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

Abstract Osteoarthritis (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.
PMID
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Authors

Mayor MeshTerms
Keywords

Bone morphogenetic protein

Cartilage

Casein kinase II

Hyaluronic acid

Osteoarthritis

Journal Title stem cell research & therapy
Publication Year Start




PMID- 28420447
OWN - NLM
STAT- In-Process
DA  - 20170419
LR  - 20170423
IS  - 1757-6512 (Electronic)
IS  - 1757-6512 (Linking)
VI  - 8
IP  - 1
DP  - 2017 Apr 18
TI  - CK2.1, a bone morphogenetic protein receptor type Ia mimetic peptide, repairs
      cartilage in mice with destabilized medial meniscus.
PG  - 82
LID - 10.1186/s13287-017-0537-y [doi]
AB  - BACKGROUND: Osteoarthritis (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. METHODS: We
      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. RESULTS:
      Immunohistochemical 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.
      CONCLUSIONS: Our 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.
FAU - Akkiraju, Hemanth
AU  - Akkiraju H
AD  - Quantitative Proteomics and Metabolomics Center, Columbia University, New York,
      NY, 10027, USA.
FAU - Srinivasan, Padma Pradeepa
AU  - Srinivasan PP
AD  - Helen F Graham Cancer center, Christiana Care, University of Delaware, Newark,
      DE, 19716, USA.
FAU - Xu, Xian
AU  - Xu X
AD  - Department of Material Sciences and Engineering, University of Delaware, Newark, 
      DE, 19716, USA.
AD  - Present address: NAL Pharmaceuticals Ltd, Monmouth Junction, NJ, 08852, USA.
FAU - Jia, Xinqiao
AU  - Jia X
AD  - Department of Material Sciences and Engineering, University of Delaware, Newark, 
      DE, 19716, USA.
FAU - Safran, Catherine B Kirn
AU  - Safran CBK
AD  - Department of Biological Sciences, University of Delaware, Newark, DE, 19716,
      USA.
FAU - Nohe, Anja
AU  - Nohe A
AUID- ORCID: http://orcid.org/0000-0002-6801-771X
AD  - Department of Biological Sciences, University of Delaware, Newark, DE, 19716,
      USA. [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170418
PL  - England
TA  - Stem Cell Res Ther
JT  - Stem cell research & therapy
JID - 101527581
PMC - PMC5395786
OTO - NOTNLM
OT  - Bone morphogenetic protein
OT  - Cartilage
OT  - Casein kinase II
OT  - Hyaluronic acid
OT  - Osteoarthritis
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/20 06:00
PHST- 2017/01/16 [received]
PHST- 2017/03/14 [accepted]
PHST- 2017/02/22 [revised]
AID - 10.1186/s13287-017-0537-y [doi]
AID - 10.1186/s13287-017-0537-y [pii]
PST - epublish
SO  - Stem Cell Res Ther. 2017 Apr 18;8(1):82. doi: 10.1186/s13287-017-0537-y.

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