Evidence map›Paper›PMID 25187480›Full record

ArticleStem cells (Dayton, Ohio)2015

Adiponectin regulates bone marrow mesenchymal stem cell niche through a unique signal transduction pathway: an approach for treating bone disease in diabetes.

Liming Yu, Qisheng Tu, Qianqian Han, Lan Zhang, Lei Sui, Leilei Zheng, Shu Meng, Yin Tang, Dongying Xuan, Jin Zhang and 8 more

Open access · greenAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

50 citing papers in PubMed, 84 citations in OpenAlex.

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  14. Stem cells mobilization by cardiopulmonary bypass after coronary artery bypass grafting.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2022
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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

18 authors at 5 institutions in 3 countries.

Liming YuDepartment of Oral and Maxillofacial Surgery, Shanghai Stomatological Disease Center, Shanghai, China; Division of Oral Biology, Tufts University School of Dental Medicine, Boston, Massachusetts, USA.
Qisheng Tu
Qianqian Han
Lan Zhang
Lei Sui
Leilei Zheng
Shu Meng
Yin Tang
Dongying Xuan
Jin Zhang
Dana Murray
Qingping Shen
Jessica Cheng
Sung-Hoon Kim
Lily Q Dong
Paloma Valverde
Xinming Cao
Jake Chen
Tufts University · USShanghai Stomatological Hospital · CNKyung Hee University · KRThe University of Texas Health Science Center at San Antonio · USWentworth Institute of Technology · US

Funding

Mechanisms of cross talk between insulin and adiponectin signaling pathwaysR01DK080344 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DONG, LILY Q · 2009 to 2013
$1.8M
Therapeutic Strategies for Treating Type 2 Diabetes Mellitus -Associated PeriodonR01DE021464 · NIDCR · TUFTS UNIVERSITY BOSTON · PI CHEN, JAKE JINKUN · 2011 to 2013
$1.3M
NIDCR NIH HHS DE21464NIDCR NIH HHS R01 DE021464NIDDK NIH HHS DK80344NIDDK NIH HHS R01 DK080344
6 · The paper itself

Abstract

Adiponectin (APN) is an adipocyte-secreted adipokine that exerts well-characterized antidiabetic properties. Patients with type 2 diabetes (T2D) are characterized by reduced APN levels in circulation and impaired stem cell and progenitor cell mobilization from the bone marrow for tissue repair and remodeling. In this study, we found that APN regulates the mobilization and recruitment of bone marrow-derived mesenchymal stem cells (BMSCs) to participate in tissue repair and regeneration. APN facilitated BMSCs migrating from the bone marrow into the circulation to regenerate bone by regulating stromal cell-derived factor (SDF)-1 in a mouse bone defect model. More importantly, we found that systemic APN infusion ameliorated diabetic mobilopathy of BMSCs, lowered glucose concentration, and promoted bone regeneration in diet-induced obesity mice. In vitro studies allowed us to identify Smad1/5/8 as a novel signaling mediator of APN receptor (AdipoR)-1 in BMSCs and osteoblasts. APN stimulation of MC3T3-E1 osteoblastic cells led to Smad1/5/8 phosphorylation and nuclear localization and increased SDF-1 mRNA expression. Although APN-mediated phosphorylation of Smad1/5/8 occurred independently from adaptor protein, phosphotyrosine interaction, pleckstrin homology domain, and leucine zipper containing 1, it correlated with the disassembly of protein kinase casein kinase 2 and AdipoR1 in immunoprecipitation experiments. Taken together, this study identified APN as a regulator of BMSCs migration in response to bone injury. Therefore, our findings suggest APN signaling could be a potential therapeutic target to improve bone regeneration and homeostasis, especially in obese and T2D patients.

Indexed as

3T3 CellsAdiponectinAnimalsBone DiseasesBone Marrow CellsCell ProliferationChemokine CXCL12Diabetes Mellitus, Type 2HumansMaleMesenchymal Stem CellsMiceMice, Inbred C57BLMice, TransgenicReceptors, CXCR4Signal TransductionAdiponectinChemokine CXCL12Cxcl12 protein, mouseCXCR4 protein, mouseReceptors, CXCR4AdiponectinBone regenerationCell mobilizationMesenchymal stem cells

Identifiers

PMID25187480
PMCPMC4681406
OpenAlexW1533033831

What OpenQuestion holds

Textmetadata
LicenceTDM
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.