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| 1 | The role of GPCRs in bone diseases and dysfunctions显示文摘The superfamily of G protein-coupled receptors (GPCRs) contains immense structural and functional diversity and mediates a myriad of biological processes upon activation by various extracellular signals.Critical roles of GPCRs have been established in bone development,remodeling,and disease.Multiple human GPCR mutations impair bone development or metabolism,resulting in osteopathologies.Here we summarize the disease phenotypes and dysfunctions caused by GPCR gene mutations in humans as well as by deletion in animals.To date,92 receptors (5 glutamate family,67 rhodopsin family,5 adhesion,4 frizzled/taste2 family,5 secretin family,and 6 other 7TM receptors) have been associated with bone diseases and dysfunctions (36 in humans and 72 in animals).By analyzing data from these 92 GPCRs,we found that mutation or deletion of different individual GPCRs could induce similar bone diseases or dysfunctions,and the same individual GPCR mutation or deletion could induce different bone diseases or dysfunctions in different populations or animal models.Data from human diseases or dysfunctions identified 19 genes whose mutation was associated with human BMD:9 genes each for human height and osteoporosis;4 genes each for human osteoarthritis (OA) and fracture risk;and 2 genes each for adolescent idiopathic scoliosis (AIS),periodontitis,osteosarcoma growth,and tooth development.Reports from gene knockout animals found 40 GPCRs whose deficiency reduced bone mass,while deficiency of 22 GPCRs increased bone mass and BMD;deficiency of 8 GPCRs reduced body length,while 5 mice had reduced femur size upon GPCR deletion.Furthermore,deficiency in 6 GPCRs induced osteoporosis;4 induced osteoarthritis;3 delayed fracture healing;3 reduced arthritis severity;and reduced bone strength,increased bone strength,and increased cortical thickness were each observed in 2 GPCR-deficiency models.The ever-expanding number of GPCR mutation-associated diseases warrants accelerated molecular analysis,population studies,and investigation of phenotype correlation with SNPs to elucidate GPCR function in human diseases. | Jian Luo Peng Sun Stefan Siwko Mingyao Liu Jianru Xiao | 2019 | Bone Research2019，7，2： | 5 |
| 2 | 花鲈OPN5基因克隆及其在光周期处理下的表达特征显示文摘【目的】通过克隆花鲈视蛋白5(OPN5)基因(LmOPN5)序列,检测视网膜、血管囊、下丘脑和垂体中LmOPN5基因在不同光周期下的表达水平,探究光周期对LmOPN5基因表达的影响,为深入研究花鲈感知光周期信号提供参考依据。【方法】通过PCR和RACE克隆获得LmOPN5基因全长序列,并进行生物信息学分析;应用实时荧光定量PCR检测LmOPN5基因在各组织中的相对表达量;再比较不同光周期(常光周期组12 L∶12 D,短光周期组8 L∶16D,长光周期组16L∶8D;L:光照时间,D:黑暗时间)条件下,视网膜、血管囊、下丘脑和垂体中LmOPN5基因表达的变化。【结果】LmOPN5基因cDNA全长1732 bp,其中开放阅读框(ORF)长1056 bp,共编码351个氨基酸残基。Lm OPN5蛋白分子量为39.26 kD,理论等电点(pI)为9.17。LmOPN5蛋白二级结构中α-螺旋占40.17%、无规则卷曲占34.76%、延伸链占22.51%、β-转角占2.56%,以α-螺旋和无规则卷曲为主。氨基酸序列同源比对分析结果显示,LmOPN5氨基酸序列与其他硬骨鱼类的OPN5氨基酸序列相似性为82.7%~92.0%,与哺乳动物OPN5氨基酸序列相似性较低。LmOPN5基因在花鲈脑组织分布广泛,尤其在下丘脑、视叶、垂体、端脑和血管囊中的相对表达量较高;同时在视网膜的相对表达量也较高。在视网膜中,LmOPN5基因相对表达量在不同光周期处理下发生显著变化(P<0.05,下同),其中长光照周期促进LmOPN5基因表达,短光照周期抑制LmOPN5基因表达;在血管囊中,长光周期条件下LmOPN5基因相对表达量显著高于常光周期;在下丘脑中,LmOPN5基因相对表达量在3种光周期处理下无显著变化(P>0.05);在垂体中,短光周期条件下LmOPN5基因相对表达量显著高于长光周期和常光周期。【结论】LmOPN5基因序列在硬骨鱼中较保守;不同光周期处理影响视网膜、血管囊和垂体中LmOPN5基因表达,表明花鲈不同组织对光周期的反应不一致,花鲈对光周期的感应具有组织特异性。 | 任红乐 邱丽华 闫路路 赵超 张博 丘高峰 王鹏飞 | 2023 | 南方农业学报2023，54，9： | 0 |
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