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10.1007/s10456-018-9594-9 http://scihub22266oqcxt.onion/10.1007/s10456-018-9594-9 C5878206!5878206 !29332242     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29332242 &cmd=llinks): Failed to open stream: HTTP request failed! 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Selective IKK2 inhibitor IMD0354 disrupts NF-?B signaling to suppress corneal inflammation and angiogenesis |pdf=|usr=}}{{29332242 }} gab.com Text Selective IKK2 inhibitor IMD0354 disrupts NF- B signaling to suppress corneal inflammation and angiogenesis JO: Angiogenesis http://www.kidney.de/pget.php?&tw=1&pmid=29332242 #FOAvip Corneal neovascularization is a sight-threatening condition caused by angiogenesis in the normally avascular cornea. Neovascularization of the cornea is often associated with an inflammatory response, thus targeting VEGF-A alone yields only a limited efficacy. The NF-?B signaling pathway plays important roles in inflammation and angiogenesis. Here, we study consequences of the inhibition of NF-?B activation through selective blockade of the IKK complex I?B kinase ? (IKK2) using the compound IMD0354, focusing on the effects of inflammation and pathological angiogenesis in the cornea. In vitro, IMD0354 treatment diminished HUVEC migration and tube formation without an increase in cell death and arrested rat aortic ring sprouting. In HUVEC, the IMD0354 treatment caused a dose-dependent reduction in VEGF-A expression, suppressed TNF?-stimulated expression of chemokines CCL2 and CXCL5, and diminished actin filament fibers and cell filopodia formation. In developing zebrafish embryos, IMD0354 treatment reduced expression of Vegf-a and disrupted retinal angiogenesis. In inflammation-induced angiogenesis in the rat cornea, systemic selective IKK2 inhibition decreased inflammatory cell invasion, suppressed CCL2, CXCL5, Cxcr2, and TNF-? expression and exhibited anti-angiogenic effects such as reduced limbal vessel dilation, reduced VEGF-A expression and reduced angiogenic sprouting, without noticeable toxic effect. In summary, targeting NF-?B by selective IKK2 inhibition dampened the inflammatory and angiogenic responses in vivo by modulating the endothelial cell expression profile and motility, thus indicating an important role of NF-?B signaling in the development of pathologic corneal neovascularization. Twit Text FOAVip Selective IKK2 inhibitor IMD0354 disrupts NF- B signaling to suppress corneal inflammation and angiogenesis ????Angiogenesis http://www.kidney.de/pget.php?&tw=1&pmid=29332242 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29332242 #FOAvip English Wikipedia <ref>{{Cite pmid|29332242 }}</ref> Selective IKK2 inhibitor IMD0354 disrupts NF-?B signaling to suppress corneal inflammation and angiogenesis #MMPMID29332242 Lennikov A ; Mirabelli P ; Mukwaya A ; Schaupper M ; Thangavelu M ; Lachota M ; Ali Z ; Jensen L ; Lagali N Angiogenesis 2018[May]; 21 (2 ): 267-285 PMID29332242 show ga Corneal neovascularization is a sight-threatening condition caused by angiogenesis in the normally avascular cornea. Neovascularization of the cornea is often associated with an inflammatory response, thus targeting VEGF-A alone yields only a limited efficacy. The NF-?B signaling pathway plays important roles in inflammation and angiogenesis. Here, we study consequences of the inhibition of NF-?B activation through selective blockade of the IKK complex I?B kinase ? (IKK2) using the compound IMD0354, focusing on the effects of inflammation and pathological angiogenesis in the cornea. In vitro, IMD0354 treatment diminished HUVEC migration and tube formation without an increase in cell death and arrested rat aortic ring sprouting. In HUVEC, the IMD0354 treatment caused a dose-dependent reduction in VEGF-A expression, suppressed TNF?-stimulated expression of chemokines CCL2 and CXCL5, and diminished actin filament fibers and cell filopodia formation. In developing zebrafish embryos, IMD0354 treatment reduced expression of Vegf-a and disrupted retinal angiogenesis. In inflammation-induced angiogenesis in the rat cornea, systemic selective IKK2 inhibition decreased inflammatory cell invasion, suppressed CCL2, CXCL5, Cxcr2, and TNF-? expression and exhibited anti-angiogenic effects such as reduced limbal vessel dilation, reduced VEGF-A expression and reduced angiogenic sprouting, without noticeable toxic effect. In summary, targeting NF-?B by selective IKK2 inhibition dampened the inflammatory and angiogenic responses in vivo by modulating the endothelial cell expression profile and motility, thus indicating an important role of NF-?B signaling in the development of pathologic corneal neovascularization. |Animals [MESH] |Animals, Genetically Modified [MESH] |Benzamides/*pharmacology [MESH] |Cornea/*metabolism/pathology [MESH] |Corneal Neovascularization/*drug therapy/genetics/metabolism/pathology [MESH] |Eye Proteins/*antagonists & inhibitors/genetics/metabolism [MESH] |Human Umbilical Vein Endothelial Cells [MESH] |Humans [MESH] |I-kappa B Kinase/*antagonists & inhibitors/genetics/metabolism [MESH] |Keratitis/*drug therapy/genetics/metabolism/pathology [MESH] |Male [MESH] |NF-kappa B/genetics/*metabolism [MESH] |Rats [MESH] |Rats, Wistar [MESH] |Signal Transduction/*drug effects/genetics [MESH]Selective IKK2 inhibitor IMD0354 disrupts NF-?B signaling to suppress (epmc).pdf DeepDyve Pubget Overpricing