Evidence map›Paper›PMID 22034075›Full record

ArticleJournal of cellular biochemistry2012

Downregulation of PKD1 by shRNA results in defective osteogenic differentiation via cAMP/PKA pathway in human MG-63 cells.

Ni Qiu, Honghao Zhou, Zhousheng Xiao

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Role of Primary Cilia in Skeletal Disorders.Stem cells international · 2022
    Review
  6. Role of KInternational journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Deciphering signaling networks in osteosarcoma pathobiology.Experimental biology and medicine (Maywood, N.J.) · 2016
    Review
  15. Physiological mechanisms and therapeutic potential of bone mechanosensing.Reviews in endocrine & metabolic disorders · 2015
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Ni QiuInstitute of Clinical Pharmacology, Central South University, Changsha, Hunan, 410078, China.
Honghao Zhou
Zhousheng Xiao
University of Tennessee Health Science Center · USCentral South University · CN

Funding

Mechanosensing Function of Primary Cilium-Polycysin Complex in BoneR21AR056794 · NIAMS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI XIAO, ZHOUSHENG · 2009 to 2010
$367k
NIAMS NIH HHS R21 AR056794NIAMS NIH HHS R21-AR056794
6 · The paper itself

Abstract

Mutations and/or deletions of Pkd1 in mouse models resulted in attenuation of osteoblast function and defective bone formation; however, the function of PKD1 in human osteoblast and bone remains uncertain. In the current study, we used lentivirus-mediated shRNA technology to stably knock down PKD1 in the human osteoblastic MG-63 cell line and to investigate the role of PKD1 on human osteoblast function and molecular mechanisms. We found that a 53% reduction of PKD1 by PKD1 shRNA in stable, transfected MG-63 cells resulted in increased cell proliferation and impaired osteoblastic differentiation as reflected by increased BrdU incorporation, decreased alkaline phosphatase activity, and calcium deposition and by decreased expression of RUNX2 and OSTERIX compared to control shRNA MG-63 cells. In addition, knockdown of PKD1 mRNA caused enhanced adipogenesis in stable PKD1 shRNA MG-63 cells as evidenced by elevated lipid accumulation and increased expression of adipocyte-related markers such as PPARγ and aP2. The stable PKD1 shRNA MG-63 cells exhibited lower basal intracellular calcium, which led to attenuated cytosolic calcium signaling in response to fluid flow shear stress, as well as increased intracellular cAMP messages in response to forskolin (10 µM) stimulation. Moreover, increased cell proliferation, inhibited osteoblastic differentiation, and osteogenic and adipogenic gene markers were significantly reversed in stable PKD1 shRNA MG-63 cells when treated with H89 (1 µM), an inhibitor of PKA. These findings suggest that downregulation of PKD1 in human MG-63 cells resulted in defective osteoblast function via intracellular calcium-cAMP/PKA signaling pathway.

Indexed as

Down-RegulationAdipogenesisCalciumCell DifferentiationCell LineCell ProliferationCiliaCyclic AMPCyclic AMP-Dependent Protein KinasesHumansLentivirusOsteoblastsOsteogenesisRNA, Small InterferingSignal TransductionTRPP Cation ChannelsCalciumCyclic AMPCyclic AMP-Dependent Protein KinasesRNA, Small InterferingTRPP Cation Channels

Identifiers

PMID22034075
PMCPMC3264804
OpenAlexW2132742350

What OpenQuestion holds

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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.