Evidence map›Paper›PMID 20617875›Full record

ArticleTissue engineering. Part A2010

Effect of phosphatidyl inositol 3-kinase, extracellular signal-regulated kinases 1/2, and p38 mitogen-activated protein kinase inhibition on osteogenic differentiation of muscle-derived stem cells.

Karin A Payne, Laura B Meszaros, Julie A Phillippi, Johnny Huard

Open access · greenAbstract read
In one paragraph

Article in Tissue engineering. Part A, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Stem cell death and survival in heart regeneration and repair.Apoptosis : an international journal on programmed cell death · 2016
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Matrix metalloproteinase inhibition negatively affects muscle stem cell behavior.International journal of clinical and experimental pathology · 2013
    Article
  15. Article
  16. 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

4 authors at 2 institutions in 1 country.

Karin A PayneStem Cell Research Center, Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania 15219, USA.
Laura B Meszaros
Julie A Phillippi
Johnny Huard
Children's Hospital of Pittsburgh · USUniversity of Pittsburgh · US

Funding

Muscle Based Tissue Engineering to Improve Bone HealingR01DE013420 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HUARD, JOHNNY · 2001 to 2010
$3.6M
NIDCR NIH HHS 1 R01 DE13420-06
6 · The paper itself

Abstract

Skeletal muscle-derived stem cells (MDSCs) can undergo osteogenesis when treated with bone morphogenetic proteins (BMPs), making them a potential cell source for bone tissue engineering. The signaling pathways that regulate BMP4-induced osteogenesis in MDSCs are not well understood, although they may provide a means to better regulate differentiation during bone regeneration. The objective of this study was to characterize the signaling pathways involved in the BMP4-induced osteogenesis of MDSCs. Cells were treated with BMP4 and specific inhibitors to the extracellular signal-regulated kinases 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and phosphatidyl inositol 3-kinase (PI3K) pathways (PD98059, SB203580, and Ly294002, respectively). Cellular proliferation, expression of osteoblast-related genes, alkaline phosphatase (ALP) activity, and tissue mineralization were measured to determine the role of each pathway in the osteogenic differentiation of MDSCs. Inhibition of the ERK1/2 pathway increased ALP activity and mineralization, whereas inhibition of the p38 MAPK pathway decreased osteogenesis, suggesting opposing roles of these pathways in the BMP4-induced osteogenesis of MDSCs. Inhibition of the PI3K pathway significantly increased mineralization by MDSCs. These findings highlight the involvement of the ERK1/2, p38 MAPK, and PI3K pathways in opposing capacities in MDSC differentiation and warrant further investigation, as it may identify novel therapeutic targets for the development of stem cell-based therapies for bone tissue engineering.

Indexed as

AnimalsBone Morphogenetic Protein 4Cell DifferentiationCell ProliferationCells, CulturedCell SurvivalChromonesEnzyme InhibitorsFlavonoidsImidazolesMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MorpholinesMuscle Cells2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneBone Morphogenetic Protein 4ChromonesEnzyme InhibitorsFlavonoidsImidazolesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Morpholinesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPyridinesSB 203580

Identifiers

PMID20617875
PMCPMC2991210
OpenAlexW2031451353

What OpenQuestion holds

Textmetadata
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.