ArticleBlood2012
Activated Gs signaling in osteoblastic cells alters the hematopoietic stem cell niche in mice.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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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.
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.
Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- Teriparatide (PTH 1-34) treatment increases peripheral hematopoietic stem cells in postmenopausal women.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Trial
- The RANK/RANKL axis controls vascular dynamics in the bone marrow.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Single-cell analysis of human fibrous dysplasia bone reveals a fibrotic transcriptome and GNAS variants in endothelial, perivascular, and stromal cells.American journal of human genetics · 2025Article
- Wnt pathway inhibition with the porcupine inhibitor LGK974 decreases trabecular bone but not fibrosis in a murine model with fibrotic bone.JBMR plus · 2024Article
- Osteoblast Lineage Support of Hematopoiesis in Health and Disease.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Review
- TIRAP drives myelosuppression through an Ifnγ-Hmgb1 axis that disrupts the endothelial niche in mice.The Journal of experimental medicine · 2022Article
- Histone variant H3.3 maintains adult haematopoietic stem cell homeostasis by enforcing chromatin adaptability.Nature cell biology · 2022Article
- Deletion ofFrontiers in immunology · 2022Article
- ACVR1Bone · 2021Article
- Modeling theeLife · 2021Article
- Sclerostin Depletion Induces Inflammation in the Bone Marrow of Mice.International journal of molecular sciences · 2021Article
- Group 2 innate lymphoid cells support hematopoietic recovery under stress conditions.The Journal of experimental medicine · 2021Article
- SLPI is a critical mediator that controls PTH-induced bone formation.Nature communications · 2021Article
- Article
- Aged marrow macrophages expand platelet-biased hematopoietic stem cells via Interleukin1B.JCI insight · 2019Article
- Advances in Models of Fibrous Dysplasia/McCune-Albright Syndrome.Frontiers in endocrinology · 2019Review
- Attenuation of PKCδ enhances metabolic activity and promotes expansion of blood progenitors.The EMBO journal · 2018Article
- NF-κB/MAPK activation underlies ACVR1-mediated inflammation in human heterotopic ossification.JCI insight · 2018Article
- The Majority of CD45Immunity · 2018Article
- ICAM-1 Deficiency in the Bone Marrow Niche Impairs Quiescence and Repopulation of Hematopoietic Stem Cells.Stem cell reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Adult hematopoiesis occurs primarily in the BM space where hematopoietic cells interact with stromal niche cells. Despite this close association, little is known about the specific roles of osteoblastic lineage cells (OBCs) in maintaining hematopoietic stem cells (HSCs), and how conditions affecting bone formation influence HSC function. Here we use a transgenic mouse model with the ColI(2.3) promoter driving a ligand-independent, constitutively active 5HT4 serotonin receptor (Rs1) to address how the massive increase in trabecular bone formation resulting from increased G(s) signaling in OBCs impacts HSC function and blood production. Rs1 mice display fibrous dysplasia, BM aplasia, progressive loss of HSC numbers, and impaired megakaryocyte/erythrocyte development with defective recovery after hematopoietic injury. These hematopoietic defects develop without compensatory extramedullary hematopoiesis, and the loss of HSCs occurs despite a paradoxical expansion of stromal niche cells with putative HSC-supportive activity (ie, endothelial, mesenchymal, and osteoblastic cells). However, Rs1-expressing OBCs show decreased expression of key HSC-supportive factors and impaired ability to maintain HSCs. Our findings indicate that long-term activation of G(s) signaling in OBCs leads to contextual changes in the BM niche that adversely affect HSC maintenance and blood homeostasis.
Indexed as
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What Socratic holds
Registered trials
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 Socratic graph.