Evidence map›Paper›PMID 22289892›Full record

ArticleBlood2012

Rantes/Ccl5 influences hematopoietic stem cell subtypes and causes myeloid skewing.

Aysegul V Ergen, Nathan C Boles, Margaret A Goodell

Abstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

183 citing papers in PubMed, 274 citations in OpenAlex.

  1. Cytotoxic CD4Nature aging · 2026
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  12. CCR5 marks a subset of mouse hematopoietic stem cells that are myeloid primed and expand with age.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  14. Review
  15. Article
  16. Article
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  18. Hallmarks of stem cell aging.Cell stem cell · 2025
    Review
  19. Article
  20. Article

123 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Aysegul V ErgenInterdepartmental Program of Developmental Biology, Baylor College of Medicine, One Baylor Plaza, N1030, Houston, TX 77030, USA.
Nathan C Boles
Margaret A Goodell
Baylor College of Medicine · USRegenerative Medicine Institute · MX

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
REGULATION OF HEMATOPOIETIC PROGENITORS BY DE NOVO DNA METHYLATIONR01DK092883 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2012 to 2024
$7.4M
Training In Cell and Gene TherapyT32HL092332 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MALCOLM K. BRENNER, Bruno Di Stefano · 2008 to 2026
$6.9M
MUSCLE-DERIVED HEMATOPOIETIC STEM CELLSR01DK058192 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2000 to 2010
$3.6M
Epigenetic Changes with Age in Hematopoietic Stem CellsRC2AG036562 · NIA · BAYLOR COLLEGE OF MEDICINE · PI DARLINGTON, GRETCHEN J. · 2009 to 2010
$2.5M
Cell Fate Tracking in the Aging Hematopoietic SystemR21AG034451 · NIA · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2009 to 2010
$420k
Regulation of Hematopoietic Progenitors by de novo DNA MethylationR56DK092883 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI GOODELL, MARGARET A. · 2011 to 2011
$344k
NCI NIH HHS P30 CA125123NHLBI NIH HHS T32 HL092332NIA NIH HHS 1RC2AG036562NIA NIH HHS AG034451NIA NIH HHS R21 AG034451NIA NIH HHS RC2 AG036562NIDDK NIH HHS DK092883NIDDK NIH HHS R01 DK058192NIDDK NIH HHS R01 DK092883NIDDK NIH HHS R56 DK092883
6 · The paper itself

Abstract

HSCs undergo dramatic changes with aging. An increase in absolute numbers of HSCs along with a functional deficit in reconstitution potential and a shift toward production of myeloid cells are the hallmarks of murine hematopoietic aging. Here, we show that high levels of the inflammatory cytokine Rantes are found in the aging stem cell milieu. Forced overproduction of Rantes by retroviral expression in BM progenitors resulted in a deficit of T-cell output, and brief ex vivo exposure of HSCs to Rantes resulted in a decrease in T-cell progeny concomitant with an increase in myeloid progenitors. In contrast, Rantes knockout (KO) animals exhibit a decrease in myeloid-biased HSCs and myeloid progenitors and an increase in T cells and lymphoid-biased HSCs. KO HSCs retained their HSC subtype distribution and they produced more lymphoid-biased HSCs in transplantations. Rantes deficiency also resulted in a decreased mammalian target of rapamycin (mTOR) activity in KLS cells. In a heterochronic transplantation setting, we further show that aged HSCs placed in a young environment generate less myeloid cells. These data establish a critical role for environmental factors in the establishment of the aged-associated myeloid skewing phenotype, which may contribute to age-associated immune deficiency.

Indexed as

AnimalsBlotting, WesternBone MarrowCell DifferentiationCell LineageCell ProliferationCellular SenescenceChemokine CCL5Hematopoietic Stem CellsHematopoietic Stem Cell TransplantationMiceMice, Inbred C57BLMice, KnockoutMyeloid Progenitor CellsReal-Time Polymerase Chain ReactionRNA, MessengerCcl5 protein, mouseChemokine CCL5mTOR protein, mouseRNA, MessengerTOR Serine-Threonine Kinases

Identifiers

PMID22289892
PMCPMC3311273
OpenAlexW2027066896

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.