title: [Effects of chemerin on the proliferation of 3T3-L1 adipocytes].
abstract: OBJECTIVE
  To explore the effects of chemerin on the proliferation of 333-Li preadipocytes and elucidate its possible mechanism.
  
  
  METHODS
  Recombinant lentivirus-mediated silencing or over-expression of chemerin gene were constructed in 3T3-L1 cells. The proliferation of 3T3-L1 cells was examined by the assays of methyl thiazolyl tetrazolium (MTT) and 5-bromo-2-deoxyuridine (BrdU) incorporation. The expressions of chemerin, ERK1, ERK2 and cyclinD1 in 3T3-L1 cells were detected by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). The protein levels of chemerin, ERK1/2 and p-ERK1/2 were detected by Western blot.
  
  
  RESULTS
  MT and BrdU results showed that absorbance (A) value and BrdU incorporation increased in chemerin over-expression group compared with over-expression control group [1. 09 ± 0. 08 vs 0. 90 ± 0. 09, (126. 5 ± 14. 6)% vs (100. 0 ± 7. 0) %, both P <0. 05]. The increase of A value and BrdU incorporation in chemerin over-expression group could be inhibited by PD98059, a blocker of ERK1/2 signal pathway. A value (0. 91 ± 0. 13) and BrdU incorporation [(104. 3 ± 10. 7)%] decreased compared with over-expression group (P <0. 05). They also decreased in chemerin gene silencing group compared to silencing control group [ 0. 72 ± 0. 11 vs 0. 90 ± 0. 09, (77. 6 ± 11. 8) % vs ( 99. 7 ± 6. 3) %, both P < 0. 05]. Quantitative real-time PCR revealed that over-expression group had a higher expression in chemerin, ERK, ERK2 and cyclinDl than over-expression control group (2. 77 ± 0. 31 vs 1. 01 ± 0. 12, 1. 39 ± 0. 19 vs 0. 76 ± 0. 30, 1. 46 ± 0. 14 vs 0. 88 ± 0. 14, 1. 44 ± 0. 17 vs 1. 03 0. 15, all P <0. 05). Chemerin gene silencing group had lower expressions of chemerin, ERKI, ERK2 and cyclinD1 than silencing control group (0. 35 ± 0. 12 vs 1. 25 ± 0. 31, 0. 64 ± 0. 15 vs 1. 03 ± 0. 14, 0. 56 ± 0. 10 vs 1. 06 ± 0. 29, 0. 66 ± 0. 13 vs 1. 09 0. 19, all P <0. 05). Western blot showed that the expressiond of chemerin, ERK1/2 and p-ERK1/2 increased in chemerin over-expression group versus over-expression control group (2. 18 ± 0. 32 vs 1. 18 ± 0. 14, 1. 37 ± 0. 05 vs 0. 97 ± 0. 12, 1. 06 ± 0. 09 vs 0. 56 ± 0. 08, all P < 0. 05). The expressiond of chemerin, ERK1/2 and p-ERK1/2 decreased in chemerin gene silencing group versus silencing control group (1. 00 ± 0. 07 vs 1. 40 ± 0. 17, 0. 87 ± 0. 15 vs 1. 20 ± 0. 12, 0. 49 ± 0. 07 vs 0. 91 ± 0. 11, all P < 0. 05).
  
  
  CONCLUSIONS
  Chemerin may promote the proliferation of 3T3-L1 cells. And it may be achieved via an up-regulated expression of ERK1/2.
authors.forename: Xuemei
authors.initials: X
authors.lastname: Li
authors.forename: Lidong
authors.initials: L
authors.lastname: Zhai
authors.forename: Penghua
authors.initials: P
authors.lastname: Wang
authors.forename: Min
authors.initials: M
authors.lastname: Ding
authors.forename: Jun
authors.initials: J
authors.lastname: Xu
authors.forename: Shuhong
authors.initials: S
authors.lastname: Feng
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes; D000818:Animals; D049109:Cell Proliferation; D005419:Flavonoids; D020868:Gene Silencing; D051379:Mice; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D060888:Real-Time Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D005419:Flavonoids; C535148:Mapk1 protein, mouse; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one