简介:摘要目的分析儿童急性偏瘫患者与正常对照之间血清成纤维细胞生长因子水平的差异。方法应用酶联免疫吸附双抗体夹心法(ELISA)检测52例儿童急性偏瘫患者(感染23例,颅脑损伤18例,脑血管11例)及50例健康对照者的血清b-FGF水平。结果疾病组和对照组血清b-FGF水平差异有统计学意义(P<0.05)。不同病因的急性偏瘫患者组间血清b-FGF水平差异无统计学意义(P>0.05)。结论儿童急性偏瘫患者血清b-FGF明显升高,恢复期更为显著,提示b-FGF等细胞因子可能在血管炎症反应/局部脑血管闭塞及血管闭塞后新生血管形成等儿童急性偏瘫的病理机制中具有重要作用。
简介:(FRS2)成纤维细胞生长因素(FGF)受体底层2是在FGF小径发信号的主要调停人。最近的研究在FRS2显示出那激活mitogen的蛋白质kinase(MAPK)phosphorylates丝氨酸和threonine残余,否定地影响FRS2的导致FGF的酷氨酸phosphorylation(PY)。几种刺激能导致FRS2的serine/threoninephosphorylation(PS/T),显示FRS2可能为学习在表明小径的生长因素之间的串音是有用的。这里,我们报导FRS2的导致FGF的PY能被EGF合作刺激在PC12房间稀释;这禁止的效果能被U0126完全颠倒,MEK的一个禁止者。我们进一步在FRS2识别了ERK1/2-binding主题并且在FGF或EGF刺激之上产生了FRS2-3KL,变异的缺乏MAPK绑定和磅。不同野类型(WT)FRS2,FRS2-3KL的导致FGF的PY不能被EGF合作刺激,和更展出的FRS2-3KL-expressingPC12房间禁止响应FGF处理比FRS2-WT-expressing房间区分潜力。这些结果建议FRS2的PS/T由FRS2-MAPK否定规章的循环调停了可以作为从另外的小径把否定规章的信号集成到产生FGFR的信号transduction的一个分子的开关工作。
简介:AbstractFibroblast growth factor 21 (FGF21) is a fasting or stress inducible metabolic hormone produced mainly in the liver. It plays important roles in regulating both glucose and lipid homeostasis via interacting with a heterodimeric receptor complex comprising FGF receptor 1 (FGFR1) and β-klotho (KLB). For the past decade, great effort has been made on developing FGF21 derivatives or specific FGF21 receptor agonists into therapeutic agents for various metabolic disorders including type 2 diabetes (T2D), obesity, and more importantly, nonalcoholic fatty liver disease (NAFLD). Here we have reviewed FGF21 gene and protein structures, its expression pattern, cellular signaling cascades that mediate FGF21 production and function. We have then summarized the six clinical trials utilizing four FGF21 analogues. Finally, two recent literatures on the development of GLP-1 and FGF21 dual agonists were presented briefly.
简介:AbstractObjective:To explore the levels of fibroblast growth factor 23 (FGF23) during pregnancy and its relationship with intrauterine growth restriction (IUGR).Methods:Pregnant rats were classified into an ad libitum rat chow group (ad libitum rat chow, AD group, n = 25) and an undernutrition group (50% of their daily food requirement, UN group, n= 25). The levels of maternal serum FGF23, tissue homogenate FGF23, and bone gla protein in fetal rats, and placental FGF23 mRNA and protein expression were examined by enzyme-linked immunosorbent assay, real-time qPCR analysis respectively. Finally, the effect of recombinant FGF23 on the viability of MG-63 cells was determined by cell proliferation assay. Data were analyzed with independent two-tailed t test and one-way analysis of variance. Spearman rank-order correlation coefficients (continuous variables) was performed to determine the relationship of results.Results:The diet restriction induced IUGR in rat offsprings, and the UN group exhibited a significantly lower FGF23 level (P < 0.05, n= 5). The FGF23 level was increased and peaked in maternal serum on gestation day (GD) 15, but peaked in fetal and placenta on GD20. Moreover, the tissue homogenate levels of FGF23 and bone gla protein in fetal rats in both groups were positively correlated (r= 0.923, P < 0.05; r= 0.925, P < 0.05, respectively, n = 15), FGF23 was localized to both decidual and labyrinth zones, with remarkably higher expression on GD20, P < 0.05, n= 5. In vitro, recombinant human FGF23 enhanced MG-63 cell viability, P < 0.05, n= 5.Conclusion:Prenatal undernutrition could decrease the FGF23 expression in fetal rats caused by the mother through the placenta, and induced the IUGR and hindered the ossification. And the FGF23 levels are peaked on GD15 mother but peaked on GD20 placenta and fetuses, these might be associated with the over compensation of maternal placenta on GD20.
简介:AbstractIn the past decades, skeletal muscle has become the focus of numerous studies due to its potential physiological role as an endocrine organ secreting hundreds of myokines. Among these myokines, fibroblast growth factor 21 (FGF21) and irisin are novel hormone polypeptides sending signals to regulate the function of specific organs, like skeletal muscle, liver, pancreas, and adipose tissue. Both hormones have been reported to normalize glucose, improve insulin resistance, and promote lipid homeostasis, thereby preventing the development of metabolic disorders, such as obesity and diabetes. Besides preserving pancreatic β-cell functions, FGF21 also protects pancreatic acini from inflammation and reduces proteotoxic stress via facilitating digestive enzyme secretion. Meanwhile, irisin is found to inhibit the pancreatic cancer cell growth as well. This review attempts to focus on the current knowledge of FGF21 and irisin and their effective roles in pancreas including pancreatic β- and acinar cells under various physiological conditions, its anti-diabetic actions, and the clinical implications.
简介:碱性成纤维细胞生长因子2(fibroblastgrowthfactor2,FGF2)是一类功能多样的多肽,可由视网膜的多种细胞分泌产生。随着对视网膜血管性疾病的研究深入,FGF2在其中的作用也得到广泛重视。FGF2可与血管内皮生长因子(vascularendothelialgrowthfactor,VEGF)、肿瘤坏死因子-α(tumornecrosisfactor-α,TNF-α)等细胞因子相互作用,通过发挥促血管生成作用、促炎作用以及一定的神经保护作用而参与视网膜血管性疾病的发生与发展。此外,FGF2的表达上调很可能是部分患者使用抗VEGF治疗效果不显著的重要因素。本文就FGF2的分子特征、分子作用机制及FGF2与视网膜血管性疾病的相关性进行总结,旨在为FGF2作为视网膜血管性疾病的治疗靶点提供理论依据。
简介:摘要2例FGF12基因变异所致早发型婴儿癫痫性脑病患儿就诊年龄分别为4月龄(男)和2月龄(女),分别于2018年9月和2019年4月收入广州市妇女儿童医疗中心,均为新生儿期出现反复抽搐,主要表现为癫痫发作形式多样,恶化期为痉挛后强直,伴或不伴痉挛发作,另伴有喂养困难和运动发育迟缓以及难治性肺炎。2例患儿均有FGF12基因杂合变异,变异位点分别为p.R52H和p.R114H。1例患儿因重症肺炎死亡,1例患儿加用钠离子通道阻滞剂后癫痫控制,运动发育进步,脑电图好转。
简介:摘要对2020年2月在山东大学齐鲁儿童医院住院治疗的1例早发性癫痫性脑病患儿进行回顾性分析。患儿,女,4月龄时因"反复抽搐发作4个月、喂养困难1个月"入院。患儿出生1 d起病,发作类型为强直发作,发育严重落后,脑电图示多灶放电,后转为高度失律,头颅影像学阴性,3月龄时出现喂养困难。基因检测结果示FGF12基因新发杂合错义突变(Arg114His)。多种抗癫痫药物、生酮饮食治疗均无效,加用苯妥英钠后2个月未发作。患儿发作控制后可自行进食,但智力运动发育无进步。FGF12基因突变致早发性癫痫性脑病预后不佳,发作较难控制,应尽早应用苯妥英钠等钠离子通道阻滞剂。