Shedding of the matrix metalloproteinases MMP-2, MMP-9, and MT1-MMP as membrane vesicle-associated components by endothelial cells.
By G. Taraboletti, S. D'Ascenzo, Patrizia Borsotti, R. Giavazzi, A. Pavan, V. Dolo. American Journal of Pathology, 2002
598 citations recorded by the source corpus.
Subfields: Cancer Research, Cardiology and Cardiovascular Medicine, Hematology
View Paper: https://www.semanticscholar.org/paper/76103310ea16d25bb24934245ec88b0b96ad6446
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- G. Raposo
- P. E. Van den Steen
- J. Vandooren
- D. Lyden
- G. Opdenakker
- E. Koivunen
- M. Björklund
- Raghu Kalluri
In Hematology
Citations in the corpus
- Gelatinase-mediated migration and invasion of cancer cells. (2005, background): “In endothelial and tumor cells, the gelatinases are secreted in specific transport vesicles containing also other proteins such as integrins and components of the plasminogen activation system (Dolo et al., 1999; Ginestra et al., 1997; Taraboletti et al., 2002).”
- Biochemistry and molecular biology of gelatinase B or matrix metalloproteinase-9 (MMP-9): The next decade (2013, background): “In pancreatic cancer, neutrophil-derived MMP-9 acts as a potent and direct VEGF-independent angiogenic factor (Bausch et al., 2011).”
- The blood–brain barrier in systemic infection and inflammation (2021, background): “Additionally, enzymes from the family of matrix metalloproteinases (MMPs) secreted by rolling leukocytes or endothelial cells [20] may degrade glycocalyx components such as syndecan, as shown in human and mouse cell lines [21] and rat mesenteric vessels [22].”
- ARF6-regulated shedding of tumor cell-derived plasma membrane microvesicles. (2009, background): “For example, microvesicles secreted by skeletal cells enable bone mineralization in vivo, whereas microvesicles secreted by normal endothelial cells have been implicated in angiogenesis [41].”
- Fibroblast growth factor/fibroblast growth factor receptor system in angiogenesis. (2005, background): “These vesicles stimulate capillary-like structure formation when added to endothelial cells seeded on a solubilized basement membrane preparation (Matrigel) [26].”
- FGF/FGFR signaling in health and disease (2020, background): “FGF2 can stimulate shedding of MMP2 and MMP9 in cell surface membrane vesicles from ECs, which is able to stimulate the angiogenesis of ECs seeded in Matrigel.(463) Another essential step of angiogenesis is endothelium migration.”
- Endothelial progenitor cell derived microvesicles activate an angiogenic program in endothelial cells by a horizontal transfer of mRNA. (2007, unknown): “Moreover, it has been shown that metalloproteinases harboured by endothelial MVs regulate the proteolytic activity on matrix required to elicit angiogenesis.(40) In the present study we demonstrate that MVs derived from EPCs may induce proliferation, apoptosis resistance and in vitro organization in”
- Microvesicles: mediators of extracellular communication during cancer progression (2010, background): “Consistent with this understanding is the knowledge that multiple cell lines of both normal and transformed origin remain viable in culture even when stimulated to release microvesicles (Dolo et al., 1998; Ginestra et al., 1998; Muralidharan-Chari et al., 2009a; Taraboletti et al., 2002).”
- Role of Matrix Metalloproteinases in Angiogenesis and Cancer (2019, background): “Additionally, it is known that ECs secrete MMP2 and−9-containing vesicles stimulated by VEGF and FGF2 and thus regulate the proteolytic activity critical for the angiogenesis-related invasive and morphogenic processes (115).”
- Extracellular vesicles in cancer: cell-to-cell mediators of metastasis (2016, background): “Endothelial cells stimulated by VEGF and FGF-2 release EVs containing MMPs that initiate the proteolysis necessary for tumor invasion and uninhibited angiogenesis (Taraboletti et al., 2002).”