4.5 Article

KIF13B regulates angiogenesis through Golgi to plasma membrane trafficking of VEGFR2

期刊

JOURNAL OF CELL SCIENCE
卷 127, 期 20, 页码 4518-4530

出版社

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.156109

关键词

VEGFR2; Angiogenesis; Kinesin; Signal transduction; Trafficking

资金

  1. National Institutes of Health [T32 HL07829, RO1 HL079356, RO1 HL103922]
  2. American Heart Association [13SDG14680053]

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Although the trafficking of newly synthesized VEGFR2 to the plasma membrane is a key determinant of angiogenesis, the molecular mechanisms of Golgi to plasma membrane trafficking are unknown. Here, we have identified a key role of the kinesin family plus-end molecular motor KIF13B in delivering VEGFR2 cargo from the Golgi to the endothelial cell surface. KIF13B is shown to interact directly with VEGFR2 on microtubules. We also observed that overexpression of truncated versions of KIF13B containing the binding domains that interact with VEGFR2 inhibited VEGF-induced capillary tube formation. KIF13B depletion prevented VEGF-mediated endothelial migration, capillary tube formation and neo-vascularization in mice. Impairment in trafficking induced by knockdown of KIF13B shunted VEGFR2 towards the lysosomal degradation pathway. Thus, KIF13B is an essential molecular motor required for the trafficking of VEGFR2 from the Golgi, and its delivery to the endothelial cell surface mediates angiogenesis.

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