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DTSTART;TZID=America/New_York:20220317T130000
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SUMMARY:Journal Club - March 2022
DESCRIPTION:Join us as we discuss: "Macrophage IL-1 promotes arteriogenesis by autocrine STAT3- and NF- B-mediated transcription of pro-angiogenic VEGF-A" originally published in Cell Reports. To review the paper\, click here: https://www.cell.com/cell-reports/fulltext/S2211-1247(22)00021-3 Authors: Chris S. Mantsounga\, Cadence Lee\, Jade Neverson\, Sheila Sharma\, Abigail Healy\, Joshua M. Berus\, Crystal Parry\, Nicolle M. Ceneri\, Francesc L pez-Gir ldez\, Hyung J. Chun\, Qing Lu\, Frank Sellke\, Gaurav Choudhary\, Alan R. Morrison Summary: Peripheral artery disease (PAD) leads to considerable morbidity\, yet strategies for therapeutic angiogenesis fall short of being impactful. Inflammatory macrophage subsets play an important role in orchestrating post-developmental angiogenesis\, but the underlying mechanisms are unclear. Here\, we find that macrophage VEGF-A expression is dependent upon the potent inflammatory cytokine\, IL-1 . IL-1 promotes pro-angiogenic VEGF-A165a isoform transcription via activation and promoter binding of STAT3 and NF- B\, as demonstrated by gene-deletion\, gain-of-function\, inhibition\, and chromatin immunoprecipitation assays. Conversely\, IL-1 -deletion or inhibition of STAT3 or NF- B increases anti-angiogenic VEGF-A165b isoform expression\, indicating IL-1 signaling may also direct splice variant selection. In an experimental PAD model of acute limb ischemia\, macrophage IL-1 expression is required for pro-angiogenic VEGF-A expression and for VEGF-A-induced blood flow recovery via angio- or arteriogenesis. Though further study is needed\, macrophage IL-1 -dependent transcription of VEGF-A via STAT3 and NF- B may have potential to therapeutically promote angiogenesis in the setting of PAD.
X-ALT-DESC;FMTTYPE=text/html:Join us as we discuss: "\;Macrophage IL-1&beta\; promotes arteriogenesis by autocrine STAT3- and NF-&kappa\;B-mediated transcription of pro-angiogenic VEGF-A&rdquo\; originally published in Cell Reports. \;
To review the paper\, click here: https://www.cell.com/cell-reports/fulltext/S2211-1247(22)00021-3 \;
Authors: Chris S. Mantsounga\, Cadence Lee\, Jade Neverson\, Sheila Sharma\, Abigail Healy\, Joshua M. Berus\, Crystal Parry\, Nicolle M. Ceneri\, Francesc Ló\;pez-Girá\;ldez\, Hyung J. Chun\, Qing Lu\, Frank Sellke\, Gaurav Choudhary\, Alan R. Morrison \;
Summary: Peripheral artery disease (PAD) leads to considerable morbidity\, yet strategies for therapeutic angiogenesis fall short of being impactful. Inflammatory macrophage subsets play an important role in orchestrating post-developmental angiogenesis\, but the underlying mechanisms are unclear. Here\, we find that macrophage VEGF-A expression is dependent upon the potent inflammatory cytokine\, IL-1&beta\;. IL-1&beta\; promotes pro-angiogenic VEGF-A165a isoform transcription via activation and promoter binding of STAT3 and NF-&kappa\;B\, as demonstrated by gene-deletion\, gain-of-function\, inhibition\, and chromatin immunoprecipitation assays. Conversely\, IL-1&beta\;-deletion or inhibition of STAT3 or NF-&kappa\;B increases anti-angiogenic VEGF-A165b isoform expression\, indicating IL-1&beta\; signaling may also direct splice variant selection. In an experimental PAD model of acute limb ischemia\, macrophage IL-1&beta\; expression is required for pro-angiogenic VEGF-A expression and for VEGF-A-induced blood flow recovery via angio- or arteriogenesis. Though further study is needed\, macrophage IL-1&beta\;-dependent transcription of VEGF-A via STAT3 and NF-&kappa\;B may have potential to therapeutically promote angiogenesis in the setting of PAD.
LOCATION:
UID:e.2142.592042
SEQUENCE:3
DTSTAMP:20261028T173650Z
URL:https://members.navbo.org/calendar-of-events/Details/journal-club-march-2022-608839?sourceTypeId=Hub
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