abstract

• Intracerebral hemorrhage (ICH) leads to delayed cell death in the regions around the hemorrhagic mass. Apoptosis has been identified in the dying cells, but the mechanism involved is unclear. Others and us have shown that matrix metalloproteinases (MMPs) are increased in ICH and could directly contribute to cell death. Tissue inhibitor to metalloproteinases-3 (TIMP-3) facilitates apoptosis in cancer cells and neurons by inhibiting the shedding of tumor necrosis factor-alpha (TNF-alpha) death receptors, Fas and p55TNF receptor 1, by MMP-3 and TNF-alpha converting enzyme (TACE), respectively. Therefore, TIMP-3 may contribute to cell death in ICH. We adapted the bacterial collagenase-induced hemorrhage (CIH) model to the mouse. Adult C57Bl/6 and Timp-3 knockout mice had CIH. Expression of mRNA for TIMP-3 was determined by real-time PCR. Hemorrhage volume and numbers of apoptotic cells were measured by unbiased stereology. Timp-3 mRNA was similar in the knockout and wild-type mice prior to injury and induction of CIH failed to cause an increase in Timp-3 mRNA in the wild-type. Furthermore, there were no differences found in the hemorrhage size or in the numbers of apoptotic cells between the Timp-3 knockout or wild-type. We were unable to prove the hypothesis that TIMP-3 is involved cell death in CIH in the mouse.

authors

• Grossetete, Mark
• Rosenberg, Gary

publication date

• January 1, 2008

published in

• Acta neurochirurgica. Supplement  Journal

keywords

• Animals
• Apoptosis
• Cell Count
• Cerebral Hemorrhage
• Collagenases
• Disease Models, Animal
• Gene Expression Regulation
• In Situ Nick-End Labeling
• Male
• Matrix Metalloproteinase 2
• Matrix Metalloproteinase 9
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• RNA, Messenger
• Time Factors
• Tissue Inhibitor of Metalloproteinase-3

PubMed ID

• 19066089

start page

• 89

end page

• 93

volume

• 105

number