Evidence map›Paper›PMID 22213341›Full record

ArticleJournal of cellular physiology2012

Biochemical and proteomic characterization of alkaptonuric chondrocytes.

Daniela Braconi, Giulia Bernardini, Claretta Bianchini, Marcella Laschi, Lia Millucci, Loredana Amato, Laura Tinti, Tommaso Serchi, Federico Chellini, Adriano Spreafico and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Alkaptonuria.Nature reviews. Disease primers · 2024
    Review
  7. Article
  8. Article
  9. Interactive alkaptonuria database: investigating clinical data to improve patient care in a rare disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  10. Article
  11. Angiogenesis in alkaptonuria.Journal of inherited metabolic disease · 2016
    Article
  12. Amyloidosis in alkaptonuria.Journal of inherited metabolic disease · 2015
    Review
  13. Review
  14. Article
  15. Chondroptosis in alkaptonuric cartilage.Journal of cellular physiology · 2015
    Article
  16. Article
  17. Article
  18. Secondary amyloidosis in an alkaptonuric aortic valve.International journal of cardiology · 2014
    Article
  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

11 authors at 1 institution in 1 country.

Daniela BraconiDipartimento di Biotecnologie, Università degli Studi di Siena, Siena, Italy.
Giulia Bernardini
Claretta Bianchini
Marcella Laschi
Lia Millucci
Loredana Amato
Laura Tinti
Tommaso Serchi
Federico Chellini
Adriano Spreafico
Annalisa Santucci
University of Siena · IT

Funding

Telethon GGP10058
6 · The paper itself

Abstract

Alkaptonuria (AKU) is a rare genetic disease associated with the accumulation of homogentisic acid (HGA) and its oxidized/polymerized products which leads to the deposition of melanin-like pigments (ochronosis) in connective tissues. Although numerous case reports have described ochronosis in joints, little is known on the molecular mechanisms leading to such a phenomenon. For this reason, we characterized biochemically chondrocytes isolated from the ochronotic cartilage of AKU patients. Based on the macroscopic appearance of the ochronotic cartilage, two sub-populations were identified: cells coming from the black portion of the cartilage were referred to as "black" AKU chondrocytes, while those coming from the white portion were referred to as "white" AKU chondrocytes. Notably, both AKU chondrocytic types were characterized by increased apoptosis, NO release, and levels of pro-inflammatory cytokines. Transmission electron microscopy also revealed that intracellular ochronotic pigment deposition was common to both "white" and "black" AKU cells. We then undertook a proteomic and redox-proteomic analysis of AKU chondrocytes which revealed profound alterations in the levels of proteins involved in cell defence, protein folding, and cell organization. An increased post-translational oxidation of proteins, which also involved high molecular weight protein aggregates, was found to be particularly relevant in "black" AKU chondrocytes.

Indexed as

AgedAlkaptonuriaApoptosisCartilageCell ProliferationChondrocytesCytokinesFemaleGene Expression RegulationHumansMaleMicroscopy, Electron, TransmissionMiddle AgedNitric OxideOchronosisOxidation-ReductionCytokinesNitric OxideProteome

Identifiers

PMID22213341
PMCPMC3427902
OpenAlexW2037308721

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.