Evidence map›Paper›PMID 22123845›Full record

ArticleBlood2012

Rac signaling in osteoblastic cells is required for normal bone development but is dispensable for hematopoietic development.

Steven W Lane, Serena De Vita, Kylie A Alexander, Ruchan Karaman, Michael D Milsom, Adrienne M Dorrance, Amy Purdon, Leeann Louis, Mary L Bouxsein, David A Williams

Open access · greenAbstract 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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. AnJBMR plus · 2021
    Article
  6. The Rho GTPase RAC1 in Osteoblasts Controls Their Function.International journal of molecular sciences · 2020
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Rac1 and Cdc42 GTPases regulate shear stress-driven β-catenin signaling in osteoblasts.Biochemical and biophysical research communications · 2013
    Article
  14. Article
  15. The regulation of normal and leukemic hematopoietic stem cells by niches.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2012
    Article
  16. Article
  17. Review
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

10 authors at 5 institutions in 2 countries.

Steven W LaneDivision of Hematology/Oncology, Children's Hospital Boston, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Serena De Vita
Kylie A Alexander
Ruchan Karaman
Michael D Milsom
Adrienne M Dorrance
Amy Purdon
Leeann Louis
Mary L Bouxsein
David A Williams
QIMR Berghofer Medical Research Institute · AUBeth Israel Deaconess Medical Center · USHarvard Stem Cell Institute · USHarvard University · USDana-Farber Cancer Institute · US

Funding

Rac proteins in hematopoietic cell survival and functionR01DK062757 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLIAMS, DAVID A · 2002 to 2016
$5.7M
NIDDK NIH HHS DK62757NIDDK NIH HHS R01 DK062757
6 · The paper itself

Abstract

Hematopoietic stem cells (HSCs) interact with osteoblastic, stromal, and vascular components of the BM hematopoietic microenvironment (HM) that are required for the maintenance of long-term self-renewal in vivo. Osteoblasts have been reported to be a critical cell type making up the HSC niche in vivo. Rac1 GTPase has been implicated in adhesion, spreading, and differentiation of osteoblast cell lines and is critical for HSC engraftment and retention. Recent data suggest a differential role of GTPases in endosteal/osteoblastic versus perivascular niche function. However, whether Rac signaling pathways are also necessary in the cell-extrinsic control of HSC function within the HM has not been examined. In the present study, genetic and inducible models of Rac deletion were used to demonstrate that Rac depletion causes impaired proliferation and induction of apoptosis in the OP9 cell line and in primary BM stromal cells. Deletion of Rac proteins caused reduced trabecular and cortical long bone growth in vivo. Surprisingly, HSC function and maintenance of hematopoiesis in vivo was preserved despite these substantial cell-extrinsic changes. These data have implications for therapeutic strategies to target Rac signaling in HSC mobilization and in the treatment of leukemia and provide clarification to our evolving concepts of HSC-HM interactions.

Indexed as

Signal TransductionAnimalsApoptosisBlotting, WesternBone DevelopmentBone Marrow CellsCell CommunicationCell DifferentiationCell MovementCell ProliferationCells, CulturedFlow CytometryHematopoiesisHematopoietic Stem CellsImmunoenzyme TechniquesMiceNeuropeptidesrac1 GTP-Binding ProteinRac1 protein, mouseRAC2 GTP-Binding ProteinRac3 protein, mouserac GTP-Binding ProteinsRNA, MessengerRNA, Small Interfering

Identifiers

PMID22123845
PMCPMC3265198
OpenAlexW1976258760

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.