Matrix metalloproteinase expression and function during fin regeneration in zebrafish: Analysis of MT1-MMP, MMP2 and TIMP2

Bai, Shan; Thummel, Ryan; Godwin, Alan R.; Nagase, Hideaki; Itoh, Yoshifumi; Li, Li; Evans, Richard D.; McDermott, Jeffrey; Seiki, Motoharu; Sarras, Michael P.

doi:10.1016/j.matbio.2005.03.007

Cited by 103 publications

(80 citation statements)

References 49 publications

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“…We found no obvious differences between genotypes in the neuroepithelial expression of genes encoding Wnt (wnt1), VEGF-A (vegfaa and vegfab) and SDF (sdf1b; also known as cxcl12b) ligands and Reck-targeted MPs (mmp2 and mmp14a). Analysis of the expression of pan-endothelial genes [ fli1a, tie1 and ve-cdh (also known as cdh5)] and markers of specific cerebral vessels (dab2, dll4 and cxcr4a) failed to reveal any obvious expression abnormalities, beyond the anticipated CtA labeling deficit in reck y72 mutants (Amoyel et al, 2005;Bai et al, 2005;Brown et al, 2000;Bussmann et al, 2011;Fujita et al, 2011;Janssens et al, 2013;Larson et al, 2004;Lyons et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Reck enables cerebrovascular development by promoting canonical Wnt signaling

et al. 2015

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The cerebral vasculature provides the massive blood supply that the brain needs to grow and survive. By acquiring distinctive cellular and molecular characteristics it becomes the blood-brain barrier (BBB), a selectively permeable and protective interface between the brain and the peripheral circulation that maintains the extracellular milieu permissive for neuronal activity. Accordingly, there is great interest in uncovering the mechanisms that modulate the formation and differentiation of the brain vasculature. By performing a forward genetic screen in zebrafish we isolated no food for thought (nft y72 ), a recessive late-lethal mutant that lacks most of the intracerebral central arteries (CtAs), but not other brain blood vessels. We found that the cerebral vascularization deficit of nft y72 mutants is caused by an inactivating lesion in reversion-inducing cysteine-rich protein with Kazal motifs [reck; also known as suppressor of tumorigenicity 15 protein (ST15)], which encodes a membrane-anchored tumor suppressor glycoprotein. Our findings highlight Reck as a novel and pivotal modulator of the canonical Wnt signaling pathway that acts in endothelial cells to enable intracerebral vascularization and proper expression of molecular markers associated with BBB formation. Additional studies with cultured endothelial cells suggest that, in other contexts, Reck impacts vascular biology via the vascular endothelial growth factor (VEGF) cascade. Together, our findings have broad implications for both vascular and cancer biology.

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Section: Introductionmentioning

confidence: 99%

Reck enables cerebrovascular development by promoting canonical Wnt signaling

et al. 2015

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“…The expression and functional role of MMPs has been studied in adult zebrafish regenerating fin and have demonstrated that membrane-type mmp, mmp-2, and timp-2 mRNA transcripts were expressed in the regenerating fin tissue. Fin outgrowth was significantly reduced by GM6001, an MMP inhibitor, emphasizing the magnitude of these proteinases during fin regeneration (Bai et al, 2005). Likewise, MMP inhibitor studies demonstrate that these enzymes are required for normal newt limb regeneration, and mmp3/10a, mmp3/10b, and mmp-9 are up-regulated within hours of limb amputation.…”

Section: Downloaded Frommentioning

confidence: 94%

Aryl Hydrocarbon Receptor Activation Inhibits Regenerative Growth

2005

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There is considerable literature supporting the conclusion that inappropriate activation of the aryl hydrocarbon receptor (AHR) alters cellular signaling. We have established previously that fin regeneration is specifically inhibited by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult zebrafish and have used this in vivo endpoint to evaluate interactions between AHR and growth-controlling pathways. Because there are experimental limitations in studying regeneration in adult animals, we have developed a larval model to evaluate the effect of AHR activation on tissue regeneration. Two-day-old zebrafish regenerate their amputated caudal fins within 3 days. Here, we demonstrate that TCDD specifically blocks regenerative growth in larvae. The AHR pathway in zebrafish is considerably more complex than in mammals, with at least three zebrafish AHR genes (zfAHR1a, zfAHR1b, and zfAHR2) and two ARNT genes (zfARNT1 and zfARNT2). Although it was presumed that the block in regeneration was mediated by AHR activation, it had not been experimentally demonstrated. Using antisense morpholinos and mutant fish lines, we report that zfAHR2 and zfARNT1 are the in vivo dimerization partners that are required for inhibition of regeneration by TCDD. Several pathways including fibroblast growth factor (FGF) signaling are essential for fin regeneration. Even though impaired FGF signaling and TCDD exposure both inhibit fin regeneration, their morphometric response is distinct, suggesting that the mechanisms of impairment are different. With the plethora of molecular and genetic techniques that can be applied to larval-stage embryos, this in vivo regeneration system can be further exploited to understand cross-talk between AHR and other signaling pathways.

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“…Although the mouse double mutants that have been examined survive to birth 7,8,56 , it is not feasible to knockout all the MMPs in a mouse to test the general role of the MMP family. MMP expression and inhibition have been examined in many other model systems, including Xenopus laevis 65,66 , hydra 67 , zebrafish [68][69][70] and Caenorhabditis elegans 71,72 ; in C. elegans, genetic analysis indicates that a worm MMP contributes to a developmentally regulated cell-invasion event 71 . The fruitfly D. melanogaster has fewer MMPs than any other model system studied, with only two MMPs 73,74 , and mutants have been generated that lack both genes 75 .…”

Section: Mmps Regulate Tissue Remodelling In Fliesmentioning

confidence: 99%

Matrix metalloproteinases and the regulation of tissue remodelling

Page-McCaw

Ewald

Werb

2007

Nat Rev Mol Cell Biol

2,589

2,180

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Matrix metalloproteinases (MMPs) were discovered because of their role in amphibian metamorphosis, yet they have attracted more attention because of their roles in disease. Despite intensive scrutiny in vitro, in cell culture and in animal models, the normal physiological roles of these extracellular proteases have been elusive. Recent studies in mice and flies point to essential roles of MMPs as mediators of change and physical adaptation in tissues, whether developmentally regulated, environmentally induced or disease associated.The founding member of the matrix metalloproteinase (MMP) family, collagenase, was identified in 1962 by Gross and Lapiere, who found that tadpole tails during metamorphosis contained an enzyme that could degrade fibrillar collagen 1,2 . Subsequently, an interstitial collagenase, collagenase-1 or MMP1, was found in diseased skin and synovium 3 . In vitro, MMP1 initiates degradation of native fibrillar collagens, crucial components of vertebrate extracellular matrix (ECM), by cleaving the peptide bond between Gly775-Ile776 or Gly775-Lys776 in native type I, II or III collagen molecules 3,4 . Further research led to the discovery of a family of structurally related proteinases (23 in human, 24 in mice), now referred to as the MMP family.Interest in MMPs increased in the late 1960s and early 1970s following observations that MMPs are upregulated in diverse human diseases including rheumatoid arthritis and cancer. Importantly, high levels of MMPs often correlated with poor prognosis in human patients (reviewed in REF. 5 ). However, recent clinical data indicate that the relationship between § These authors contributed equally to this paper. Competing interests statementThe authors declare no competing financial interests. DATABASESThe following terms in this article are linked online to: Entrez Genome: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=gene DmMmp1 | DmMmp2 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptMMPs and disease is not simple; for example, increased MMP activity can enhance tumour progression or can inhibit it (reviewed in REF. 6 ). This complex relationship between MMP expression and cancer has increased the basic and clinical interest in understanding MMP function in vivo, but it has also focused attention on MMPs and pathology, and relatively less attention has been focused on the normal roles of these enzymes. MMP proteolysisMMPs are members of the metzincin group of proteases, which are named after the zinc ion and the conserved Met residue at the active site 11,12 . Recent work has generated a unified peptidase nomenclature 13 Functions of MMP proteolysisHistorically, MMPs were thought to function mainly as enzymes that degrade structural components of the ECM. However, MMP proteolysis can create space for cells to migrate, can produce specific substrate-cleavage fragments with independent biological activity, can MMPs in bone modelling and remodellingBone is an important site of ongoing tissue remodelling during development...

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Matrix metalloproteinase expression and function during fin regeneration in zebrafish: Analysis of MT1-MMP, MMP2 and TIMP2

Cited by 103 publications

References 49 publications

Reck enables cerebrovascular development by promoting canonical Wnt signaling

Reck enables cerebrovascular development by promoting canonical Wnt signaling

Aryl Hydrocarbon Receptor Activation Inhibits Regenerative Growth

Matrix metalloproteinases and the regulation of tissue remodelling

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