المؤلفون: Avraham Bayer, Takuya Mishima, Yoel Sadovsky, Carolyn B. Coyne, Jean-Francois Mouillet, Yingshi Ouyang, Tianjiao Chu, Elena Sadovsky, Guojing Chang

المصدر: Placenta. 35:A5

مصطلحات موضوعية: Genetically modified mouse, Genetics, Cell, Obstetrics and Gynecology, RNA, Transplacental, Biology, Microvesicles, medicine.anatomical_structure, Reproductive Medicine, Placenta, embryonic structures, microRNA, medicine, Function (biology), Developmental Biology

الوصف: Positioned at the maternal-fetal interface, the placenta generates regulatory signals and serves as a communication junction that governs pregnancy health. In addition to hormones, growth factors and diverse proteins, we and others have recently shown that small non-coding RNA molecules, including microRNAs (miRNAs), traffic among the maternalplacental-fetal compartments, and may have a central role in maternalfetal adaptation to homeostatic perturbations. Although common and unique types of miRNAs are expressed by the placenta during pregnancy, the function of placental miRNA species remains largely unknown. We recently showed that primary human trophoblasts are resistant to infection by a heterogeneous panel of viruses, and that this resistance can be partly conferred to non-trophoblast cells by exogenous expression of trophoblast-specific miRNAs, expressed from the chromosome 19 miRNA cluster (C19MC). This effect was not observed during cell infection by nonviral placental pathogens, including Listeria monocytogenes, and Toxoplasma gondii. Trophoblastic miRNAs can be released to the extracellular space within several types of vesicles, including cell fragments, apoptotic bodies, microvesicles, and nanovesicles (exosomes), or can be packaged with non-vesicular protein complexes, such as argonaute-2. To examine the trafficking of trophoblastic miRNAs to maternal-fetal tissues we engineered a transgenic mouse that expresses a 160 kb segment of human genomic DNA harboring the human C19MC cluster. We coupled this technology with RNAseq analysis of miRNA expression in triads of placenta, maternal plasma and fetal plasma from pregnant women at term. Together, these analyses shed new light on transplacental bidirectional miRNA trafficking patterns (Supported by NIH HD06589, HD075665, HD071707, AI081759, and the Pennsylvania Department of Health Research Formula Funds)

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::d583cb574102c6f98834f99d318500f0Test
https://doi.org/10.1016/j.placenta.2014.06.016Test

المؤلفون: Cyclin E, Yingshi Ouyang, Yan Song, Bingwei Lu

المساهمون: The Pennsylvania State University CiteSeerX Archives

المصدر: ftp://ftp.ncbi.nlm.nih.gov/pub/pmc/19/61/PLoS_One_2011_Nov_28_6(11)_e28098.tar.gz

الوصف: Accumulating evidence suggests that tumor-initiating stem cells or cancer stem cells (CSCs) possibly originating from normal stem cells may be the root cause of certain malignancies. How stem cell homeostasis is impaired in tumor tissues is not well understood, although certain tumor suppressors have been implicated. In this study, we use the Drosophila neural stem cells (NSCs) called neuroblasts as a model to study this process. Loss-of-function of Numb, a key cell fate determinant with well-conserved mammalian counterparts, leads to the formation of ectopic neuroblasts and a tumor phenotype in the larval brain. Overexpression of the Drosophila tumor suppressor p53 (dp53) was able to suppress ectopic neuroblast formation caused by numb loss-of-function. This occurred in a non-apoptotic manner and was independent of Dacapo, the fly counterpart of the well-characterized mammalian p53 target p21 involved in cellular senescence. The observation that dp53 affected Edu incorporation into neuroblasts led us to test the hypothesis that dp53 acts through regulation of factors involved in cell cycle progression. Our results show that the inhibitory effect of dp53 on ectopic neuroblast formation was mediated largely through its regulation of Cyclin E (Cyc E). Overexpression of Cyc E was able to abrogate dp539s ability to rescue numb loss-of-function phenotypes. Increasing Cyc E levels by attenuating Archipelago (Ago), a recently identified transcriptional target of dp53 and a negative regulator of Cyc E, had similar effects. Conversely, reducing Cyc E activity by overexpressing Ago blocked ectopic neuroblast formation in numb mutant. Our results reveal an intimate connection

وصف الملف: application/zip

العلاقة: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.287.1322Test

المؤلفون: Yufeng Yang^1,2, Yingshi Ouyang^1,2, Lichuan Yang³, Beal, M. Flint³, McQuibban, Angus⁴, Vogel, Hannes¹, Bingwei Lu^1,2 bingwei@stanford.edu

المصدر: Proceedings of the National Academy of Sciences of the United States of America. 5/13/2008, Vol. 105 Issue 19, p7070-7075. 6p. 4 Diagrams.

مصطلحات موضوعية: *MATERIAL plasticity, *NEURONS, *MITOCHONDRIA, *NEURODEGENERATION, *PARKINSON'S disease

مستخلص: Mitochondria form dynamic tubular networks that undergo frequent morphological changes through fission and fusion, the imbalance of which can affect cell survival in general and impact synaptic transmission and plasticity in neurons in particular. Some core components of the mitochondrial fission/fusion machinery, including the dynamin-like GTPases Drp1, Mitofusin, Opa1, and the Drp1-interacting protein Fis1, have been identified. How the fission and fusion processes are regulated under normal conditions and the extent to which defects in mitochondrial fission/fusion are involved in various disease conditions are poorly understood. Mitochondrial malfunction tends to cause diseases with brain and skeletal muscle manifestations and has been implicated in neurodegenerative diseases such as Parkinson's disease (PD). Whether abnormal mitochondrial fission or fusion plays a role in PD pathogenesis has not been shown. Here, we show that Pink1, a mitochondria-targeted Ser/Thr kinase linked to familial PD, genetically interacts with the mitochondrial fission/fusion machinery and modulates mitochondrial dynamics. Genetic manipulations that promote mitochondrial fission suppress Drosophila Pink 1 mutant phenotypes in indirect flight muscle and dopamine neurons, whereas decreased fission has opposite effects. In Drosophila and mammalian cells, overexpression of Pink1 promotes mitochondrial fission, whereas inhibition of Pink1 leads to excessive fusion. Our genetic interaction results suggest that Fis1 may act in-between Pink1 and Drp1 in controlling mitochondrial fission. These results reveal a cell biological role for Pink1 and establish mitochondrial fission/fusion as a paradigm for PD research. Compounds that modulate mitochondrial fission/fusion could have therapeutic value in PD intervention. [ABSTRACT FROM AUTHOR]

المؤلفون: Yufeng Yang, Gehrke, Stephan, Imai, Yuzuru, Zhinong Huang, Yingshi Ouyang, Ji-Wu Wang, Lichuan Yang, Beal, M. Flint, Vogel, Hannes, Bingwei Lu

المصدر: Proceedings of the National Academy of Sciences of the United States of America; 7/11/2006, Vol. 103 Issue 28, p10793-10798, 6p, 2 Diagrams, 3 Graphs

مصطلحات موضوعية: MITOCHONDRIAL pathology, DOPAMINERGIC neurons, PARKINSON'S disease, DEGENERATION (Pathology), MUSCLE diseases, DROSOPHILA, MEDICAL genetics

مستخلص: Mutations in Pink1, a gene encoding a Ser/Thr kinase with a mitochondrial-targeting signal, are associated with Parkinson's disease (PD), the most common movement disorder characterized by selective loss of dopaminergic neurons. The mechanism by which loss of Pink1 leads to neurodegeneration is not understood. Here we show that inhibition of Drosophila Pink1 (dPink1) function results in energy depletion, shortened lifespan, and degeneration of select indirect flight muscles and dopaminergic neurons. The muscle pathology was preceded by mitochondrial enlargement and disintegration. These phenotypes could be rescued by the wild type but not the pathogenic C-terminal deleted form of human Pink1 (hPink1). The muscle and dopaminergic phenotypes associated with dPink1 inactivation show similarity to that seen in parkin mutant flies and could be suppressed by the overexpression of Parkin but not DJ-1. Consistent with the genetic rescue results, we find that, in dPink1 RNA interference (RNAi) animals, the level of Parkin protein is significantly reduced. Together, these results implicate Pink1 and Parkin in a common pathway that regulates mitochondrial physiology and cell survival in Drosophila. [ABSTRACT FROM AUTHOR]

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المؤلفون: Krawczynski, Kamil, Yingshi Ouyang, Mouillet, Jean-Francois, Tianjiao Chu, Coyne, Carolyn B., Yoel Sadovsky

المصدر: Journal of Cell Science. 2021 Special Issue, Vol. 134, p1-1. 1p.

مصطلحات موضوعية: *VESICULAR stomatitis, *CHROMOSOMES, *MICRORNA, *VIRAL replication, *GENE targeting, *DNA replication

مستخلص: The function of microRNAs (miRNAs) can be cell autonomous or communicated to other cell types and has been implicated in diverse biological processes. We previously demonstrated that miR-517a-3p (miR-517a), a highly expressed member of the chromosome 19 miRNA cluster (C19MC) that is transcribed almost exclusively in human trophoblasts, attenuates viral replication via induction of autophagy in non-trophoblastic recipient cells. However, the molecular mechanisms underlying these effects remain unknown. Here, we identified unc-13 homolog D (UNC13D) as a direct, autophagy-related gene target of miR-517a, leading to repression of UNC13D. In line with the antiviral activity of miR-517a, silencing UNC13D suppressed replication of vesicular stomatitis virus (VSV), whereas overexpression of UNC13D increased VSV levels, suggesting a role for UNC13D silencing in the antiviral activity of miR-517a. We also found that miR-517a activated NF-κB signaling in HEK-293XL cells expressing TLR8, but the effect was not specific to C19MC miRNA. Taken together, our results define mechanistic pathways that link C19MC miRNA with inhibition of viral replication. [ABSTRACT FROM AUTHOR]

المؤلفون: Yuyang Gu¹, Chuyi Chen¹, Zhangming Mao², Bachman, Hunter¹, Becker, Ryan³, Rufo, Joseph¹, Zeyu Wang¹, Peiran Zhang¹, Mai, John⁴, Shujie Yang¹, Jinxin Zhang¹, Shuaiguo Zhao¹, Yingshi Ouyang⁵, Wong, David T. W.⁶, Sadovsky, Yoel^5,7, Jun Huang, Tony¹ tony.huang@duke.edu

المصدر: Science Advances. Jan2021, Vol. 7 Issue 1, p1-10. 10p.

مصطلحات موضوعية: *CENTRIFUGATION, *MICROFLUIDICS, *DROPLETS, *CENTRIFUGES, *MATERIALS science, *ACOUSTIC surface wave devices, *CIRCULAR motion

مستخلص: The article presents research report on acoustofluidic centrifuge for nanoparticle enrichment and separation. Topics include liquid droplets have been studied for decades and have recently experienced renewed attention as a simplified model for numerous fascinating physical phenomena occurring on size scales from the cell nucleus to stellar black holes; and entanglement of acoustic wave actuation and the spin of a fluidic droplet to enable nanoparticle enrichment and separation.