Evidence map›Paper›PMID 9121441›Full record

ArticleMolecular and cellular biology1997

Suppression of autocrine and paracrine functions of basic fibroblast growth factor by stable expression of perlecan antisense cDNA.

D Aviezer, R V Iozzo, D M Noonan, A Yayon

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.Matrix biology : journal of the International Society for Matrix Biology · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Proteoglycan form and function: A comprehensive nomenclature of proteoglycans.Matrix biology : journal of the International Society for Matrix Biology · 2015
    Review
  11. Review
  12. Review
  13. Article
  14. Endorepellin evokes autophagy in endothelial cells.The Journal of biological chemistry · 2014
    Article
  15. The role of vascular-derived perlecan in modulating cell adhesion, proliferation and growth factor signaling.Matrix biology : journal of the International Society for Matrix Biology · 2014
    Article
  16. Article
  17. Article
  18. Antithetic roles of proteoglycans in cancer.Cellular and molecular life sciences : CMLS · 2012
    Review
  19. Article
  20. Proteoglycans in cancer biology, tumour microenvironment and angiogenesis.Journal of cellular and molecular medicine · 2011
    Review
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

4 authors at 3 institutions in 3 countries.

D AviezerDepartment of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel.
R V Iozzo
D M Noonan
A Yayon
Weizmann Institute of Science · ILAlleanza Contro il Cancro · ITThomas Jefferson University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heparan sulfate proteoglycans (HSPG) play a critical role in the formation of distinct fibroblast growth factor (FGF)-HS complexes, augmenting high-affinity binding and receptor activation. Perlecan, a secreted HSPG abundant in proliferating cells, is capable of inducing FGF-receptor interactions in vitro and angiogenesis in vivo. Stable and specific reduction of perlecan levels in mouse NIH 3T3 fibroblasts and human metastatic melanoma cells has been achieved by expression of antisense cDNA corresponding to the N-terminal and HS attachment domains of perlecan. Long-term perlecan downregulation is evidenced by reduced levels of perlecan mRNA and core protein as indicated by Northern blot analysis, immunoblots, and immunohistochemistry, using DNA probes and antibodies specific to mouse or human perlecan. The response of antisense perlecan-expressing cells to increasing concentrations of basic FGF (bFGF) is dramatically reduced in comparison to that in wild-type or vector-transfected cells, as measured by thymidine incorporation and rate of proliferation. Furthermore, receptor binding and affinity labeling of antisense perlecan-transfected cells with 125I-bFGF is markedly inhibited, indicating that eliminating perlecan expression results in reduced high-affinity bFGF binding. Both the binding and mitogenic response of antisense-perlecan-expressing clones to bFGF can be rescued by exogenous heparin or perlecan. These results support the notion that perlecan is a major accessory receptor for bFGF in mouse fibroblasts and human melanomas and point to the possible use of perlecan antisense constructs as specific modulators of bFGF-mediated responses.

Indexed as

Heparan Sulfate Proteoglycans3T3 CellsAnimalsCell DivisionDNA, AntisenseFibroblast Growth Factor 2Gene ExpressionHeparan SulfateHeparinHumansMiceProteoglycansRNA, MessengerTransfectionTumor Cells, CulturedDNA, AntisenseFibroblast Growth Factor 2Heparan SulfateHeparan Sulfate ProteoglycansHeparinperlecanProteoglycansRNA, Messenger

Identifiers

PMID9121441
PMCPMC232040
OpenAlexW2142355688

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.