Role for Matrix Metalloproteinase 9 after Focal Cerebral Ischemia: Effects of Gene Knockout and Enzyme Inhibition with BB-94

By M. Asahi, Kazuko Asahi, Jae Chang Jung, G. del Zoppo, M. E. Fini, Eng H. Lo. Journal of Cerebral Blood Flow and Metabolism, 2000

604 citations recorded by the source corpus.

Subfields: Cancer Research, Hematology, Immunology and Allergy

View Paper: https://www.semanticscholar.org/paper/d6197c6b7851acce90173fa928e2807e569b2787

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. Gary A. Rosenberg
2. S. Doré
3. T. Mabuchi
4. G. D. del Zoppo
5. B. Bauer
6. A. Hartz
7. R. Rempe
8. G. Moalem-Taylor

In Hematology

1. S. Doré
2. T. Mabuchi
3. G. D. del Zoppo
4. Gary A. Rosenberg
5. G. Moalem-Taylor
6. P. Austin

In Immunology and Allergy

1. B. Bauer
2. A. Hartz
3. R. Rempe

Citations in the corpus

• Blood-brain barrier pathophysiology in traumatic brain injury (2011, background): “Genetic deletion of the Mmp9 gene or the pharmacological inhibition of activity of MMPs was found to significantly reduce the extent of brain tissue damage and to improve functional outcome in murine models of cerebral ischemia and TBI [108, 109].”
• Effects of Matrix Metalloproteinase-9 Gene Knock-Out on the Proteolysis of Blood–Brain Barrier and White Matter Components after Cerebral Ischemia (2001, methodology): “After separation by electrophoresis, the gel was renatured and then incubated with developing buffer at 37°C for 24 hr as previously described (Asahi et al., 2000b).”
• Matrix metalloproteinases in the brain and blood–brain barrier: Versatile breakers and makers (2016, background): “Third, MMP inhibition with GM6001 or BB-94 in rodent stroke models shortly (hours) after stroke reduced edema, infarct size, and the number of hemorrhagic events.(180,185,300,301) Long-term (days) MMP inhibition with the MMP-inhibitor BB-1101 for up to 48 h after stroke in rats reduced barrier leaka”
• Role of extracellular matrix in adaptation of tendon and skeletal muscle to mechanical loading. (2004, background): “Collagen degradation is initiated extracellularly by MMPs (or matrixins), which are presented in tissues mostly as latent proMMPs (38, 49, 475).”
• The inflammatory response in stroke. (2007, methodology): “compared to wildtype controls (Asahi et al., 2000); however, such an effect was not observed in MMP-2 deficient mice (Asahi et al.”
• Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke. (2019, background): “Different inhibitors of MMPs, such as BB-94 and KB-R7785, administered after ischemia, reduced the damage induced by MCAO in mice (9, 89).”
• Matrix metalloproteinases in neuroinflammation (2002, background): “A MMP-9 knockout mouse was found to have reduced infarct size and less BBB damage (Asahi et al., 2000, 2001).”
• Cerebral Microvessel Responses to Focal Ischemia (2003, background): “Lo and investigators have confirmed that pro-MMP-9, but not pro-MMP-2, expression is associated with focal ischemia in the rodent (Asahi et al., 2000, 2001a,b), and that deletion of the MMP-9 gene is associated with a decrease in microvascular permeability, but not in laminin immunoreactivity…”
• Resveratrol regulates neuro-inflammation and induces adaptive immunity in Alzheimer’s disease (2017, background): “Animal studies have also revealed significant increases in MMP9 levels after traumatic brain injury [17], but damage to the BBB and behavioral deficits are significantly attenuated in MMP9 knockout animals [18, 19].”