Tissue inhibitor of metalloproteinase 1 inhibits excitotoxic cell death in neurons

Tan, Hiang Khoon; Heywood, Darren; Ralph, G; Bienemann, Alison; Baker, Andrew H.; Uney, James B.

doi:10.1016/s1044-7431(02)00024-6

Cited by 80 publications

(84 citation statements)

References 37 publications

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“…Levels of TIMP-1 expression were found to be increased in the hippocampal formation after transient forebrain ischemia or seizure and in the retinal ganglion cell layer after elevation of intraocular pressure (Rivera et al, 1997(Rivera et al, , 2002Jourquin et al, 2005). Manipulations increasing TIMP-1 were shown to protect neurons in dissociated and organotypic hippocampal cultures from excitotoxicity but not from apoptosis induced by withdrawal of nerve growth factor or chemical-induced ischemia (Tan et al, 2003). Developmental regulation of TIMP-2 was demonstrated in neural progenitor and neuroblastoma cell lines treated with neurotrophic factors or retinoic acid (Jaworski and Perez-Martinez, 2006).…”

Section: Introductionmentioning

confidence: 97%

Tissue inhibitor of metalloproteinases-3 (TIMP-3) expression is increased during serum deprivation-induced neuronal apoptosis in vitro and in the G93A mouse model of amyotrophic lateral sclerosis: A potential modulator of Fas-mediated apoptosis

Lee

Shin

Suh

et al. 2008

Neurobiology of Disease

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Section: Introductionmentioning

confidence: 97%

Tissue inhibitor of metalloproteinases-3 (TIMP-3) expression is increased during serum deprivation-induced neuronal apoptosis in vitro and in the G93A mouse model of amyotrophic lateral sclerosis: A potential modulator of Fas-mediated apoptosis

Lee

Shin

Suh

et al. 2008

Neurobiology of Disease

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“…In hippocampal primary and organotypic cultures, TIMP-1 protected against glutamate-induced cytotoxicity by decreasing neuronal calcium influx (Tan et al, 2003). Adenovirus-mediated gene transfer of TIMP-1 and TIMP-2 were neuroprotective in global ischemia (Magnoni et al, 2007).…”

Section: Introductionmentioning

confidence: 98%

Tissue Inhibitor of Metalloproteinases Protect Blood—Brain Barrier Disruption in Focal Cerebral Ischemia

Fujimoto

Takagi

Aoki

et al. 2008

J Cereb Blood Flow Metab

140

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Enhanced matrix metalloproteinases (MMPs) can cause vasogenic edema and hemorrhagic transformation after cerebral ischemia, and affect the extent of ischemic injury. We hypothesized that the endogenous MMP inhibitors, tissue inhibitor of MMPs (TIMPs), were essential to protect against blood-brain barrier (BBB) disruption after ischemia by regulating the activities of MMPs. We confirmed the transition of MMP-2 and MMP-9, and the TIMPs family after 30 mins of middle cerebral artery occlusion, and elucidated the function of TIMP-1 and TIMP-2 in focal ischemia, using TIMP-1 À/À and TIMP-2 À/À mice. TIMP-1 mRNA expression was gradually increased until 24 h after reperfusion. In TIMP-1 À/À mice, MMP-9 protein expression and gelatinolytic activity were significantly more augmented after cerebral ischemia than those in WT mice, and were accompanied by exacerbated BBB disruption, neuronal apoptosis, and ischemic injury. In contrast, TIMP-2 gene deletion mice exhibited no significant difference in MMP expressions and the degree of ischemic injury despite an increased Evans blue leakage. These results suggest that TIMP-1 inhibits MMP-9 activity and can play a neuroprotective role in cerebral ischemia.

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“…Induction of TIMP overexpression may therefore reduce ischemic damage by either reducing exaggerated MMP activity or activating neuroprotective signals and is likely dependent on the choice of inhibitor. Notably, synthetic MMP inhibitors could not mimic this beneficial effect (22), and studies highlight the importance of a therapeutic window for MMP inhibition with such suppression resulting in exacerbation of lesion size and reduced recovery (23,24). Gene transfer can result in efficient production of proteins for a transient or long period by a single injection of vector, overcoming disadvantages of infection caused by retention of catheters and brain damage caused by repeated therapeutic injections.…”

mentioning

confidence: 99%

Brain protection using autologous bone marrow cell, metalloproteinase inhibitors, and metabolic treatment in cerebral ischemia

Baker

Sica

Work

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Despite advances in imaging, understanding the underlying pathways, and clinical translation of animal models of disease there remains an urgent need for therapies that reduce brain damage after stroke and promote functional recovery in patients. Blocking oxidant radicals, reducing matrix metalloproteinase-induced neuronal damage, and use of stem cell therapy have been proposed and tested individually in prior studies. Here we provide a comprehensive integrative management approach to reducing damage and promoting recovery by combining biological therapies targeting these areas. In a rat model of transient cerebral ischemia (middle cerebral artery occlusion) gene delivery vectors were used to overexpress tissue inhibitor of matrix metalloproteinase 1 and 2 (TIMP1 and TIMP2) 3 days before ischemia. After occlusion, autologous bone marrow cells alone or in combination with agents to improve NO bioavailability were administered intraarterially. When infarct size, BrdU incorporation, and motor function recovery were determined in the treatment groups the largest beneficial effect was seen in rats receiving the triple combined therapy, surpassing effects of single or double therapies. Our study highlights the utility of combined drug, gene, and cell therapy in the treatment of stroke.

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Tissue inhibitor of metalloproteinase 1 inhibits excitotoxic cell death in neurons

Cited by 80 publications

References 37 publications

Tissue inhibitor of metalloproteinases-3 (TIMP-3) expression is increased during serum deprivation-induced neuronal apoptosis in vitro and in the G93A mouse model of amyotrophic lateral sclerosis: A potential modulator of Fas-mediated apoptosis

Tissue inhibitor of metalloproteinases-3 (TIMP-3) expression is increased during serum deprivation-induced neuronal apoptosis in vitro and in the G93A mouse model of amyotrophic lateral sclerosis: A potential modulator of Fas-mediated apoptosis

Tissue Inhibitor of Metalloproteinases Protect Blood—Brain Barrier Disruption in Focal Cerebral Ischemia

Brain protection using autologous bone marrow cell, metalloproteinase inhibitors, and metabolic treatment in cerebral ischemia

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