Evidence map›Paper›PMID 25464512›Full record

ArticlePloS one2014

Osteoblast-specific deletion of Pkd2 leads to low-turnover osteopenia and reduced bone marrow adiposity.

Zhousheng Xiao, Li Cao, Yingjuan Liang, Jinsong Huang, Amber Rath Stern, Mark Dallas, Mark Johnson, Leigh Darryl Quarles

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 46 citations in OpenAlex.

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  7. Progress on the mechanism of Polycystin-1 in bone remodeling.Frontiers in cell and developmental biology · 2025
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  17. Role of KInternational journal of molecular sciences · 2021
    Review
  18. Review
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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

8 authors at 2 institutions in 1 country.

Zhousheng XiaoDepartment of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, 38165, United States of America.
Li CaoDepartment of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, 38165, United States of America.
Yingjuan LiangDepartment of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, 38165, United States of America.
Jinsong HuangDepartment of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, 38165, United States of America.
Amber Rath SternDepartment of Oral Biology, School of Dentistry, University of Missouri-Kansas City, Kansas City, Missouri, 64108, United States of America; Engineering Systems, Inc., Charlotte, North Carolina, 28227, United States of America.
Mark DallasDepartment of Oral Biology, School of Dentistry, University of Missouri-Kansas City, Kansas City, Missouri, 64108, United States of America.
Mark JohnsonDepartment of Oral Biology, School of Dentistry, University of Missouri-Kansas City, Kansas City, Missouri, 64108, United States of America.
Leigh Darryl QuarlesDepartment of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, 38165, United States of America.
University of Tennessee Health Science Center · USUniversity of Missouri–Kansas City · US

Funding

DIFFERENTIAL FUNCTION AND REGULATION OF RUNX2 ISOFORMSR01AR049712 · NIAMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI QUARLES, L DARRYL · 2003 to 2007
$1.7M
Extrarenal Functions of Polycystin-1R01DK083303 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI QUARLES, L DARRYL · 2010 to 2014
$1.6M
NIAMS NIH HHS R01 AR049712NIDDK NIH HHS R01 DK083303NIDDK NIH HHS R01-DK083303
6 · The paper itself

Abstract

Polycystin-1 (Pkd1) interacts with polycystin-2 (Pkd2) to form an interdependent signaling complex. Selective deletion of Pkd1 in the osteoblast lineage reciprocally regulates osteoblastogenesis and adipogenesis. The role of Pkd2 in skeletal development has not been defined. To this end, we conditionally inactivated Pkd2 in mature osteoblasts by crossing Osteocalcin (Oc)-Cre;Pkd2+/null mice with floxed Pkd2 (Pkd2flox/flox) mice. Oc-Cre;Pkd2flox/null (Pkd2Oc-cKO) mice exhibited decreased bone mineral density, trabecular bone volume, cortical thickness, mineral apposition rate and impaired biomechanical properties of bone. Pkd2 deficiency resulted in diminished Runt-related transcription factor 2 (Runx2) expressions in bone and impaired osteoblastic differentiation ex vivo. Expression of osteoblast-related genes, including, Osteocalcin, Osteopontin, Bone sialoprotein (Bsp), Phosphate-regulating gene with homologies to endopeptidases on the X chromosome (Phex), Dentin matrix protein 1 (Dmp1), Sclerostin (Sost), and Fibroblast growth factor 23 (FGF23) were reduced proportionate to the reduction of Pkd2 gene dose in bone of Oc-Cre;Pkd2flox/+ and Oc-Cre;Pkd2flox/null mice. Loss of Pkd2 also resulted in diminished peroxisome proliferator-activated receptor γ (PPARγ) expression and reduced bone marrow fat in vivo and reduced adipogenesis in osteoblast culture ex vivo. Transcriptional co-activator with PDZ-binding motif (TAZ) and Yes-associated protein (YAP), reciprocally acting as co-activators and co-repressors of Runx2 and PPARγ, were decreased in bone of Oc-Cre;Pkd2flox/null mice. Thus, Pkd1 and Pkd2 have coordinate effects on osteoblast differentiation and opposite effects on adipogenesis, suggesting that Pkd1 and Pkd2 signaling pathways can have independent effects on mesenchymal lineage commitment in bone.

Indexed as

AdiposityGene DeletionAnimalsBone Diseases, MetabolicBone MarrowFibroblast Growth Factor-23Gene Expression RegulationMiceOsteoblastsSignal TransductionTRPP Cation ChannelsX-Ray MicrotomographyFgf23 protein, mouseFibroblast Growth Factor-23TRPP Cation Channels

Identifiers

PMID25464512
PMCPMC4252138
OpenAlexW1990008878

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.