Matrix metalloproteinases in neuroinflammation

By Gary A. Rosenberg. Glia, 2002

856 citations recorded by the source corpus.

Subfields: Cancer Research, Hematology, Oncology

View Paper: https://www.semanticscholar.org/paper/8c38025ed89a14049974151251007ee9bf74bf5a

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. G. Moalem-Taylor
2. Jian Wang
3. P. Austin
4. T. Mabuchi
5. J. McGuire
6. A. Manicone
7. S. Doré
8. G. D. del Zoppo

In Hematology

1. G. Moalem-Taylor
2. Jian Wang
3. P. Austin
4. T. Mabuchi
5. J. McGuire
6. A. Manicone
7. S. Doré
8. G. D. del Zoppo

In Oncology

1. G. Moalem-Taylor
2. Jian Wang
3. P. Austin
4. T. Mabuchi
5. J. McGuire
6. A. Manicone
7. S. Doré
8. G. D. del Zoppo

Citations in the corpus

• The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. (2010, positive): “, 2006), possibly to assist in the demyelinating process (Rosenberg, 2002).”
• The inflammatory response in stroke. (2007, background): “MMPs are normally found in the cytosol in a pro- or inactivated state, but are cleaved by proteases such as plasmin or other MMPs to their active state (Rosenberg, 2002).”
• Matrix metalloproteinases as modulators of inflammation. (2008, background): “Similarly, MMP2 and MMP9 can regulate endothelial permeability by cleaving occludin, the transmembrane component of endothelial tight junctions, in the opening of the blood-brain barrier (BBB) [15], a process that may contribute to enhanced permeability and inflammation in autoimmune encephalitis, h”
• Resveratrol regulates neuro-inflammation and induces adaptive immunity in Alzheimer’s disease (2017, background): “MMP9-mediated breakdown of the basal lamina and destruction of gap junctions in the neurovascular unit result in increased CNS permeability and inflammation in autoimmune encephalitis, hypoxic brain injury, and other diseases [9, 10].”
• Cerebral Microvessel Responses to Focal Ischemia (2003, background): “The appearance of the u-PA activity in the ischemic core (relative to PAI-1) does not clearly allow the conclusion that pro–MMP-2 is activated but suggests that u-PA may be an indirect activator.”
• CNS immune privilege: hiding in plain sight (2006, background): “Finally, inflammation can promote both cell death and cell regeneration (4).”
• Inflammation after Intracerebral Hemorrhage (2007, background): “Many investigators have reviewed the role of MMPs in mediating acute brain injury after ischemia and trauma (Cunningham et al, 2005; Gasche et al, 2006; Rosenberg, 2002; Rosenberg and Mun-Bryce, 2004; Wang and Lo, 2003), but because MMPs are essential for neurogenesis, myelin formation, and axonal g”