Estradiol-17 beta regulates the expression of insulin-like growth factors 1 and 2 via estradiol receptors in spotted scat (Scatophagus argus)
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY
Authors: Zhang, Ke-Wei; Wu, Tian-Li; Chen, Hua-Pu; Jiang, Dong-Neng; Zhu, Chun-Hua; Deng, Si-Ping; Zhang, Yong; Li, Guang-Li
Abstract
Insulin-like growth factors (Igf1 and Igf2) play a key role in growth and development of vertebrates. In mammals, the expression of IGFs is regulated by estradiol-17 beta (E-2) via estrogen receptors (ESRs). The expression of igfs can also be regulated by E-2 in fish, while comparative study of this is still lacking. The present study examined tissue distribution of igfs and hepatic expression of igfs and esrs during gonad development in Scatophagus argus by real-time PCR. Serum E-2 concentration was measured by enzyme-linked immunosorbent assay (ELISA). The hepatic expression of igfs and esrs at gonadal phase III, incubated with either E-2 (0.1, 1 or 10 mu M) alone or in combination with estrogen receptor antagonists-fulvestrant, MPP or PHTPP, was measured. igf1 and igf2 expressed highest in liver of both sexes. Igf1, esr1 and esr2b expressions and serum E-2 concentration increased, while igf2 and esr2a expressions decreased, during ovary development. Igfs and esrs expressions increased while serum E-2 concentration maintained low during testis development. In females, E-2 incubation enhanced the expressions of igf1 and esr1 but inhibited that of igf2 and esr2a. Both fulvestrant and MPP inhibited up-regulation effect of E-2 on igf1 and esr1. Fulvestrant enhanced down-regulation effect of E-2 on igf2 and esr2a, but MPP conversely. In males, E-2 incubation enhanced the expressions of igfs, esr1 and esr2a. Fulvestrant and MPP inhibited up-regulation effect of E-2 on igfs and esr1. PHTPP inhibited igf1 and esr2 expressions in both sexes. Our results indicated that the expression of igfs is regulated by E-2 via Esrs in S. argus.
Systematic Review and Meta-Analysis of Candidate Gene Association Studies With Fracture Risk in Physically Active Participants
FRONTIERS IN GENETICS
Authors: Ryan-Moore, Edward; Mavrommatis, Yiannis; Waldron, Mark
Abstract
Background:Fractures are common in physically active populations and genetic differences may mediate injury risk. Objective:To meta-analyse the pooled results of candidate gene association studies with non-osteoporotic fracture risk in physically active humans. Methods:Systematic searching of databases returned 11 eligible studies published in English. Pooled odds ratios (ORs) with 95% confidence intervals (CI) were produced using allele contrast, recessive and homozygote contrast meta-analysis models to evaluate associations of risk alleles in theCOL1A1(rs1800012),COL2A1(rs412777),CTR(rs1801197),ESR1(rs2234693 and rs9340799)LRP5(rs3736228),VDR(rs10735810, rs7975232, rs1544410, and rs731236) genes with fracture incidence. Results:Eligible study quality was generally low (7/11) and no significant overall effect was found for any genetic variant with any comparison model (p> 0.05). Atrivialreduction in fracture risk was found for female participants with theCOL1A1Sp1 (rs1800012) T allele (OR= 0.48, 95% CI = 0.25-0.91,p= 0.03,d= -0.18). Conclusions:No overall effect was found from the pooled results of included genetic variants on fracture risk in physically active participants. TheCOL1A1Sp1 rs1800012 T allele may reduce fracture risk in physically active females but further high-quality research with sex-specific analysis is required.