Evidence map›Paper›PMID 26090483›Full record

ArticleJournal of immunology research2015

Induction of Apoptosis Coupled to Endoplasmic Reticulum Stress through Regulation of CHOP and JNK in Bone Marrow Mesenchymal Stem Cells from Patients with Systemic Lupus Erythematosus.

Genkai Guo, Yan Meng, Wei Tan, Yunfei Xia, Chun Cheng, Xiaolan Chen, Zhifeng Gu

Open access · goldAbstract read
In one paragraph

Article in Journal of immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. IFN-γ and TNF-α Pre-licensing Protects Mesenchymal Stromal Cells from the Pro-inflammatory Effects of Palmitate.Molecular therapy : the journal of the American Society of Gene Therapy · 2018
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. 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 2 institutions in 1 country.

Genkai GuoDepartment of Rheumatology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Yan MengDepartment of Rheumatology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Wei TanDepartment of Rheumatology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Yunfei XiaDepartment of Rheumatology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Chun ChengJiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College, Nantong University, Nantong 226001, China.
Xiaolan ChenDepartment of Nephrology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Zhifeng GuDepartment of Rheumatology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies indicated that bone marrow mesenchymal stem cells (BM-MSCs) from patients with systemic lupus erythematosus (SLE) exhibited the phenomenon of apoptosis. In this study, we aimed to investigate whether apoptosis of BM-MSCs from SLE patients were dysregulated. In this paper, endoplasmic reticulum stress (ERS) was evidenced by increased expression of phosphorylated protein kinase RNA-like ER kinase (PERK) and inositol-requiring protein-1 (IRE-1). We also found the activation of downstream target eukaryotic translation initiator factor 2α (eIF 2α) and CCAAT/enhancer-binding protein- (C/EBP-) homologous protein (CHOP) in BM-MSCs from SLE patients. Interestingly, we discovered that 4-phenylbutyric acid (4-PBA), a selective inhibitor of ERS, blocked the apoptosis of BM-MSCs from SLE patients and alleviated the level of Jun N-terminal kinase1/2 (JNK1/2) and CHOP. Furthermore, blockage of PERK signaling expression by siRNA not only significantly reduced the expression of CHOP, but also activated the anti-apoptotic regulator B-cell lymphoma-2 (Bcl-2). Blockage of IRE-1 or JNK1/2 by siRNA resulted in the decreased expression of JNK1/2 and proapoptosis protein Bcl-2 associated protein X (BAX). These results implicated that ERS-mediated apoptosis was a critical determinant of BM-MSCs from SLE patients.

Indexed as

AdolescentAdultApoptosisbcl-2-Associated X ProteinBone Marrow CellsCase-Control StudiesCCAAT-Enhancer-Binding ProteinseIF-2 KinaseEndoplasmic Reticulum StressEndoribonucleasesEukaryotic Initiation Factor-2FemaleHumansJNK Mitogen-Activated Protein KinasesLupus Erythematosus, SystemicMesenchymal Stem Cellsbcl-2-Associated X ProteinCCAAT-Enhancer-Binding ProteinsDDIT3 protein, humanEIF2AK3 protein, humaneIF-2 KinaseEndoribonucleasesERN1 protein, humanEukaryotic Initiation Factor-2JNK Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2Transcription Factor CHOP

Identifiers

PMID26090483
PMCPMC4452351
OpenAlexW1579851397

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.