Evidence map›Paper›PMID 19429683›Full record

ArticleThe Journal of biological chemistry2009

Differential regulation of cell type-specific apoptosis by stromelysin-3: a potential mechanism via the cleavage of the laminin receptor during tail resorption in Xenopus laevis.

Smita Mathew, Liezhen Fu, Maria Fiorentino, Hiroki Matsuda, Biswajit Das, Yun-Bo Shi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
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  8. Article
  9. Article
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  12. Apoptosis in amphibian organs during metamorphosis.Apoptosis : an international journal on programmed cell death · 2010
    Review
  13. Review
  14. Article
  15. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Smita MathewSection on Molecular Morphogenesis, Laboratory of Gene Regulation and Development, Program in Cellular Regulation and Metabolism, NICHD, National Institutes of Health, Bethesda, Maryland 20892, USA.
Liezhen Fu
Maria Fiorentino
Hiroki Matsuda
Biswajit Das
Yun-Bo Shi
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · US

Funding

Regulation and function of matrix metalloproteinases during frog metamorphosisZIAHD008859 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SHI, YUN-BO · 2009 to 2010
$594k
Regulation and function of matrix metalloproteinases during frog metamorphosisZ01HD008859 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI SHI, YUN-BO · 2008 to 2008
$506k
Intramural NIH HHS
6 · The paper itself

Abstract

Matrix metalloproteinases (MMPs) have been extensively studied because of their functional attributes in development and diseases. However, relatively few in vivo functional studies have been reported on the roles of MMPs in postembryonic organ development. Amphibian metamorphosis is a unique model for studying MMP function during vertebrate development because of its dependence on thyroid hormone (T3) and the ability to easily manipulate this process with exogenous T3. The MMP stromelysin-3 (ST3) is induced by T3, and its expression correlates with cell death during metamorphosis. We have previously shown that ST3 is both necessary and sufficient for larval epithelial cell death in the remodeling intestine. To investigate the roles of ST3 in other organs and especially on different cell types, we have analyzed the effect of transgenic overexpression of ST3 in the tail of premetamorphic tadpoles. We report for the first time that ST3 expression, in the absence of T3, caused significant muscle cell death in the tail of premetamorphic transgenic tadpoles. On the other hand, only relatively low levels of epidermal cell death were induced by precocious ST3 expression in the tail, contrasting what takes place during natural and T3-induced metamorphosis when ST3 expression is high. This cell type-specific apoptotic response to ST3 in the tail suggests distinct mechanisms regulating cell death in different tissues. Furthermore, our analyses of laminin receptor, an in vivo substrate of ST3 in the intestine, suggest that laminin receptor cleavage may be an underlying mechanism for the cell type-specific effects of ST3.

Indexed as

AnimalsApoptosisEpidermisGene Expression Regulation, DevelopmentalHeat-Shock ResponseLarvaMatrix Metalloproteinase 11Metamorphosis, BiologicalMusclesOrganisms, Genetically ModifiedReceptors, LamininTailTransgenesTriiodothyronineXenopus laevisMatrix Metalloproteinase 11Receptors, LamininTriiodothyronine

Identifiers

PMID19429683
PMCPMC2709371
OpenAlexW2074032055

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.