ArticleJournal of cell science2016
Hic-5 mediates the initiation of endothelial sprouting by regulating a key surface metalloproteinase.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Identification of New Markers of Angiogenic Sprouting Using Transcriptomics: New Role for RND3.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Hic-5 regulates extracellular matrix-associated gene expression and cytokine secretion in cancer associated fibroblasts.Experimental cell research · 2024Article
- The age of bone marrow dictates the clonality of smooth muscle-derived cells in atherosclerotic plaques.Nature aging · 2023Article
- Physiological and pathological roles of Hic‑5 in several organs (Review).International journal of molecular medicine · 2022Review
- Dynamic Expression of Membrane Type 1-Matrix Metalloproteinase (Mt1-mmp/Mmp14) in the Mouse Embryo.Cells · 2021Article
- Identification of a tumor microenvironment-associated prognostic gene signature in bladder cancer by integrated bioinformatic analysis.International journal of clinical and experimental pathology · 2021Article
- Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.International review of cell and molecular biology · 2020Article
- Filopodia and focal adhesions: An integrated system driving branching morphogenesis in neuronal pathfinding and angiogenesis.Developmental biology · 2019Review
- Hic-5 regulates Src-induced invadopodia rosette formation and organization.Molecular biology of the cell · 2019Article
- Pericyte ALK5/TIMP3 Axis Contributes to Endothelial Morphogenesis in the Developing Brain.Developmental cell · 2018Article
- Establishment of a three-dimensional model to study human uterine angiogenesis.Molecular human reproduction · 2018Article
- Genistein inhibits the growth and regulates the migration and invasion abilities of melanoma cells via the FAK/paxillin and MAPK pathways.Oncotarget · 2017Article
- NIK regulates MT1-MMP activity and promotes glioma cell invasion independently of the canonical NF-κB pathway.Oncogenesis · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
During angiogenesis, endothelial cells must coordinate matrix proteolysis with migration. Here, we tested whether the focal adhesion scaffold protein Hic-5 (also known as TGFB1I1) regulated endothelial sprouting in three dimensions. Hic-5 silencing reduced endothelial sprouting and lumen formation, and sprouting defects were rescued by the return of Hic-5 expression. Pro-angiogenic factors enhanced colocalization and complex formation between membrane type-1 matrix metalloproteinase (MT1-MMP, also known as MMP14) and Hic-5, but not between paxillin and MT1-MMP. The LIM2 and LIM3 domains of Hic-5 were necessary and sufficient for Hic-5 to form a complex with MT1-MMP. The degree of interaction between MT1-MMP and Hic-5 and the localization of the complex within detergent-resistant membrane fractions were enhanced during endothelial sprouting, and Hic-5 depletion lowered the surface levels of MT1-MMP. In addition, we observed that loss of Hic-5 partially reduced complex formation between MT1-MMP and focal adhesion kinase (FAK, also known as PTK2), suggesting that Hic-5 bridges MT1-MMP and FAK. Finally, Hic-5 LIM2-LIM3 deletion mutants reduced sprout initiation. Hic-5, MT1-MMP and FAK colocalized in angiogenic vessels during porcine pregnancy, supporting that this complex assembles during angiogenesis in vivo. Collectively, Hic-5 appears to enhance complex formation between MT1-MMP and FAK in activated endothelial cells, which likely coordinates matrix proteolysis and cell motility.
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Registered trials
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