Adiponectin is a special protein with many biological functions produced by adipose cells.It can increase insulin sen- sitivity,protect hypertension,suppress atherosclerosis,liver fibrosis,and tumor growth,and also can increase bone mass by suppressing osteoclast and activating osteoblast.When compared with other adipokines,the levels of adiponectin are inversely proportional to body fat content.Recent studies pay attention to the roles that adiponectin played in the homeostasis of adipose tissue,pathogenesis of the metabolic syndrome,type 2 diabetes,and atherosclerosis.These pleiotropic effects make it being an attractive therapeutic target for obe- sity-related conditions.Two adiponectin receptors are identified,termed AdiopR1 and AdipoR2.These both are ubiquitously expressed. AdipoR1 is mos't highly expressed in skeletal muscle,and AdipoR2 is most highly expressed in liver.This paper rcvicws the latest re- search progress of adiponectin and its receptors.
Objective To study the regulatory effect of interferons(IFNs) on retinoic acid-inducible gene-Ⅰ(RIG-Ⅰ) and the roles of RIG-Ⅰ in IFNs signaling pathway. Methods RIG-Ⅰ expression before and after IFNs treatment in mouse embryonic fibroblasts(MEFs) were analyzed with Northern blotting and semi-quantitative RT-PCR assay.MEFs isolated from wild-type and RIG-Ⅰ-/-mice were used to test growth inhibition and antiviral activity of IFNs with MTT assay and cytopathic effect inhibition assay. Results Both IFN-γ and IFN-β could induce RIG-Ⅰ expression in MEFs.Treated with 100 U/mL IFN-γ,growth inhibition and antiviral activity of MEFs from wild-type mice were more significant than those from RIG-Ⅰ-/-mice.With the absence of RIG-Ⅰ,the antiviral protective role IFN-β plays was significantly weaker than the wild type. Conclusion RIG-Ⅰ gene is a novel mediator of interferon effects on cells.It may participate in the inflammation responses mediated by IFNs through modulating cytokines production.
Osteogenesis imperfecta(OMIM 166200)is an autosomal dominant disorder characterized by bone fragility and abnormalities of connective tissue.Over 90% of patients with osteogenesis imperfecta have mutations in the COL1A1 and COL1A2 genes which encode the chains of typeⅠprocollagen.This disease has genetic heterogeneity.Clinical characteristics of osteogenesis imperfecta(OI)are variable and its clinical clas- sification is complex.Different phenotypes may be involved different mechanism.Here,we generally summa- rize the clinical classification and progress of genetic studies on osteogenesis imperfecta.
Objective To explore the biological functions of retinoic acid-inducible gene-I(RIG-I) in vivo through phenotype analysis of RIG-I knockout mice. Methods The gene expression of RIG-Ⅰ in various tissues of mice was examined with Northern blotting and semi-quantitative RT-PCR.The phenotypes observed included body weight measurement,differential count of peripheral blood cells,metabolic parameters measurement and histopathologic examination. ResultsRIG-Ⅰ expressed in various tissues of mice with different levels.No gross developmental abnormalities and expected maturation arrest in granulocytic differentiation were observed in RIG-Ⅰ knockout mice.However,RIG-Ⅰ knockout mice exhibited an unexpected increase in the ratios of neutrophiles to lymphocytes in peripheral blood and increased susceptibility to bacteria infection. Conclusion RIG-Ⅰ may play an important role in immune regulation in mice.
Objective To investigate the relationships between serum levels of receptor activator of nuclear factor-kappa B ligand(RANKL),estrogen and heart function in osteoprotegerin(OPG) deficience-induced mouse osteoporosis. MethodsOPG knockout mouse model and control group were established.Serum OPG and RANKL levels were measured by ELISA.Serum estrogen was detected by radioimmunology,and cardiac ultrasonography was performed to assess the heart function.Results The heart weight,the ratio of heart weight to body weight and transverse area of myocardial cells of left ventricle were significantly increased in OPG knockout mice compared to the control group(P0.01).Left ventricular systolic diameter and left ventricular end-systolic volume in OPG knockout mice were significantly higher than those in the control group(P0.05).The serum RANKL level in OPG knockout mice was higher than that of the control group(P0.001),while there was no significant change in the serum estrogen level(P0.05). Conclusion Deficience of OPG induces up-regulation of serum RANKL level and myocardial hypertrophy,but has no effect on serum estrogen level.
Objective:To investigate the expression and regulation mechanism of SATB1 in various cancer cells through assaying 5' upstream sequence and 3'untranslated region of SATB1.Methods:mRNA of SATB1 is assayed by semi-quantitative PCR in six cell lines including BT549,MCF7,NCI-H-446,SPC-A1,QG56,HL60.Western blot is used for detecting SATB1.Reporter vectors composed of truncated 5'upstream sequence of SATB1 were constructed.Then these vectors were transected into QG56 and SPC-A1 cells.In addition,3'UTR of SATB1 was inserted into PGL3 control.PGL3-control-3'UTR was transfected into three lung cancer cell lines.Dual-luciferase reporter assay is used to detect the activity of luciferase.Bioinformatics analysis is used to predict transcription factors binding-site of two sequence segment including-638～+404 and-1218～+48.Resaults:T1 exists in BT549,NCI-H-446,SPC-A1,and QG56;T2 exists in BT549 and QG56.For QG56,PGL3-T1-638～+404 has highest luciferase activity,while for SPC-A1,transfected PGL3-T2-1218～+48 has highest luciferase activity.In NCI-H-446,luciferase activity of PGL3-control-3'UTR is markedly lower than that of PGL3-control(P0.05).Conclusions:Metastasis of lung cancer isn't related with SATB1.RT-PCR,luciferase activity and bioinformatics analysis show that two transcription of SATB1 are regulated by respective 5'upstream sequence.In NCI-H-446,expression of SATB1 is inhibited by 3'UTR.
Objective To investigate the leukemogenic potential of AML1-ETO fusion gene in vivo, and to provide an ideal animal model for anti-leukemia drug screening. Methods The molecular cloning technology was used to construct the AML1-ETO transgenic plasmid. The recombined DNA was microinjected into the zygotes, which was then implanted into the pseudopregnant mice. And then the G0 transgenic mice were obtained. The integration of the transgene was tested by PCR and the expression was examined by reverse transcription-polymerase chain reaction (RT-PCT). Results PCR testing revealed a total of 10 G0 transgenic mice, 8 of whom had their F1 offsprings and then 8 AML1-ETO transgenic mouse lines was established. RT-PCR showed the AML1-ETO fusion gene stably expressed only in one line, which had no abnormal changes in the blood routine, liver and spleen tissues. The AML1-ETO gene was found to express stably in liver, spleen, heart and muscle except brain. Conclusions A transgenic mouse model in which the AML1-ETO fusion gene can stably express has been established.
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