Evidence map›Paper›PMID 15877047›Full record

ArticleGene therapy2005

Silencing p21(Waf1/Cip1/Sdi1) expression increases gene transduction efficiency in primitive human hematopoietic cells.

J Zhang, E Attar, K Cohen, C Crumpacker, D Scadden

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Gene therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Gene Therapy For Beta-Thalassemia: Updated Perspectives.The application of clinical genetics · 2019
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. The brain-specific factor FEZ1 is a determinant of neuronal susceptibility to HIV-1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Primitive hematopoietic cells resist HIV-1 infection via p21.The Journal of clinical investigation · 2007
    Article
  19. An intrinsic host defense against HIV-1 integration?The Journal of clinical investigation · 2007
    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

5 authors at 3 institutions in 1 country.

J ZhangDivision of Infectious Diseases, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.
E Attar
K Cohen
C Crumpacker
D Scadden
Beth Israel Deaconess Medical Center · USHarvard University · USMassachusetts General Hospital · US

Funding

MECHANISMS OF HEMATOPOIESIS IN AIDSR01HL044851 · NHLBI · NEW ENGLAND DEACONESS HOSPITAL · PI SCADDEN, DAVID T · 1991 to 2015
$7.7M
Stem Cell Cycling and TransductionK18AI055313 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ZHANG, JIELIN · 2003 to 2004
$173k
NHLBI NIH HHS HL044851-13NIAID NIH HHS AI055313
6 · The paper itself

Abstract

Adult hematopoietic and other tissue stem cells have highly constrained cell cycling that limits their susceptibility to standard gene therapy vectors, which depend upon chromosomal integration. Using cytokine cocktails to increase transduction efficiency often compromises subsequent stem cell function in vivo. We previously showed that p21(Waf1/Cip1/Sdi1) (p21) mediates stem cell quiescence in vivo and decreasing its expression ex vivo leads to an expansion of stem cell pool in vivo. Here, we report that application of p21 specific siRNA increased the gene transduction efficiency in hematopoietic stem cells while preserving cell multipotentiality. Both types of siRNA, synthesized siRNA and transcribed shRNA, reduced p21 expression in target cells by 85-98%. The effect of RNAi in these cells was transient and the level of p21 mRNA returned to base line 14-28 days after siRNA treatment. This brief interval of reduction, however, was sufficient to increase transduction efficiency to two- to four-fold in cell cultures, and followed by a seven- to eight-fold increase in mice. The RNAi treated, lentivector-transduced CD34+ cells retained multipotentiality as assessed in vitro by colony formation assay and in vivo by NOD/SCID mouse transplantation assay. Reduction of p21 resulted in an increased chromosomal integration of lentivector into target cellular DNA. Taken together, both synthesized and transcribed siRNA knocked down p21 expression in human CD34+ hematopoietic stem/progenitor cells. Silencing p21 expression increased gene transduction efficiency and vector integration while retaining stem cell multipotentiality. Thus, RNAi targeting of p21 is a useful strategy to increase stem cell gene transfer efficiency. Decreasing p21 expression transiently while increasing gene-transfer vector integration may ultimately facilitate clinical applications of gene therapy.

Indexed as

Gene SilencingAdultAnalysis of VarianceAnimalsAntigens, CD34Blotting, WesternCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Flow CytometryGenetic TherapyGenetic VectorsHumansLentivirusMiceMice, SCIDAntigens, CD34CDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21RNA, Small Interfering

Identifiers

PMID15877047
OpenAlexW1975438827

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.