Matrix metalloproteinase processing of monocyte chemoattractant proteins generates CC chemokine receptor antagonists with anti-inflammatory properties in vivo.

By G. A. McQuibban, J. Gong, J. Wong, J. Wallace, I. Clark‐Lewis, Christopher M. Overall. Blood, 2002

649 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology and Allergy, Oncology

View Paper: https://www.semanticscholar.org/paper/33d225f62cba941cb2a392dc4a1dd26f1507281f

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

1. Zena Werb
2. W. Parks
3. J. Campisi
4. S. Gill
5. Andrew J. Ewald
6. V. Plaks
7. E. Koivunen
8. M. Björklund

In Immunology and Allergy

1. S. Gill
2. W. Parks
3. Zena Werb
4. J. McGuire
5. A. Manicone

In Oncology

1. J. Campisi
2. Zena Werb
3. W. Parks
4. Andrew J. Ewald
5. S. Gill
6. V. Plaks
7. E. Koivunen
8. M. Björklund

Citations in the corpus

• Matrix metalloproteinases as modulators of inflammation. (2008, methodology): “Additionally, in an in vivo model of carrageenan-induced inflammation in rat paws, the MMP-truncated CC chemokines induced a greater than 66% reduction in inflammatory edema progression after 12 hours [5].”
• Inflammation in wound repair: molecular and cellular mechanisms. (2007, background): “Interestingly, recent in vitro data suggested that matrix metalloproteinases (MMPs) can downregulate inflammation via cleavage of chemokines, which then act as antagonists (McQuibban et al., 2000, 2002).”
• Chemokine and cytokine processing by matrix metalloproteinases and its effect on leukocyte migration and inflammation (2007, background): “The closely related chemokines CCL2 (MCP-1) and CCL13 (MCP-4) could also be cleaved by MMP-1 and MMP-3, the latter of which also cleaved CCL8 (MCP-2) [19].”
• Hypertrophic Scarring and Keloids: Pathomechanisms and Current and Emerging Treatment Strategies (2011, background): “Also, recent in vitro data suggested that MMPs may downregulate inflammation via cleavage of chemokines, which then act as antagonists (74,75).”
• Senescent cells as a source of inflammatory factors for tumor progression (2010, background): “For example, these MMPs can cleave MCP-1, -2, and -4 and IL-8 [63].”
• The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression (2010, background): “During angiogenesis, endothelial cells can undergo proliferation, which is stimulated by vascular endothelial growth factor (VEGF), IL-8, I-309, and eotaxin (125–127).”
• Phagocyte partnership during the onset and resolution of inflammation (2010, background): “103 ); cleaved CCL7 continues to bind chemokine receptors CCR1, CCR2 and CCR3, but fails to induce downstream signalling and chemotaxi”
• Matrix metalloproteinases and the regulation of tissue remodelling (2007, background): “Truncation of macrophage-derived CCL7 by MMP2 and MMP14 results in the formation of peptides that can bind to the CC chemokine receptor and function as antagonist”
• Processing of VEGF-A by matrix metalloproteinases regulates bioavailability and vascular patterning in tumors (2005, background): “…cleavage of growth factors has been implicated in activation, in the alteration of biological properties, and in growth factor degradation (Fuentes-Prior et al., 2000; Junttila et al., 2000; McQuibban et al., 2000, 2002; Bergsten et al., 2001; Borrell-Pages et al., 2003; Nanba et al., 2003).”