression, which suggests an increase in EC tip cell population. Finally, siRNA screening studies revealed that transient knockdown of Hey1, a downstream Notch signaling mediator, resulted in increased Irx3 expression in response to VEGF treatment. Strategies to pharmacologically regulate Irx3 function in adult endothelial cells may provide new therapies for angiogenesis." @default.
• W2022023305 created "2016-06-24" @default.
• W2022023305 creator A5023181168 @default.
• W2022023305 creator A5048930457 @default.
• W2022023305 creator A5073990636 @default.
• W2022023305 creator A5081448344 @default.
• W2022023305 creator A5087769693 @default.
• W2022023305 date "2015-03-01" @default.
• W2022023305 modified "2023-10-11" @default.
• W2022023305 title "The Proangiogenic Effect of Iroquois Homeobox Transcription Factor Irx3 in Human Microvascular Endothelial Cells" @default.
• W2022023305 cites W112392588 @default.
• W2022023305 cites W1969110441 @default.
• W2022023305 cites W1971324461 @default.
• W2022023305 cites W1973333497 @default.
• W2022023305 cites W1978393368 @default.
• W2022023305 cites W1978565769 @default.
• W2022023305 cites W1979675055 @default.
• W2022023305 cites W1983038328 @default.
• W2022023305 cites W1985789529 @default.
• W2022023305 cites W1992112921 @default.
• W2022023305 cites W1993523135 @default.
• W2022023305 cites W1995827857 @default.
• W2022023305 cites W1997508706 @default.
• W2022023305 cites W2001772382 @default.
• W2022023305 cites W2005279322 @default.
• W2022023305 cites W2015922937 @default.
• W2022023305 cites W2017516431 @default.
• W2022023305 cites W2033522367 @default.
• W2022023305 cites W2041569441 @default.
• W2022023305 cites W2049529144 @default.
• W2022023305 cites W2053444552 @default.
• W2022023305 cites W2058734213 @default.
• W2022023305 cites W2066018349 @default.
• W2022023305 cites W2070222135 @default.
• W2022023305 cites W2092827213 @default.
• W2022023305 cites W2095696977 @default.
• W2022023305 cites W2099436620 @default.
• W2022023305 cites W2100063887 @default.
• W2022023305 cites W2100393234 @default.
• W2022023305 cites W2103886590 @default.
• W2022023305 cites W2107146765 @default.
• W2022023305 cites W2108839432 @default.
• W2022023305 cites W2116317116 @default.
• W2022023305 cites W2118432271 @default.
• W2022023305 cites W2119470055 @default.
• W2022023305 cites W2121992723 @default.
• W2022023305 cites W2130380865 @default.
• W2022023305 cites W2131637001 @default.
• W2022023305 cites W2141012207 @default.
• W2022023305 cites W2146415477 @default.
• W2022023305 cites W2148141447 @default.
• W2022023305 cites W2148688467 @default.
• W2022023305 cites W2149483845 @default.
• W2022023305 cites W2156714600 @default.
• W2022023305 cites W2157893542 @default.
• W2022023305 cites W2159181129 @default.
• W2022023305 cites W2159788711 @default.
• W2022023305 cites W2166227518 @default.
• W2022023305 cites W2166807613 @default.
• W2022023305 cites W2168645747 @default.
• W2022023305 cites W4253074478 @default.
• W2022023305 doi "https://doi.org/10.1074/jbc.m114.601146" @default.
• W2022023305 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4358267" @default.
• W2022023305 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25512384" @default.
• W2022023305 hasPublicationYear "2015" @default.
• W2022023305 type Work @default.
• W2022023305 sameAs 2022023305 @default.
• W2022023305 citedByCount "15" @default.
• W2022023305 countsByYear W20220233052016 @default.
• W2022023305 countsByYear W20220233052017 @default.
• W2022023305 countsByYear W20220233052018 @default.
• W2022023305 countsByYear W20220233052019 @default.
• W2022023305 countsByYear W20220233052020 @default.
• W2022023305 countsByYear W20220233052021 @default.
• W2022023305 countsByYear W20220233052022 @default.
• W2022023305 crossrefType "journal-article" @default.
• W2022023305 hasAuthorship W2022023305A5023181168 @default.
• W2022023305 hasAuthorship W2022023305A5048930457 @default.
• W2022023305 hasAuthorship W2022023305A5073990636 @default.
• W2022023305 hasAuthorship W2022023305A5081448344 @default.
• W2022023305 hasAuthorship W2022023305A5087769693 @default.
• W2022023305 hasBestOaLocation W20220233051 @default.
• W2022023305 hasConcept C104317684 @default.
• W2022023305 hasConcept C121587040 @default.
• W2022023305 hasConcept C189165786 @default.
• W2022023305 hasConcept C2780394083 @default.
• W2022023305 hasConcept C502942594 @default.
• W2022023305 hasConcept C54355233 @default.
• W2022023305 hasConcept C86339819 @default.
• W2022023305 hasConcept C86803240 @default.
• W2022023305 hasConcept C95444343 @default.
• W2022023305 hasConceptScore W2022023305C104317684 @default.
• W2022023305 hasConceptScore W2022023305C121587040 @default.
• W2022023305 hasConceptScore W2022023305C189165786 @default.
• W2022023305 hasConceptScore W2022023305C2780394083 @default.
• W2022023305 hasConceptScore W2022023305C502942594 @default.
• W2022023305 hasConceptScore W2022023305C54355233 @default.
• W2022023305 hasConceptScore W2022023305C86339819 @default.

• next