Matrilysin shedding of syndecan-1 regulates chemokine mobilization and transepithelial efflux of neutrophils in acute lung injury.

By Qinglang Li, P. Park, Carole L Wilson, W. Parks. Cell, 2002

771 citations recorded by the source corpus.

Subfields: Cell Biology, Immunology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/a4c4f00d474288938de1cf0f2581121b5b11e7ef

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. S. Sarrazin
2. William C. Lamanna
3. J. Esko
4. J. McGuire
5. A. Manicone
6. Andrew J. Ewald
7. W. Parks
8. Zena Werb

In Immunology

1. Zena Werb
2. V. Plaks
3. J. McGuire
4. A. Manicone
5. Andrew J. Ewald
6. Pengfei Lu
7. Valerie M. Weaver

In Pulmonary and Respiratory Medicine

1. J. McGuire
2. A. Manicone

Citations in the corpus

• Extracellular matrix remodelling: the role of matrix metalloproteinases (2003, background): “Shedding of ICAM-1 has recently been shown to be MMP-9 mediated [39], and MMP-7 has been found to cleave the proteoglycan syndecan-1 [60].”
• Metalloproteinases and their inhibitors: regulators of wound healing. (2008, background): “As a result, neutrophils fail to migrate into the alveolar lumen and instead, are sequestered in the interstitial space (Li et al., 2002).”
• Matrix metalloproteinases as modulators of inflammation. (2008, methodology): “With the use of gene-targeting strategies, combined with observation and deduction, physiologic substrates have been identified (Table 1) [2,7,8].”
• Matrix metalloproteinases as modulators of inflammation and innate immunity (2004, background): “, which results in enhancement, inactivation or antagonism of chemokine activities, or it can be indirect, by the proteinases acting on other substrates that bind, retain or concentrate the chemotactic molecules in particular location”
• Heparan sulphate proteoglycans fine-tune mammalian physiology (2007, background): “A number of studies have shown that syndecan-1 expressed by alveolar epithelia undergoes rapid shedding in response to lung injury, apparently through the matrix metalloproteinase matrilysi”
• Chemokine and cytokine processing by matrix metalloproteinases and its effect on leukocyte migration and inflammation (2007, background): “Instillation of a bacterial chemotactic protein in the lungs of MMP-7-deficient mice did trigger neutrophils to infiltrate the luminal tissue, and the outcome was worse in these animals than in their wild-type counterparts [25].”
• Heparan sulfate proteoglycans. (2011, background): “Syndecan shedding is mediated by matrix metalloproteinases (MMP1, MMP7, MMP9, ADAM17) (Fitzgerald et al. 2000; Li et al. 2002; Endo et al. 2003; Ding et al. 2005; Brule et al. 2006; Cite this article as Cold Spring Harb Perspect Biol 2011;3:a004952 15 Pruessmeyer et al. 2010).”
• Matrix Metalloproteinases: Regulators of the Tumor Microenvironment (2010, background): “MMP-8, -9, and -12 also modulate the bioactivity of CXCL11/ I-TAC, a potent Th1 lymphocyte-attracting chemokine (Cox et al., 2008).”
• Matrix metalloproteinase inhibitors as therapy for inflammatory and vascular diseases (2007, background): “MMP7 was found to be essential to generate a chemotactic gradient for neutrophils from the perivascular space to the alveolar lumen, by cleaving the proteoglycan syndecan-1, which associates with the chemokine K”
• Physiology and pathophysiology of matrix metalloproteases (2010, background): “MMP-7 further enables migration of neutrophils through the epithelium during inflammation, since MMP-7 null mice show accumulation of neutrophils in the interstitium without them crossing over into the epithelium (Li et al. 2002).”
• Matrix metalloproteinases. (2010, background): “MMPs can also modulate antitumour immune reactions by efficiently cleaving several chemokines or regulating their mobilization [143-145].”
• Control of matrix metalloproteinase catalytic activity. (2007, background): “, 1999) (clearly beneficial functions), but it also promotes neutrophil activation, which can be damaging and lethal (Li et al., 2002; McGuire et al., 2003).”