Evidence map›Paper›PMID 22066471›Full record

ArticleStem cells and development2012

Processing of CXCL12 by different osteoblast-secreted cathepsins.

Nicole D Staudt, Andreas Maurer, Bärbel Spring, Hubert Kalbacher, Wilhelm K Aicher, Gerd Klein

Abstract read
In one paragraph

Article in Stem cells and development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Cathepsin Z/X: Breaking Down the Known and Unknown.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Review
  4. Review
  5. Proteases Regulate Cancer Stem Cell Properties and Remodel Their Microenvironment.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Periarteriolar Glioblastoma Stem Cell Niches Express Bone Marrow Hematopoietic Stem Cell Niche Proteins.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018
    Article
  11. Article
  12. Article
  13. 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

6 authors at 3 institutions in 1 country.

Nicole D StaudtSection for Transplantation Immunology and Immunohematology, Center for Medical Research, University Medical Clinic, University of Tübingen, Tübingen, Germany.
Andreas Maurer
Bärbel Spring
Hubert Kalbacher
Wilhelm K Aicher
Gerd Klein
University of Tübingen · DEBernstein Center for Computational Neuroscience Tübingen · DEUniversity Children's Hospital Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematopoietic stem and progenitor cells (HSPCs) are known to reside in specialized niches at the endosteum in the trabecular bone. Osteoblasts are the major cell type of the endosteal niche. It is well established that secreted proteases are involved in cytokine-induced mobilization processes that release stem cell from their niches. However, migratory processes such as the regular trafficking of HSPCs between their niches and the periphery are not fully understood. In the current study we analyzed whether osteoblast-secreted cysteine cathepsins are able to reduce the direct interaction of HSPCs with bone-forming osteoblasts. Isolated human osteoblasts were shown to secrete proteolytically active cysteine cathepsins, such as cathepsins B, K, L, and X. All of these cathepsins were able to digest, although with different efficacy, the chemokine CXCL12, which is known to be important for retaining HSPCs in their niches. Of the 4 identified cathepsins, only cathepsin X was able to reduce binding of HSPCs to osteoblasts. Interestingly, nonactivated pro-cathepsin X and mature cathepsin X did not interfere with HSPC-osteoblast interactions. Only pro-cathepsin X treated with dithiothreitol, which unfolds but does not lead to full maturation of cathepsin X, significantly reduced HSPC adhesion to osteoblasts. These observations argue for a role of the accessible cathepsin X prodomain in diminishing cell binding. Our findings strongly suggest that the cysteine cathepsins B, K, and L constitutively secreted by osteoblasts are part of the fine-tuned regulation of CXCL12 in the bone marrow, whereas pro-cathepsin X with its prodomain can affect HSPC trafficking in the niche.

Indexed as

Antigens, CD34Cathepsin BCathepsin KCathepsinsCell AdhesionCell MovementCellular MicroenvironmentChemokine CXCL12Culture Media, ConditionedDithiothreitolEnzyme ActivationEnzyme AssaysHematopoietic Stem CellsHumansOsteoblastsPrimary Cell CultureAntigens, CD34Cathepsin BCathepsin KCathepsinsChemokine CXCL12CTSB protein, humanCTSK protein, humanCulture Media, ConditionedCXCL12 protein, humanDithiothreitolprocathepsin X, humanProtein PrecursorsRecombinant Proteins

Identifiers

PMID22066471
PMCPMC3396142
OpenAlexW2120487295

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.