Evidence map›Paper›PMID 25024173›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2014

Specific collagen XVIII isoforms promote adipose tissue accrual via mechanisms determining adipocyte number and affect fat deposition.

Mari Aikio, Harri Elamaa, David Vicente, Valerio Izzi, Inderjeet Kaur, Lotta Seppinen, Helen E Speedy, Dorota Kaminska, Sanna Kuusisto, Raija Sormunen and 8 more

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Recent Developments in Extracellular Matrix Remodeling for Fat Grafting.Frontiers in cell and developmental biology · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Fibroblast activation protein restrains adipogenic differentiation and regulates matrix-mediated mTOR signaling.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Article
  15. Review
  16. Article
  17. Article
  18. Fat fibrosis: friend or foe?JCI insight · 2018
    Review
  19. Article
  20. 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

18 authors at 4 institutions in 3 countries.

Mari AikioFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
Harri ElamaaFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
David VicenteFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
Valerio IzziFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
Inderjeet KaurFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
Lotta SeppinenFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
Helen E SpeedyCentre for Endocrinology, William Harvey Research Institute, Queen Mary University of London and Barts and the London School of Medicine and Dentistry, London EC1M 6BQ, United Kingdom;
Dorota KaminskaDepartment of Clinical Nutrition, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, FI-70211 Kuopio, Finland;
Sanna KuusistoBiocenter Oulu,Department of Internal Medicine, Clinical Research Center, Institute of Clinical Medicine, and.
Raija SormunenBiocenter Oulu,Department of Pathology, Oulu University Hospital, University of Oulu, FI-90014 Oulu, Finland;
Ritva HeljasvaaraFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu.
Emma L JonesCentre for Endocrinology, William Harvey Research Institute, Queen Mary University of London and Barts and the London School of Medicine and Dentistry, London EC1M 6BQ, United Kingdom;
Mikko MuiluPublic Health Genomics Unit, National Institute for Health and Welfare, FI-00290 Helsinki, Finland; and.
Matti JauhiainenPublic Health Genomics Unit, National Institute for Health and Welfare, FI-00290 Helsinki, Finland; and.
Jussi PihlajamäkiDepartment of Clinical Nutrition, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, FI-70211 Kuopio, Finland;Department of Medicine, Clinical Nutrition and Obesity Center, Kuopio University Hospital, FI-70211 Kuopio, Finland.
Markku J SavolainenBiocenter Oulu,Department of Internal Medicine, Clinical Research Center, Institute of Clinical Medicine, and.
Carol C ShouldersCentre for Endocrinology, William Harvey Research Institute, Queen Mary University of London and Barts and the London School of Medicine and Dentistry, London EC1M 6BQ, United Kingdom; taina.pihlajaniemi@oulu.fi c.shoulders@qmul.ac.uk.
Taina PihlajaniemiFaculty of Biochemistry and Molecular Medicine, Oulu Center for Cell-Matrix Research,Biocenter Oulu, taina.pihlajaniemi@oulu.fi c.shoulders@qmul.ac.uk.
Matrix Research (United States) · USBiocenter Finland · FIQueen Mary University of London · GBUniversity of Eastern Finland · FI

Funding

British Heart FoundationMedical Research Council MC_U120074258
6 · The paper itself

Abstract

Collagen XVIII is an evolutionary conserved ubiquitously expressed basement membrane proteoglycan produced in three isoforms via two promoters (P). Here, we assess the function of the N-terminal, domain of unknown function/frizzled-like sequences unique to medium/long collagen XVIII by creating P-specific null mice. P2-null mice, which only produce short collagen XVIII, developed reduced bulk-adiposity, hepatic steatosis, and hypertriglyceridemia. These abnormalities did not develop in P1-null mice, which produce medium/long collagen XVIII. White adipose tissue samples from P2-null mice contain larger reserves of a cell population enriched in early adipocyte progenitors; however, their embryonic fibroblasts had ∼ 50% lower adipocyte differentiation potential. Differentiating 3T3-L1 fibroblasts into mature adipocytes produced striking increases in P2 gene-products and dramatic falls in P1-transcribed mRNA, whereas Wnt3a-induced dedifferentiation of mature adipocytes produced reciprocal changes in P1 and P2 transcript levels. P2-derived gene-products containing frizzled-like sequences bound the potent adipogenic inhibitor, Wnt10b, in vitro. Previously, we have shown that these same sequences bind Wnt3a, inhibiting Wnt3a-mediated signaling. P2-transcript levels in visceral fat were positively correlated with serum free fatty acid levels, suggesting that collagen α1 (XVIII) expression contributes to regulation of adipose tissue metabolism in visceral obesity. Medium/long collagen XVIII is deposited in the Space of Disse, and interaction between hepatic apolipoprotein E and this proteoglycan is lost in P2-null mice. These results describe a previously unidentified extracellular matrix-directed mechanism contributing to the control of the multistep adipogenic program that determines the number of precursors committing to adipocyte differentiation, the maintenance of the differentiated state, and the physiological consequences of its impairment on ectopic fat deposition.

Indexed as

3T3-L1 CellsAdipocytesAdipose TissueAdiposityAnimalsCell DifferentiationCollagen Type XVIIIEmbryo, MammalianFatty AcidsFatty LiverFemaleFibroblastsHumansMaleMiceMice, Mutant StrainsCollagen Type XVIIIFatty Acids

Identifiers

PMID25024173
PMCPMC4121773
OpenAlexW2022542180

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.