Role of miR-219 and TGFBR2 in pathogenesis of renal fibrosis

AIM:To study the role of microRNA-219 (miR-219) in regulation of transforming growth factor-β receptor type 2 (TGFBR2) in renal fibrosis. METHODS:The renal fibrosis patients (n=70) were selected in this stu-dy, and 20 cases of healthy people were selected as control group. RT-qPCR was used to detect the expression of miR-219 in the serum of the patients with renal fibrosis and control group, and the expression of miR-219 in NRK49F cells after stimulation with angiotensin Ⅱ(AngⅡ) was detected. The protein expression of α-smooth muscle actin (α-SMA) in the NRK49F cells transfected with miR-219 mimics after stimulation with AngⅡ was determined by Western blot. The potential target gene TGFBR2 of miR-219 was screened and verified by the method of luciferase reporter gene. RT-qPCR and Western blot were used to detected the effect of miR-219 mimics on the expression of TGFBR2 at mRNA and protein levels, and the mRNA expression of α-SMA, connective tissue growth factor (CTGF), type I collagen α1 (COL1A1) and COL3A1 in the NRK49F cells was also detected, respectively. The unilateral ureteral occlusion (UUO) mouse model was established and the expression of miR-219 in the renal tissue was monitored. The morphological change of renal fibrosis was observed in the UUO mice after injection of miR-219, and the mRNA expression levels of COL1A1 and COL3A1 were detected. RESULTS:The expression level of miR-219 in the patients with renal fibrosis was significantly lower than that in control group, and the expression of miR-219 in the UUO mice was decreased significantly (P<0.01). The expression level of miR-219 was significantly decreased in the NRK49F cells after AngⅡ stimulation, and miR-219 mimics inhibited the protein expression of α-SMA(P<0.01). miR-219 mimics had a targeted regulatory effect on TGFBR2 gene, which inhibited the mRNA and protein expression of TGFBR2. miR-219 mimics inhibited the mRNA expression of α-SMA, CTGF, COL1A1 and COL3A1. miR-219 also down-regulated the mRNA expression of COL1A1 and COL3A1 in the UUO mice and inhibited the process of renal fibrosis. CONCLUSION:miR-219 inhibits the development of renal fibrosis by inhibiting the expression of TGFBR2, which may become a new target for the diagnosis and treatment of renal fibrosis.     

Protective effect of C1q/tumor necrosis factor-related protein 3 on vascular endothelium in rats with hyperuricemia

AIM To study whether C1q/tumor necrosis factor （TNF）-related protein 3 （CTRP3）protect vascular endothelium in rats with hyperuricemia and its potential mechanisms. METHODS An animal model of hyperuricemia was established by using male SD rats drinking 10% fructose water （n=10）. The rats drinking normal water served as normal controls （n=10）. After 12 weeks, the rats were given a single injection with Ad-CTRP3 or Ad-GFP. The experiment was ended at 14th day after transfection.The serum levels of uric acid and nitric oxide （NO） were evaluated. The serum contents of TNF-α and interleukin-6 （IL-6） were measured by ELISA. HE staining and TUNEL assay were used to assess the morphological changes of intima and apoptosis of endothelial cells in thoracic aorta, respectively. The mRNA levels of endothelial nitric oxide synthase （eNOS）, TNF-α and IL-6 were detected by RT-qPCR. The protein levels of CTRP3 and Toll-like receptor 4 （TLR4） were determined by Western blot. RESULTS Compared with normal control group, the rats with hyperuricemia showed lower CTRP3 and higher TLR4 protein levels in the thoracic aorta （P<0.05）. Hyperuricemic rats had higher serum contents of uric acid, TNF-α and IL-6 （P<0.05）. Also, the intima structure disturbance of thoracic aorta, increased apoptotic rate, higher mRNA levels of TNF-α and IL-6 as well as lower mRNA levels of eNOS were observed （P<0.05）. By contrast, CTRP3 over-expression decreased TLR4 protein levels, reduced inflammatory cytokines, and obviously improved the morphology and function of thoracic aorta in the rats with hyperuricemia. CONCLUSION CTRP3 protect vascular endothelium in rats with hyperuricemia maybe via down-regulation of TLR4- mediated inflammatory signaling pathway.     

不同处理方法对受体牛同期发情效果的比较研究

[目的]为了进一步促进人工授精技术广泛应用以及提高胚胎移植效率，为酒泉本地胚胎移植选择高效的同期发情方法。[方法]本试验分别采用PRID＋PGF2α法和PGF2α＋PGF2α法对胚胎移植受体牛做同期友情处理。[结果]表明：两种方法处理受体牛，其同期发情率和移植妊娠率之间差异无统计意义（P〉0．05），但是用PRID＋PGF2α法处理受体牛同期发情率和移植妊娠率均高于PGF2α＋PGF2α法。[结论]在奶牛养殖及生产上，在考虑移植成本和生产效益的情况下，在农区大面积对牛只进行同期发情技术处理，应优选PGF2α＋PGF2α法处理受体牛。     

Associations of Gonadotropin-Releasing Hormone Receptor (GnRHR) and Neuropeptide Y (NPY) Genes'''' Polymorphisms with Egg-Laying Traits in Wenchang Chicken

Single nucleotide polymorphisms (SNP) of chicken gonadotropin-releasing hormone receptor (GnRHR) and neuropeptide Y (NPY) were selected to identify the genotypes of Wenchang (Chinese indigenous breed) chicken with restricton fragment length polymorphisms. The associations of the SNPs with the total egg production (NE), average days of continual laying (ADCL), and number of double-yolked eggs (DYE) traits were analyzed. The frequency of restriction enzyme A/a alleles in the population was for GnRHR 0.69 (Bpu1102 Ⅰ A) and 0.31 (Bpu1102 Ⅰ a) and for NPY 0.46 (Dra Ⅰ B) and 0.54 (Dra Ⅰ b). Trait data from a total of 120 hens, which were purebred introduced from Hainan Province, China from one generation were recorded. Two significant effects of genes' marker were found for GnRHR and number of eggs (dominant; t= 2.67, df= 116) and NPY and number of eggs (additive; t= 1.97, df= 116). The current research supports the effects of GnRHR and NPY genes on egg-laying traits of chickens.     

孕酮处理对蛋鸡蛋壳钙化过程中CaBP-d28k基因表达的影响

实验旨在研究孕酮对蛋鸡CaBP-d28k基因表达的影响。对产蛋高峰期蛋鸡进行孕酮和孕酮受体拮抗剂(RU-486)处理,利用实时荧光定量PCR技术(QRT-PCR),测定在蛋壳形成过程中输卵管子宫部钙结合蛋白(CaBP-d28k)、孕酮受体(PGR)的表达量;同时对血液中钙离子和孕酮浓度变化进行测定。结果表明:孕酮处理后,血液中钙离子浓度显著降低(P<0.05),输卵管子宫部CaBP-d28k表达量也显著降低(P<0.05);孕酮受体拮抗剂处理后,血液中钙离子浓度显著升高(P<0.05),输卵管子宫部CaBP-d28k表达量极显著升高(P<0.01)。结果提示,在蛋壳钙化过程中,孕酮对CaBP-d28k表达和钙离子转运起负调控作用。     

死亡受体6的作用机制及其生物学功能

死亡受体6(death receptor 6,DR6)是肿瘤坏死因子受体超家族中的成员。DR6是Ⅰ型跨膜受体,拥有4个胞外半胱氨酸基序和1个胞内死亡结构域。在人的大多数组织表达中,已经发现其在心、脑、胎盘、胰脏、胸腺、淋巴结和几个非淋巴癌细胞系中表达。DR6可以和TRADD相互作用,激活JNK和NF-κB途径。DR6能下调T、B细胞的增殖和活化,诱导神经细胞的凋亡等。     

催乳素及其受体对乳腺发育研究进展

本文主要对催乳素受体的结构、作用机理、功能及其在不同时期的乳腺发育的不同作用进行的论述。总结了近几年来的有关研究进展,为进一步的研究工作提供参考资料。     

Advance in receptor type protein tyrosine phosphatase Q

Receptor type protein tyrosine phosphatase Q (PTPRQ) is an unusual protein tyrosine phosphatase that has intrinsic dephosphorylating activity for various phosphatidylinositiol and phospho-tyrosine substrates, especially the phosphatidylinositol activity. Recent data show that PTPRQ has an important role in various biological processes and is associated with some diseases. In this article, the structure and function of PTPRQ and the relationship between PTPRQ and diseases were briefly summarized.