ArticleExperimental & molecular medicine2019
Peroxiredoxin II negatively regulates BMP2-induced osteoblast differentiation and bone formation via PP2A Cα-mediated Smad1/5/9 dephosphorylation.
Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Therapeutic strategies for intervertebral disc degeneration: Extracellular vesicles and microRNAs derived from mesenchymal stem cells.World journal of stem cells · 2025Review
- Overexpression of miR-671-3p alleviates postmenopausal osteoporosis by targeting GREM2 to activate BMP2/SMAD signaling pathway.Hereditas · 2025Article
- ERS-PERK Pathway is Involved in the Repair of the Pulpo-Dentinal Complex Under an Inflammatory Microenvironment.Stem cells international · 2025Article
- Article
- Article
- Review
- Influence of diabetes mellitus on the pathological profile of aortic stenosis: a sex-based approach.Cardiovascular diabetology · 2023Article
- The Emerging Role of Protein Phosphatase in Regeneration.Life (Basel, Switzerland) · 2023Review
- Understanding Reactive Oxygen Species in Bone Regeneration: A Glance at Potential Therapeutics and Bioengineering Applications.Frontiers in bioengineering and biotechnology · 2022Review
- DUSP5 promotes osteogenic differentiation through SCP1/2-dependent phosphorylation of SMAD1.Stem cells (Dayton, Ohio) · 2021Article
- Active hematopoiesis triggers exosomal release of PRDX2 that promotes osteoclast formation.Physiological reports · 2021Article
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Schnurri-3 regulates BMP9-induced osteogenic differentiation and angiogenesis of human amniotic mesenchymal stem cells through Runx2 and VEGF.Cell death & disease · 2020Article
- N-myc Downstream-Regulated Gene 2 (NDRG2) Promotes Bone Morphogenetic Protein 2 (BMP2)-Induced Osteoblastic Differentiation and Calcification by Janus Kinase 3 (JAK3)/Signal Transducer and Activator of Transcription 3 (STAT3) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Peroxiredoxin II (Prx II), an antioxidant enzyme in the Prx family, reduces oxidative stress by decreasing the intracellular ROS levels. Osteoblast differentiation is promoted by bone morphogenetic protein 2 (BMP2), which upregulates the expression of osteoblast differentiation marker genes, through Smad1/5/9 phosphorylation. We found that Prx II expression was increased by a high dose of lipopolysaccharide (LPS) but was not increased by a low dose of LPS. Prx II itself caused a decrease in the osteogenic gene expression, alkaline phosphatase (ALP) activity, and Smad1/5/9 phosphorylation induced by BMP2. In addition, BMP2-induced osteogenic gene expression and ALP activity were higher in Prx II knockout (KO) cells than they were in wild-type (WT) cells. These inhibitory effects were mediated by protein phosphatase 2A Cα (PP2A Cα), which was increased and is known to induce the dephosphorylation of Smad1/5/9. The overexpression of Prx II increased the expression of PP2A Cα, and PP2A Cα was not expressed in Prx II KO cells. Moreover, PP2A Cα reduced the level of BMP2-induced osteogenic gene expression and Smad1/5/9 phosphorylation. LPS inhibited BMP2-induced Smad1/5/9 phosphorylation and the suppressed phosphorylation was restored by the PP2A inhibitor okadaic acid (OA). Bone phenotype analyses using microcomputed tomography (μCT) revealed that the Prx II KO mice had higher levels of bone mass than the levels of the WT mice. We hypothesize that Prx II has a negative role in osteoblast differentiation through the PP2A-dependent dephosphorylation of Smad1/5/9.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.