Evidence map›Paper›PMID 30813444›Full record

ArticleProteomes2019

Comparative Proteome-Wide Analysis of Bone Marrow Microenvironment of β-Thalassemia/Hemoglobin E.

Saranyoo Ponnikorn, Rungrawee Mongkolrob, Suwit Klongthalay, Sittiruk Roytrakul, Kitima Srisanga, Sumalee Tungpradabkul, Suradej Hongeng

Open access · goldAbstract read
In one paragraph

Article in Proteomes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. 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

7 authors at 4 institutions in 1 country.

Saranyoo PonnikornChulabhorn International College of Medicine, Thammasat University Rangsit campus, Pathum Thani 12121, Thailand. saranyoo@tu.ac.th.ORCID 0000-0001-6599-2301
Rungrawee MongkolrobChulabhorn International College of Medicine, Thammasat University Rangsit campus, Pathum Thani 12121, Thailand. scrmr303@gmail.com.
Suwit KlongthalayFaculty of Medical Technology, Rangsit University, Pathum Thani 12000, Thailand. suwit_klong51@hotmail.com.
Sittiruk RoytrakulNational Center for Genetic Engineering and Biotechnology (BIOTEC), Thailand Science Park, Pathum Thani 12121, Thailand. sittiruk@biotec.or.th.
Kitima SrisangaChulabhorn International College of Medicine, Thammasat University Rangsit campus, Pathum Thani 12121, Thailand. kitima_su@hotmail.com.
Sumalee TungpradabkulDepartment of Biochemistry, Faculty of Science, Mahidol University, Bangkok 10400, Thailand. pexcotung@gmail.com.
Suradej HongengDepartment of Pediatrics, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok 10400, Thailand. suradej.hon@mahidol.ac.th.
Thammasat University · THMahidol University · THNational Center for Genetic Engineering and Biotechnology · THRangsit University · TH

Funding

National Research Council of Thailand 3949National Research Council of Thailand 43000Thammasat University 1/2015
6 · The paper itself

Abstract

β-thalassemia/Hb E is a global health issue, which is characterized by a range of clinical symptoms from a mild and asymptomatic anemia to severe disorders that require transfusions from infancy. Pathological mechanisms of the disease involve the excess of unmatched alpha globin and iron overload, leading to ineffective erythropoiesis and ultimately to the premature death of erythroid precursors in bone marrow (BM) and peripheral organs. However, it is unclear as to how BM microenvironment factors contribute to the defective erythropoiesis in β-thalassemia/Hb E patients. Here, we employed mass spectrometry-based comparative proteomics to analyze BM plasma that was collected from six β-thalassemia/Hb E patients and four healthy donors. We identified that the differentially expressed proteins are enriched in secretory or exosome-associated proteins, many of which have putative functions in the oxidative stress response. Using Western blot assay, we confirmed that atypical lipoprotein, Apolipoprotein D (APOD), belonging to the Lipocalin transporter superfamily, was significantly decreased in BM plasma of the tested pediatric β-thalassemia/Hb E patients. Our results highlight that the disease condition of ineffective erythropoiesis and oxidative stress found in BM microenvironment of β-thalassemia/Hb E patients is associated with the impaired expression of APOD protein.

Indexed as

Apolipoprotein Dbone marrowineffective erythropoiesisoxidative stressproteomicsβ-thalassemia/Hb E

Identifiers

PMID30813444
PMCPMC6473223
OpenAlexW2916805753

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.