The promoting effect of retinoic acid on proliferation of chicken primordial germ cells by increased expression of cadherin and catenins |
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Authors: | Minli Yu Kun Guan Caiqiao Zhang |
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Institution: | (1) Key Laboratory of Animal Epidemic Etiology and Immunological Prevention of the Ministry of Agriculture, Department of Veterinary Medicine, College of Animal Sciences, Zhejiang University, No. 268 Kaixuan Road, Hangzhou, 310029, People’s Republic of China; |
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Abstract: | Proliferation and cellular aggregation are both crucial features for survival and self-renewal of primordial germ cells (PGCs).
Adhesive proteins play pivotal roles in cell–cell adhesion and signal exchanges under the influence of cytokines, growth factors
and bioactive metabolites such as retinoic acid (RA). In this study, proliferation-promoting effect of RA on chicken PGCs
was investigated by revealing changes in adhesive proteins E-cadherin and α/β catenins. PGCs were isolated from the genital
ridge of 4-day-old chicken embryos and cultured on embryonic fibroblast feeder. RA (10−7–10−5 M) increased PGCs aggregation and mRNA expression of E-cadherin and α/β-catenins. Furthermore, E-cadherin and β-catenin protein
expression levels were increased by RA treatment. However, RA-elicited effect was significantly attenuated by a PKC inhibitor
H7. In addition, the number and area of PGC colonies were increased by RA treatment at 10−7–10−5 M. Again, this increase was reduced by combined treatment of H7. The proliferating effect of RA on PGCs was further confirmed by increased mRNA expression of cyclins, CCND1 and CCNE1, and cyclin-dependent kinases 6 and 2, which are critical for G1–S progression in cell cycle. Moreover, flow cytometry analysis
confirmed that RA-treated PGC populations displayed a significant increase in the proportion of S and G2 phase cells. Likewise,
this stimulating action was hindered by combined H7 treatment. These results indicate that RA, as a bioactive metabolite of vitamin A, may promote PGC proliferation and increase
intercellular aggregation of PGCs via E-cadherin and α/β-catenins expression through the PKC signaling pathway. |
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