ELEVATED MMP-9 brain inflamation

[Guest guest]

J posted this back in 08.

http://ajpheart.physiology.org/cgi/content/full/289/2/H558

ELEVATED MMP-9

http://ajpheart.physiology.org/cgi/content/full/289/2/H558

[Guest guest]

Thanks k,good find,

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> J posted this back in 08.

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> http://ajpheart.physiology.org/cgi/content/full/289/2/H558

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> ELEVATED MMP-9

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> http://ajpheart.physiology.org/cgi/content/full/289/2/H558

>

>

>

[Guest guest]

check out some of the cited abstracts on this.

Blood–Brain Barrier Disruption in Humans Is Independently Associated With

Increased Matrix Metalloproteinase-9

Conclusions— Baseline MMP-9 was a significant predictor of HARM at 24-hour

follow-up, supporting the hypothesis that MMP-9 is associated with BBB

disruption. If the association between MMP-9 and BBB disruption is confirmed in

future studies, HARM may be a useful imaging marker to evaluate MMP-9 inhibition

in ischemic stroke and other populations with BBB disruption.

http://stroke.ahajournals.org/cgi/content/abstract/41/3/e123

Systemic Inflammation Alters the Kinetics of Cerebrovascular Tight Junction

Disruption after Experimental Stroke in Mice

Systemic inflammatory events, such as infection, increase the risk of stroke and

are associated with worse outcome.

Systemic inflammation caused an alteration in the kinetics of blood–brain

barrier (BBB) disruption through conversion of a transient to a sustained

disruption of the tight junction protein, claudin-5, and also markedly

exacerbated disruption to the cerebrovascular basal lamina protein, collagen-IV.

These alterations were associated with a systemic inflammation-induced increase

in neurovascular gelatinolytic activity that was mediated by a fivefold increase

in neutrophil-derived matrix metalloproteinase-9 (MMP-9).

Specific inhibition of MMP-9 abrogated the effects of systemic inflammation on

the sustained but not the acute disruption of claudin-5, which was associated

with phosphorylation of cerebrovascular myosin light chain. MMP-9 inhibition

also attenuated the deleterious impact of systemic inflammation on brain damage,

edema, neurological deficit, and incidence of hemorrhagic transformation. These

data indicate that a transformation from transient to sustained BBB disruption

caused by enhanced neutrophil-derived neurovascular MMP-9 activity is a critical

mechanism underlying the exacerbation of ischemic brain injury by systemic

inflammation.

http://www.jneurosci.org/cgi/content/abstract/28/38/9451

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> > J posted this back in 08.

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> > http://ajpheart.physiology.org/cgi/content/full/289/2/H558

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