title: Pilose antler polypeptides promote chondrocyte proliferation via the tyrosine kinase signaling pathway.
abstract: BACKGROUND
  Pilose antler polypeptides (PAP) have been reported to promote chondrocyte proliferation. However, the underlying mechanism remains unclear. The present study was to investigate the effects of PAP on the proliferation of chondrocytes and its underlying mechanism.
  
  
  METHODS
  Chondrocytes isolated from the knee of Zealand white rabbits were cultured. The second generation chondrocytes were collected and identified using safranin-O staining. The chondrocytes were divided into the following 4 groups including serum-free, PAP, genistein (an inhibitor of tyrosine kinases), and PAP plus genistein group. Cell viability was analyzed using the MTT assay. The cell cycle distribution of the chondrocytes was analyzed by flow cytometry. The expression levels of cyclin A was detected using immunocytochemical staining.
  
  
  RESULTS
  No significant difference was observed between serum-free and genistein group. Treatment of the cultures with PAP produced a significant dose-dependent increase in cell viability, the percentage proportion of chondrocytes in the S phase and Cyclin A expression as well. However, the promoting effect of PAP on chondrocyte proliferation were dose-dependently inhibited by genistein, whereas genistein alone had no effect on proliferation of isolated chondrocytes.
  
  
  CONCLUSIONS
  The data demonstrate that PAP promotes chondrocyte proliferation with the increased cell number, percentage proportion of chondrocytes in S phase and expression of protein cyclin A via the TK signaling pathway.
authors.affiliation: Orthopaedics & Traumatology College, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, PR China. Zhanglil626@yahoo.com.
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Lin
authors.forename: Ling-Xiao
authors.initials: LX
authors.lastname: Deng
authors.forename: Zhao-Yang
authors.initials: ZY
authors.lastname: Wu
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Li
authors.initials: L
authors.lastname: Zhang
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