Tissue Inhibitor of Metalloproteinase-2 Promotes Neuronal Differentiation by Acting as an Anti-Mitogenic Signal

Pérez-Martı́nez, Leonor; Jaworski, Diane M.

doi:10.1523/jneurosci.5066-04.2005

Cited by 110 publications

(107 citation statements)

References 66 publications

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“…They show that differentiation and subsequent functional plasticity recovery is correlated to an increased MMP-2 activity (Reeves et al 2003). Similarly, during brain disaggregation neurons are strained because of disruption of connections to the neighbouring cells triggering a recovery-like cell response (Pérez-Martínez and Jaworski 2005). In the present work we show that after 1 day in culture, MMP-2 expression and activity levels are higher for neurons isolated with cardosins compared to trypsin.…”

Section: Discussionsupporting

confidence: 60%

Cardosins improve neuronal regeneration after cell disruption: a comparative expression study

Duarte

Correia

et al. 2008

Cell Biol Toxicol

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The establishment of primary cell cultures is invaluable for studying cell and molecular biological questions. Although primary cell cultures more closely resemble and function like in the native environment, during the culture establishment the cells undergo several changes including the damage sustained during their removal from original tissue. The resultant cells have to rebalance the expression of their processing molecules to ascertain matrix signalling that ensure cell adaptation and consequent proliferation. Hence, we used cardosin, a novel plant enzyme for tissue disaggregation, for isolating and culturing neuronal cells from embryonic rats. The present investigation reports the molecular events, mainly related with matrix metalloproteinases (MMPs)/tissue inhibitor of metalloproteinase (TIMPs) expression, which could substantiate the superior neurite outgrowth and dendritic extension previously described. It was observed that 24 h after primary culture establishment, MMP-2 and MMP-9 messenger RNA (mRNA) are significantly upregulated, while the expression of TIMP-1 and TIMP-2 is unaltered. Regarding the role of laminin in neuronal pathfinding, it was found that the use of anti-laminin antibody and arginine-glycine-aspartate (RGD) peptide exerted inhibitory effects on neurite outgrowth after mechanical lesion where the expression of MMP-9 and TIMP-1 is upregulated under non-permissive conditions in response to mechanical injury.

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Section: Discussionsupporting

confidence: 60%

Cardosins improve neuronal regeneration after cell disruption: a comparative expression study

Duarte

Correia

et al. 2008

Cell Biol Toxicol

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“…The PFA-fixed cells were then permeabilized and stained with propidium iodide using 500 AL of low-salt solution (0.1% Triton X-100, 3% polyethylene glycol-8000, 50 Ag/mL propidium iodide, 100 Ag/mL RNase, 4 mmol/L sodium citrate, pH 7.1-7.2) for 30 min at 4jC, and subsequently added with an equal volume of high-salt solution (0.1% Triton X-100, 3% polyethylene glycol-8000, 50 Ag/mL propidium iodide, 100 Ag/mL RNase, 400 mmol/L NaCl, pH 7.1-7.2) for 30 min at 4jC (13). The propidium iodide-stained cells were analyzed by fluorescence-activated cell sorting (Beckman Coulter).…”

Section: Methodsmentioning

confidence: 99%

Lipid Raft–Specific Knockdown of Src Family Kinase Activity Inhibits Cell Adhesion and Cell Cycle Progression of Breast Cancer Cells

et al. 2007

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Src family kinase (SFK) is known to control various cell functions, but the significance of the location of its activation was largely unknown. We herein revealed that SFK activation occurs in lipid rafts. Based on this finding, we have developed a lipid raft-targeted SFK inhibitory fusion protein (LRT-SIFP) that inhibits the SFK activity in lipid rafts. LRT-SIFP has a peptide inhibitor of SFK and a lipid raft-targeting sequence in which two cysteine residues are palmitoylated for clustering in lipid rafts. LRT-SIFP was found to inhibit cell adhesion and cell cycle progression of human breast cancer cell lines MCF-7 and MDA-MB231. On the other hand, the cell functions of MCF-7 cells were found to be not affected with a previously developed peptide inhibitor of SFK that lacks the lipid rafttargeting sequence. In addition, when we replaced the targeting sequence of LRT-SIFP with the consensus sequence for geranylgeranylation to make LRT-SIFP unable to cluster in lipid rafts, this mutated LRT-SIFP did not show any effect on the above cell functions of MCF-7 cells. Furthermore, in contrast to the breast cancer cell lines, LRT-SIFP did not show any inhibitory effect on cell adhesion and cell cycle progression of human normal cell line HEK293. The present lipid raft-specific knockdown of SFK activity would potentially be useful for selective cancer therapy to prevent tumorigenesis and metastasis of breast cancer cells. [Cancer Res 2007;67(17):8139-48]

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“…In contrast, the TIMP-2-proMMP-2 complex facilitates proMMP-2 activation (Brew et al, 2000;Gasche et al, 2006). Tissue inhibitor of metalloproteinases have also been shown to play roles in cell proliferation, differentiation, and angiogenic processes through mechanisms independent of MMP inhibition (Reed et al, 2003;Perez-Martinez and Jaworski, 2005).…”

Section: Introductionmentioning

confidence: 99%

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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Tissue Inhibitor of Metalloproteinase-2 Promotes Neuronal Differentiation by Acting as an Anti-Mitogenic Signal

Cited by 110 publications

References 66 publications

Cardosins improve neuronal regeneration after cell disruption: a comparative expression study

Cardosins improve neuronal regeneration after cell disruption: a comparative expression study

Lipid Raft–Specific Knockdown of Src Family Kinase Activity Inhibits Cell Adhesion and Cell Cycle Progression of Breast Cancer Cells

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

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