Abstract：
:Brain extracellular matrix (ECM) is highly degraded after cerebral ischemia. The perlecan c-terminal fragment LG3 is generated at increased levels by proteolytic processing as long as 3 days after ischemia. It has previously been shown that oxygen-glucose deprivation (OGD), reperfusion and interleukin-1 α (IL-1α) stimulate brain cells to yield increased levels of LG3. This LG3, in turn, is neuroprotective against OGD, and may therefore represent one of the brain's defenses against ischemic injury. Here, we investigate whether, in neurons, this increased LG3 is the result of increased perlecan generation and cellular release, increased protease release (to generate LG3 from previous extracellularly deposited perlecan) or both. We found that pre-synthesized perlecan may be exocytosed by neurons during OGD and de novo synthesis of perlecan is increased during reperfusion, even 24 h after OGD. Furthermore, while cathepsin L activity was seen to be marginally important to generate LG3 during normoxic conditions, cathepsin B activity was found to be important to generate increased levels of LG3 following OGD and reperfusion. On the other hand, IL-1α treatment raised levels of cathepsin L in neuronal media, and both cathepsin L and cathepsin B were demonstrated to be important for increasing LG3 levels after IL-1α treatment.
journal_name
Brain Resjournal_title
Brain researchauthors
Saini MG,Bix GJdoi
10.1016/j.brainres.2011.12.027subject
Has Abstractpub_date
2012-02-15 00:00:00pages
65-74eissn
0006-8993issn
1872-6240pii
S0006-8993(11)02228-1journal_volume
1438pub_type
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