JULIO FLAVIO MEIRELLES MARCHINI

(Fonte: Lattes)
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Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina

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Agora exibindo 1 - 10 de 21
  • bookPart
    Endocardite infecciosa
    (2019) BRANDãO NETO, Rodrigo Antonio; MACHADO, Adriano da Silva; MARCHINI, Julio Flávio Meirelles
  • bookPart
    Fibrilação atrial
    (2019) MARCHINI, Julio Flávio Meirelles; BRANDãO NETO, Rodrigo Antonio
  • bookPart
    Emergências hipertensivas
    (2019) RODRIGUES, Caio Godoy; MARCHINI, Julio Flávio Meirelles; BRANDãO NETO, Rodrigo Antonio
  • bookPart
    Síncope
    (2019) BRANDãO NETO, Rodrigo Antonio; MARCHINI, Julio Flávio Meirelles
  • bookPart
    Taquiarritmias
    (2019) PEREIRA, Thiago Vicente; MARCHINI, Julio Flávio Meirelles
  • bookPart
    Acidentes relacionados a animais peçonhantos
    (2019) MARCHINI, Julio Flávio Meirelles; BRANDãO NETO, Rodrigo Antonio
  • bookPart
    Infarto agudo do miocárdio com supradesnivelamento do segmento ST
    (2019) MARCHINI, Julio Flávio Meirelles
  • article 54 Citação(ões) na Scopus
    MicroRNA-135a-3p regulates angiogenesis and tissue repair by targeting p38 signaling in endothelial cells
    (2019) ICLI, Basak; WU, Winona; OZDEMIR, Denizhan; LI, Hao; HAEMMIG, Stefan; LIU, Xin; GIATSIDIS, Giorgio; CHENG, Henry S.; AVCI, Seyma Nazli; KURT, Merve; LEE, Nathan; GUIMARAES, Raphael Boesche; MANICA, Andre; MARCHINI, Julio F.; RYNNING, Stein Erik; RISNES, Ivar; HOLLAN, Ivana; CROCE, Kevin; ORGILL, Dennis P.; FEINBERG, Mark W.
    Angiogenesis is a critical process in repair of tissue injury that is regulated by a delicate balance between pro- and antiangiogenic factors. In disease states associated with impaired angiogenesis, we identified that miR-135a-3p is rapidly induced and serves as an antiangiogenic microRNA (miRNA) by targeting endothelial cell (EC) p38 signaling in vitro and in vivo. MiR-135a-3p overexpression significantly inhibited EC proliferation, migration, and network tube formation in matrigel, whereas miR-135-3p neutralization had the opposite effects. Mechanistic studies using transcriptomic profiling, bioinformatics, 3'-UTR reporter and miRNA ribonucleoprotein complex -immunoprecipitation assays, and small interfering RNA dependency studies revealed that miR-135a-3p inhibits the p38 signaling pathway in ECs by targeting huntingtin-interacting protein 1 (HIP1). Local delivery of miR-135a-3p inhibitors to wounds of diabetic db/db mice markedly increased angiogenesis, granulation tissue thickness, and wound closure rates, whereas local delivery of miR-135a-3p mimics impaired these effects. Finally, through gain- and loss-of-function studies in human skin organoids as a model of tissue injury, we demonstrated that miR-135a-3p potently modulated p38 signaling and angiogenesis in response to VEGF stimulation by targeting HIP1. These findings establish miR-135a-3p as a pivotal regulator of pathophysiological angiogenesis and tissue repair by targeting a VEGF-HIP1-p38K signaling axis, providing new targets for angiogenic therapy to promote tissue repair.
  • bookPart
    Síndromes aórticas agudas
    (2019) BRANDãO NETO, Rodrigo Antonio; MARCHINI, Julio Flávio Meirelles
  • bookPart
    Ultrassonografia de tórax
    (2019) MARINO, Lucas Oliveira; PETRINI, Carla Andrade; JOãO, Eduardo Alher; MARCHINI, Julio Flávio Meirelles