PMID- 29949137
OWN - NLM
STAT- MEDLINE
DCOM- 20191119
LR  - 20191219
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 22
IP  - 12
DP  - 2018 Jun
TI  - Chemerin affects the metabolic and proliferative capabilities of chondrocytes by 
      increasing the phosphorylation of AKT/ERK.
PG  - 3656-3662
LID - 15243 [pii]
LID - 10.26355/eurrev_201806_15243 [doi]
AB  - OBJECTIVE: The purpose of the present study was to explore the mechanism of 
      action of the adipokine chemerin in osteoarthritis (OA) by means of an in vitro 
      OA model. MATERIALS AND METHODS: Primary chondrocytes were isolated from normal 
      rats. The chondrocytes were stimulated with interleukin 1 beta (IL-1beta, 10 mug/L) 
      to establish a model of induced OA. Chemerin was administered to cells of this 
      model. After culture of the chondrocytes in the presence of chemerin for 48 h, 
      the expression of the genes related to OA occurrence and protection, matrix 
      metalloproteinase-1 (MMP-1), matrix metalloproteinase-3 (MMP-3), and matrix 
      metalloproteinase-13 (MMP-13) was examined. Western blot was then performed to 
      analyze the phosphorylation of the AKT and extracellular signal-regulated kinase 
      (ERK) proteins in chondrocytes. RESULTS: Stimulation of chondrocytes with IL-1beta 
      markedly reduced the proliferative capability of chondrocytes. Chemerin (5 muM) 
      also significantly decreased the proliferative capability of chondrocytes. The 
      combined administration of IL-1beta and chemerin induced an even greater reduction 
      in the proliferative capability of chondrocytes. Polymerase chain reaction (PCR) 
      results showed that both IL-1beta and chemerin reduced the expression of the 
      protective genes in OA (MMP-1, MMP-3, and MMP-13). Also, the stimulation with 
      IL-1beta and chemerin significantly enhanced the phosphorylation of AKT/ERK in 
      chondrocytes. CONCLUSIONS: This adipokine induces changes in the metabolic and 
      proliferative capabilities of chondrocytes by increasing the phosphorylation of 
      AKT/ERK, thereby inducing OA or aggravating the symptoms of OA.
FAU - Ma, J
AU  - Ma J
AD  - Department of Orthopedics, First Affiliated Hospital of Northwest Minzu 
      University, Yinchuan, Ningxia, China. mj1849@163.com.
FAU - Ren, L
AU  - Ren L
FAU - Guo, C-J
AU  - Guo CJ
FAU - Wan, N-J
AU  - Wan NJ
FAU - Niu, D-S
AU  - Niu DS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Chemokines)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Rarres2 protein, rat)
RN  - EC 2.7.11.1 (Oncogene Protein v-akt)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Animals
MH  - Cartilage, Articular/cytology/drug effects/metabolism
MH  - Cell Proliferation/genetics
MH  - Cells, Cultured
MH  - Chemokines/*genetics
MH  - Chondrocytes/*metabolism/ultrastructure
MH  - Intercellular Signaling Peptides and Proteins/*genetics
MH  - Interleukin-1beta/pharmacology
MH  - MAP Kinase Signaling System/*genetics
MH  - Male
MH  - Matrix Metalloproteinases/metabolism
MH  - Oncogene Protein v-akt/*genetics/*metabolism
MH  - Osteoarthritis/*genetics/metabolism
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Wistar
EDAT- 2018/06/28 06:00
MHDA- 2019/11/20 06:00
CRDT- 2018/06/28 06:00
PHST- 2018/06/28 06:00 [entrez]
PHST- 2018/06/28 06:00 [pubmed]
PHST- 2019/11/20 06:00 [medline]
AID - 15243 [pii]
AID - 10.26355/eurrev_201806_15243 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2018 Jun;22(12):3656-3662. doi: 
      10.26355/eurrev_201806_15243.