Evidence map›Paper›PMID 25070889›Full record

ArticleThe Journal of biological chemistry2014

Protein kinase Cα (PKCα) regulates bone architecture and osteoblast activity.

Gabriel L Galea, Lee B Meakin, Christopher M Williams, Sarah L Hulin-Curtis, Lance E Lanyon, Alastair W Poole, Joanna S Price

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Gabriel L GaleaFrom the School of Veterinary Sciences, University of Bristol, Bristol BS2 8EJ, United Kingdom and gabriel.galea@bristol.ac.uk.
Lee B MeakinFrom the School of Veterinary Sciences, University of Bristol, Bristol BS2 8EJ, United Kingdom and.
Christopher M Williamsthe School of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, United Kingdom.
Sarah L Hulin-CurtisFrom the School of Veterinary Sciences, University of Bristol, Bristol BS2 8EJ, United Kingdom and.
Lance E LanyonFrom the School of Veterinary Sciences, University of Bristol, Bristol BS2 8EJ, United Kingdom and.
Alastair W Poolethe School of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, United Kingdom.
Joanna S PriceFrom the School of Veterinary Sciences, University of Bristol, Bristol BS2 8EJ, United Kingdom and.
University of Bristol · GB

Funding

British Heart Foundation RG/10/006/28299Wellcome TrustWellcome Trust 088560/Z/09/ZWellcome Trust 092045/Z/10/Z
6 · The paper itself

Abstract

Bones' strength is achieved and maintained through adaptation to load bearing. The role of the protein kinase PKCα in this process has not been previously reported. However, we observed a phenotype in the long bones of Prkca(-/-) female but not male mice, in which bone tissue progressively invades the medullary cavity in the mid-diaphysis. This bone deposition progresses with age and is prevented by disuse but unaffected by ovariectomy. Castration of male Prkca(-/-) but not WT mice results in the formation of small amounts of intramedullary bone. Osteoblast differentiation markers and Wnt target gene expression were up-regulated in osteoblast-like cells derived from cortical bone of female Prkca(-/-) mice compared with WT. Additionally, although osteoblastic cells derived from WT proliferate following exposure to estradiol or mechanical strain, those from Prkca(-/-) mice do not. Female Prkca(-/-) mice develop splenomegaly and reduced marrow GBA1 expression reminiscent of Gaucher disease, in which PKC involvement has been suggested previously. From these data, we infer that in female mice, PKCα normally serves to prevent endosteal bone formation stimulated by load bearing. This phenotype appears to be suppressed by testicular hormones in male Prkca(-/-) mice. Within osteoblastic cells, PKCα enhances proliferation and suppresses differentiation, and this regulation involves the Wnt pathway. These findings implicate PKCα as a target gene for therapeutic approaches in low bone mass conditions.

Indexed as

AnimalsCell DifferentiationCell ProliferationFemaleHumansMaleMiceOsteoblastsOsteogenesisProtein Kinase C-alphaWeight-BearingWnt ProteinsProtein Kinase C-alphaWnt ProteinsBoneEstrogenGaucher DiseaseMechanical LoadingOsteoblastProtein Kinase C (PKC)Wnt Signaling

Identifiers

PMID25070889
PMCPMC4162157
OpenAlexW2012390518

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.