微小RNA在血管新生和缺血性疾病中的调控作用

血管新生是一种极为重要的生物学过程,微小RNA在血管新生中发挥着重要的调控作用,相关研究已引起广泛关注.文章概述了近年来微小RNA在新生血管形成调控方面的最新研究进展,同时对一些可能参与调控缺血性疾病中血管新生的特异性微小RNA进行了概括.     

特发性肺纤维化相关微小RNA研究进展

微小RNA(microRNA)是一类高度保守的、内源性非编码小RNA,长度约20～25个核苷酸,广泛存在于植物、线虫以及人类的细胞中.其种类众多,表达具有一定组织特异性,参与基因转录后水平调控.近年来,随着对微小RNA研究的逐步深入,发现部分微小RNA参与心肌、肝脏、肾脏和肺等器官组织纤维化的发生发展及调控过程.现对微小RNA的产生、作用机制及其在特发性肺纤维化(idiopathic pulmonary fibrosis,IPF)发生发展中的作用和潜在治疗价值综述如下.     

微小RNA对心肌肥厚和心力衰竭的影响

心力衰竭的病理过程复杂,涉及心肌重构、电生理改变、细胞骨架重构以及神经体液的变化等,心肌肥厚是心力衰竭重要的病理过程之一.微小RNA是近年来新发现的一类非编码RNA,可以在转录后水平调控蛋白的表达,参与心力衰竭多个病理过程的调节,对心肌肥大的发生和发展有重要的影响.     

microRNA在肝纤维化中的研究进展

已有研究表明微小RNA(microRNA,miRNA)在肝纤维化发生过程中存在异常表达,并对肝纤维化的发生发展、诊断及治疗等均有调控作用.本文就miRNA在肝纤维化中的研究进展作一综述.     

微小RNA、缺氧诱导因子-1与血管发生

微小RNA与缺氧诱导因子-1都有着广泛而重要的生物学功能,两者都在血管发生中起着重要的调控作用,它们之间的相互作用对于深刻理解血管发生的调控机制有着重要的意义.文章着重概述了近年来对微小RNA与缺氧诱导因子-1相互调控及其对血管发生的影响.     

微小RNA与室性心律失常的研究进展

室性心律失常常发生于心肌损伤、急慢性心肌缺血或非缺血性心肌疾病导致的器质性心脏病和心脏离子通道病等,也可在正常心脏发生.微小RNA是具有约22个核苷酸的小内源性非编码RNA.近年来,微小RNA在心血管疾病中的调控作用成为研究热点.本文主要综述微小RNA与室性心律失常的研究进展,尤其是微小RNA可能是室性心律失常诊断的潜...     

微小核糖核酸和心血管疾病

微小核糖核酸（micro ribonucleic acid,microRNAs,miRNAs或miRs）是一类进化上高度保守的单链非编码RNA小分子,含18～25个核苷酸,主要通过抑制信使RNA（mRNA）翻译或促进其降解调控基因表达。近年研究发现,miRNAs在心血管系统病理状态下有显著的表达量变化。在离体和在体条件下,获得性和缺失性研究都表明,miRNAs在心血管系统发育、疾病发生过程中的调控作用。近年这个领域的研究飞速发展,本文对miRNAs在心血管系统的发育和疾病过程中的作用做一综述。     

微小 RNA-27与心血管疾病

微小 RNA（miRNA）对心血管疾病的发生发展起重要的调控作用。miR-27可以通过调节多种靶基因的表达直接或间接作用于心血管疾病的发生发展过程，该文就miR-27在心血管疾病中的调控作用机制作一综述。     

MicroRNA在急性胰腺炎中的研究进展

急性胰腺炎(acute pancreatitis,AP)是临床常见的胰腺外分泌腺急性炎症性疾病,可引起严重的局部和全身并发症,死亡率高.微小RNA(micro RNA,mi RNA)是一类非编码的转录后调控因子,随着mi RNA研究的深入,多项研究显示mi RNA参与机体生长发育过程以及多种疾病发生过程.mi RNA在AP发病过程中的作用尚不明确.本文总结近年来的研究结果,对AP与相关mi RNA的研究进展作一综述.     

环状RNA在心血管疾病中的研究进展

环状RNA(circular RNAs,circRNAs)是一类新型非编码RNA,由前体RNA反向地首尾剪接形成。circRNAs大量存在于真核细胞转录组中,并且其表达具有组织差异性。一些circRNAs可以充当微小RNA(miRNAs)海绵或者在基因转录调控中起到重要作用。已经有研究证明,circRNAs广泛存在于心血管系统中,并作为调控因子参与心血管疾病的发生和发展。本文就circRNAs的来源、形成机制以及功能做简述,并对circRNAs在心血管疾病中的研究进展做一介绍。     

microRNA与胰腺发育以及干细胞分化的研究进展

microRNA(miRNA)是一类参与基因转录后调控的非编码小分子RNA,其在胚胎发育、细胞命运决定、生长调控等方面发挥重要作用.业已证实,一些特定的miRNA通过靶向调控某些胰腺发育相关的重要转录因子而参与胰腺胚胎发育过程.通过模拟体内胰岛发育过程,可将干细胞在体外诱导定向分化为胰岛素分泌细胞.此外,miRNA在干细胞的维持和分化中也可能具有调控作用.因此,miRNA在胰腺发育和干细胞分化中的作用及其机制值得深入研究,这将为胰岛功能重建治疗糖尿病策略提供新的思路.     

微小RNA与缺血性脑血管病

微小RNA(microRNA,miRNA)是一类高度保守的非编码小RNA,在转录后水平对基因表达进行负向调控,可导致翻译抑制或mRNA降解.miRNA在进化上高度保守,广泛参与生物体的生长、发育、凋亡等生理或病理学过程.最近的研究表明,特定miRNA在缺血性脑血管病的发生和发展过程中发挥着重要作用,同时还参与了脑缺血后的损伤机制以及保护和修复机制的调控.充分认识各种miRNA的功能意义及其表达水平改变所起的调节作用,不仅有助于明确治疗靶点,阻止神经元死亡,减轻缺血性脑损伤,而且还能通过其表达水平的调控清除凋亡细胞,促进血管发生和神经发生.此外,miRNA也可能为缺血性卒中的预防和诊断提供新的策略.     

缺血性脑损伤诱导的神经发生及其调节机制

传统观点认为,中枢神经系统神经元缺乏再生能力.最近的研究发现,脑缺血可激活成年哺乳动物脑内的神经发生,为脑缺血损伤后的神经修复带来了新的希望.充分了解成年神经发生的部位、过程,缺血后神经发生及其调控机制很有必要.     

Delineating developmental and metabolic pathways in vivo by expression profiling using the RIKEN set of 18,816 full-length enriched mouse cDNA arrays

We have systematically characterized gene expression patterns in 49 adult and embryonic mouse tissues by using cDNA microarrays with 18,816 mouse cDNAs. Cluster analysis defined sets of genes that were expressed ubiquitously or in similar groups of tissues such as digestive organs and muscle. Clustering of expression profiles was observed in embryonic brain, postnatal cerebellum, and adult olfactory bulb, reflecting similarities in neurogenesis and remodeling. Finally, clustering genes coding for known enzymes into 78 metabolic pathways revealed a surprising coordination of expression within each pathway among different tissues. On the other hand, a more detailed examination of glycolysis revealed tissue-specific differences in profiles of key regulatory enzymes. Thus, by surveying global gene expression by using microarrays with a large number of elements, we provide insights into the commonality and diversity of pathways responsible for the development and maintenance of the mammalian body plan.     

Proton MR spectroscopy of neural stem cells: does the proton-NMR peak at 1.28 ppm function as a biomarker for cell type or state?

Recently, a peak at 1.28 ppm in proton magnetic resonance spectroscopy ((1)H-MRS) of neural stem cells (NSCs) was introduced as a noninterventional biomarker for neurogenesis in vivo. This would be an urgently needed requisite for translational studies in humans regarding the beneficial role of adult neurogenesis for the structural and functional integrity of the brain. However, many concerns have risen about the validity of the proposed signal as a specific marker for NSCs. The peak has also been related to cell-type-independent phenomena such as apoptosis or necrosis. Thus, we compared the 1.28-ppm peak in various immature stem cell populations, including embryonic stem cells, mouse embryonic fibroblasts, embryonic stem cell- and induced pluripotent stem cell-derived NSCs, ex vivo isolated embryonic NSCs, as well as mature and tumor cell types from different germ layers. To correlate the integral peak intensity with cell death, we induced both apoptosis with camptothecin and necrosis with sodium azide. A peak at 1.28 ppm was found in most cell types, and in most, but not all, NSCH cultures, demonstrating no specificity for NSCs. The intensities of the 1.28-ppm resonance significantly correlated with the rate of apoptosis, but not with the rate of necrosis, cell cycle phase distribution, cell size, or type. Multiple regression analysis displayed a significant predictive value of the peak intensity for apoptosis only. In this context, its specificity for apoptosis as a major selection process during neurogenesis may suggest this resonance as an indirect marker for neurogenesis in vivo.     

Neurogenesis, cellular plasticity and cognition: the impact of stem cells in the adult and aging brain--a mini-review

The hippocampus is a structure equipped with a high degree of flexibility and adaptation. In contrast to most structures of the adult central nervous system, the hippocampus can rely on a form of plasticity known as neurogenesis. The continuous provision of new neurons derived from resident adult neural stem cells appears to facilitate the execution of hippocampal-dependent tasks since reduction or blockage of neurogenesis is associated with cognitive impairments. Importantly, however, although hippocampal neurogenesis is maintained all throughout life, its levels decrease steadily along with aging. Notwithstanding some evidence that in age-matched animals neurogenesis levels and learning performance are tightly associated, these two parameters do not appear to be directly coupled when comparing individuals of various age groups. Additional components, and in particular experience, appear to play a fundamental roles in hippocampal functions. In this review, we speculate on the impact of neurogenesis level modulation on cognitive performances, putting in perspective recent studies made in the aging human population and in rodent models of aging.     

A speculative essay on retinoic acid regulation of neural stem cells in the developing and aging olfactory system

Circulating signals like the acidic derivative of vitamin A: retinoic acid (RA) may regulate resident stem cells in the adult nervous system, particularly in the olfactory pathway. RA is an essential factor for inducing neural stem or precursor cells that give rise to olfactory receptor neurons (ORNs) and olfactory bulb (OB) interneurons (OBINs) during embryonic development. Similar precursors in the adult brain constantly generate new ORNs and OBINs, and embryonic signaling pathways, like that via RA, may be retained or reactivated for this purpose. We have shown that RA regulates neural precursors in the embryonic and adult olfactory pathway. Moreover, RA administration after olfactory system damage stimulates an immune response and yields a more rapid recovery of olfactory-guided behavior. We suggest that olfactory integrity may be maintained by RA-mediated regulation of neurogenesis as well as local immune responses, and that aging compromises these mechanisms. The chemical senses, particularly olfaction, decline in aged individuals, and RA (via vitamin A) levels may also decline, perhaps due to changes in appetite and food intake. This synergy may result in a high prevalence of olfactory pathology in aged individuals.     

Activation of cAMP-response-element-binding protein (CREB) after focal cerebral ischemia stimulates neurogenesis in the adult dentate gyrus

New neurons are generated in adult mammalians and may contribute to repairing the brain after injury. Here, we show that the number of new neurons in the dentate gyrus of adult rats increased in cerebral ischemic stroke and correlated with activation of the cAMP-response-element-binding protein (CREB). Inhibition of endogenous CREB by expression of a dominant-negative mutant of CREB (CREB-S133A or CREB-R287L) blocked ischemia-induced neurogenesis in the dentate gyrus of adult rats, whereas expression of constitutively active CREB, VP16-CREB, increased the number of new neurons. Thus, our findings provide roles and regulatory mechanisms for CREB in adult neurogenesis and possibly suggest a practical strategy for replacing dead neurons in brain injury.