| 1 | Pyridoxine regulates hair follicle development via the PI3K/Akt, Wnt and Notch signalling pathways in rex rabbits显示文摘This study was conducted to evaluate the effect of pyridoxine on the development of hair follicles in Rex rabbits and the underlying molecular mechanism.Two hundred 3-month-old Rex rabbits were randomly divided into 5 groups and fed diets supplemented with 0,5,10,20,or 40 mg/kg pyridoxine.The hair follicle density on the dorsal skin and the gene and protein expression levels of components of the phosphoinositide 3-kinase(PI3 K)/protein kinase B(PKB or Akt),Wnt,Notch and bone morphogenetic protein(BMP)signalling pathways were measured.In addition,free hair follicles were isolated from Rex rabbits and cultured with pyridoxine in vitro to measure hair shaft growth.Furthermore,dermal papilla cells(DPC)were isolated from the skin of Rex rabbits and cultured with pyridoxine in vitro to measure the gene and protein expression levels of components of the PI3 K/Akt,Wnt,Notch and BMP signalling pathways.The results showed that the addition of dietary pyridoxine significantly increased the total follicle density,secondary follicle density,and secondary-to-primary ratio(S/P,P<0.05),that the growth ratio of hair stems was promoted by pyridoxine in basic culture medium,and that the growth length of tentacle hair follicles cultured in the pyridoxine group was longer than that in the control group(P<0.05).In addition,pyridoxine changed the DPC cycle progression and promoted cell proliferation,and appropriate concentrations of pyridoxine(10 and 20μmol/L)significantly inhibited cell apoptosis(P<0.05).Pyridoxine significantly affected the gene expression of components of the PI3 K/Akt,Wnt and Notch signalling pathways in the skin and DPC of Rex rabbits(P<0.05),increased the levels of phosphorylated catenin beta 1(CTNNB1)and Akt,and decreased the level of phosphorylated glycogen synthase kinase 3 beta(GSK-3β)(P<0.05).Therefore,the molecular mechanism by which pyridoxine promotes hair follicle density in Rex rabbits probably occurs through activation of the PI3 K/Akt,Wnt and Notch signalling pathways,prolonging hair follicle growth and delaying the onset of telogen. | Gongyan Liu Guangmin Cheng Yongcui Zhang Shuxia Gao Haitao Sun Liya Bai Shu Li Yanli Zhu Chunyang Wang Fuchang Li | 2021 | Animal Nutrition2021，，4： | 1 |
| 2 | Long noncoding RNA TMEM147-AS1 serves as a microRNA-326 sponge to aggravate the malignancy of gastric cancer by upregulating SMAD5显示文摘The abnormal expression of long noncoding RNAs(lncRNAs)is frequently observed in gastric cancer(GC)and considered an important driving force in GC progression.However,little is known regarding the involvement of TMEM147-AS1 in GC.Therefore,we examined TMEM147-AS1 expression in GC and determined its prognostic value.In addition,TMEM147-AS1 expression was depleted to identify the functional changes in response to TMEM147-AS1 deficiency.Using the cancer genome atlas dataset and our own cohort,we identified a strong expression of TMEM147-AS1 in GC.Increased TMEM147-AS1 levels in GC showed a significant association with poor prognosis.TMEM147-AS1 interference resulted in the inhibition of GC cell proliferation,colony-forming,migration,and invasion in vitro.Additionally,depletion of TMEM147-AS1 restricted the growth of GC cells in vivo.Mechanistically,TMEM147-AS1 functioned as a microRNA-326(miR-326)sponge.Furthermore,SMAD family member 5(SMAD5)was experimentally validated as the functional effector of miR-326.TMEM147-AS1 was demonstrated to sequester miR-326 away from SMAD5;consequently,knocking down TMEM147-AS1 downregulated SMAD5 levels in GC cells.The functional suppression of miR-326 or reintroduction of SMAD5 effectively reversed the attenuated behavior of GC cells caused by TMEM147-AS1 downregulation.In summary,TMEM147-AS1 exhibits tumorigenic activities in GC,which is likely the result of an altered miR-326/SMAD5 axis.Therefore,targeting TMEM147-AS1/miR-326/SMAD5 may represent a target for the treatment of GC. | XUFU QIN ZIYE JIANG YONGCUI ZHU HONGPENG XUE CHENGQUN WEI | 2021 | Oncology Research2021，29，4： | 0 |
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