Evidence map›Paper›PMID 28420447›Full record

ArticleStem cell research & therapy2017

CK2.1, a bone morphogenetic protein receptor type Ia mimetic peptide, repairs cartilage in mice with destabilized medial meniscus.

Hemanth Akkiraju, Padma Pradeepa Srinivasan, Xian Xu, Xinqiao Jia, Catherine B Kirn Safran, Anja Nohe

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  9. Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023
    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

6 authors at 5 institutions in 1 country.

Hemanth AkkirajuQuantitative Proteomics and Metabolomics Center, Columbia University, New York, NY, 10027, USA.
Padma Pradeepa SrinivasanHelen F Graham Cancer center, Christiana Care, University of Delaware, Newark, DE, 19716, USA.
Xian XuDepartment of Material Sciences and Engineering, University of Delaware, Newark, DE, 19716, USA.
Xinqiao JiaDepartment of Material Sciences and Engineering, University of Delaware, Newark, DE, 19716, USA.
Catherine B Kirn SafranDepartment of Biological Sciences, University of Delaware, Newark, DE, 19716, USA.
Anja NoheDepartment of Biological Sciences, University of Delaware, Newark, DE, 19716, USA. anjanohe@udel.edu.ORCID 0000-0002-6801-771X
University of Delaware · USChristiana Care Health System · USColumbia University · USMaterial Sciences (United States) · USProvid Pharmaceuticals (United States) · US

Funding

Mechanism of a mimetic peptide CK2.3 on bone formationR01AR064243 · NIAMS · UNIVERSITY OF DELAWARE · PI NOHE, ANJA G · 2013 to 2018
$1.6M
NIAMS NIH HHS R01 AR064243
6 · The paper itself

Abstract

backgroundOsteoarthritis (OA) of the knee involves degeneration of articular cartilage of the diarthrodial joints. Current treatment options temporarily relieve the joint pain but do not restore the lost cartilage. We recently designed a novel bone morphogenetic protein receptor type I (BMPRI) mimetic peptide, CK2.1, that activates BMPRIa signaling in the absence of bone morphogenetic protein (BMP). Our previous research demonstrated that CK2.1 induced chondrogenesis in vitro and in vivo; however, it is unknown if CK2.1 restores damaged articular cartilage in vivo. In this study, we demonstrate that CK2.1 induced articular cartilage (AC) repair in an OA mouse model.

methodsWe designed hyaluronic acid (HA)-based hydrogel particles (HGPs) that slowly release CK2.1. HGP-CK2.1 particles were tested for chondrogenic potency on pluripotent mesenchymal stem cells (C3H10T1/2 cells) and locally injected into the intra-articular capsule in mice with cartilage defects. C57BL/6J mice were operated on to destabilize the medial meniscus and these mice were kept for 6 weeks after surgery to sustain OA-like damage. Mice were then injected via the intra-articular capsule with HGP-CK2.1; 4 weeks after injection the mice were sacrificed and their femurs were analyzed for cartilage defects.

resultsImmunohistochemical analysis of the cartilage demonstrated complete repair of the AC compared to sham-operated mice. Immunofluorescence analysis revealed collagen type IX production along with collagen type II in the AC of mice injected with HGP-CK2.1. Mice injected with phosphate-buffered saline (PBS) and HGP alone had greater collagen type X and osteocalcin production, in sharp contrast to those injected with HGP-CK2.1, indicating increased chondrocyte hypertrophy.

conclusionsOur results demonstrate that the slow release HGP-CK2.1 drives cartilage repair without the induction of chondrocyte hypertrophy. The peptide CK2.1 could be a powerful tool in understanding the signaling pathways contributing to the repair process, and also may be used as a potential therapeutic for treating degenerative cartilage diseases such as OA.

Indexed as

ChondrogenesisAnimalsBone Morphogenetic Protein Receptors, Type ICartilage, ArticularCell LineCollagenMeniscusMesenchymal Stem CellsMiceOsteoarthritis, KneeOsteocalcinPeptidesBmpr1a protein, mouseBone Morphogenetic Protein Receptors, Type ICK2.1 peptideCollagenOsteocalcinPeptidesBone morphogenetic proteinCartilageCasein kinase IIHyaluronic acidOsteoarthritis

Identifiers

PMID28420447
PMCPMC5395786
OpenAlexW2606643986

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.