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1.
PLoS One ; 15(10): e0240996, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33091062

RESUMO

Biological invasions impact both agricultural and natural systems. The damage can be quantified in terms of both economic loss and reduction of biodiversity. Although the literature is quite rich about the impact of invasive species on plant and animal communities, their impact on environmental microbiomes is underexplored. Here, we re-analyze publicly available data using a common framework to create a global synthesis of the effects of biological invasions on environmental microbial communities. Our findings suggest that non-native species are responsible for the loss of microbial diversity and shifts in the structure of microbial populations. Therefore, the impact of biological invasions on native ecosystems might be more pervasive than previously thought, influencing both macro- and micro-biomes. We also identified gaps in the literature which encourage research on a wider variety of environments and invaders, and the influence of invaders across seasons and geographical ranges.


Assuntos
Microbiota/fisiologia , Animais , Biodiversidade , Ecossistema , Geografia , Espécies Introduzidas
2.
JCI Insight ; 2(21)2017 11 02.
Artigo em Inglês | MEDLINE | ID: mdl-29093270

RESUMO

An ascending aortic aneurysm (AscAA) is a life-threatening disease whose molecular basis is poorly understood. Mutations in NOTCH1 have been linked to bicuspid aortic valve (BAV), which is associated with AscAA. Here, we describe a potentially novel role for Notch1 in AscAA. We found that Notch1 haploinsufficiency exacerbated the aneurysmal aortic root dilation seen in the Marfan syndrome mouse model and that heterozygous deletion of Notch1 in the second heart field (SHF) lineage recapitulated this exacerbated phenotype. Additionally, Notch1+/- mice in a predominantly 129S6 background develop aortic root dilation, indicating that loss of Notch1 is sufficient to cause AscAA. RNA sequencing analysis of the Notch1.129S6+/- aortic root demonstrated gene expression changes consistent with AscAA. These findings are the first to our knowledge to demonstrate an SHF lineage-specific role for Notch1 in AscAA and suggest that genes linked to the development of BAV may also contribute to the associated aortopathy.


Assuntos
Aneurisma Aórtico/genética , Valva Aórtica/anormalidades , Predisposição Genética para Doença , Haploinsuficiência , Receptor Notch1/genética , Animais , Aorta , Aneurisma Aórtico/patologia , Valva Aórtica/diagnóstico por imagem , Valva Aórtica/patologia , Doença da Válvula Aórtica Bicúspide , Modelos Animais de Doenças , Expressão Gênica , Estudos de Associação Genética , Doenças das Valvas Cardíacas , Camundongos , Camundongos Knockout , Mutação , Fenótipo
3.
Sci Rep ; 7(1): 9263, 2017 08 23.
Artigo em Inglês | MEDLINE | ID: mdl-28835705

RESUMO

The domestic cat is an important human companion animal that can also serve as a relevant model for ~250 genetic diseases, many metabolic and degenerative conditions, and forms of cancer that are analogous to human disorders. MicroRNAs (miRNAs) play a crucial role in many biological processes and their dysregulation has a significant impact on important cellular pathways and is linked to a variety of diseases. While many species already have a well-defined and characterized miRNAome, miRNAs have not been carefully studied in cats. As a result, there are no feline miRNAs present in the reference miRNA databases, diminishing the usefulness of medical research on spontaneous disease in cats for applicability to both feline and human disease. This study was undertaken to define and characterize the cat miRNAome in normal feline tissues. High-throughput sequencing was performed on 12 different normal cat tissues. 271 candidate feline miRNA precursors, encoding a total of 475 mature sequences, were identified, including several novel cat-specific miRNAs. Several analyses were performed to characterize the discovered miRNAs, including tissue distribution of the precursors and mature sequences, genomic distribution of miRNA genes and identification of clusters, and isomiR characterization. Many of the miRNAs were regulated in a tissue/organ-specific manner.


Assuntos
Perfilação da Expressão Gênica , MicroRNAs/genética , Transcriptoma , Animais , Gatos , Biologia Computacional/métodos , Evolução Molecular , Biblioteca Gênica , Estudos de Associação Genética , Genômica/métodos , Sequenciamento de Nucleotídeos em Larga Escala , Especificidade de Órgãos/genética , Reprodutibilidade dos Testes
4.
Pediatr Res ; 80(4): 602-9, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27384406

RESUMO

BACKGROUND: Congenital obstructive nephropathy (CON) is a leading cause of pediatric chronic kidney disease (CKD). Despite optimal surgical and medical care, there is a high rate of CKD progression. Better understanding of molecular and cellular changes is needed to facilitate development of improved biomarkers and novel therapeutic approaches in CON. METHODS: The megabladder (mgb) mouse is an animal model of CKD with impaired bladder emptying, hydronephrosis, and progressive renal injury. In this study, we characterize a particular microRNA, miR-205, whose expression changes with the degree of hydronephrosis in the mgb(-/-) kidney. RESULTS: Expression of miR-205 is progressively increased in the adult mgb(-/-) mouse with worsening severity of hydronephrosis. miR-205 expression is correlated with altered expression of cytokeratins and uroplakins, which are markers of cellular differentiation in urothelium. We describe the spatial pattern of miR-205 expression, including increased expression in renal urothelium and novel miR-205 expression in medullary collecting duct epithelium in the congenitally obstructed kidney. CONCLUSION: miR-205 is increased with severity of CON and CKD in the mgb(-/-) mouse and may regulate urothelial differentiation.


Assuntos
Epitélio/metabolismo , Regulação da Expressão Gênica , Nefropatias/congênito , MicroRNAs/genética , Animais , Biomarcadores/sangue , Biomarcadores/metabolismo , Diferenciação Celular , Modelos Animais de Doenças , Progressão da Doença , Feminino , Hidronefrose/sangue , Queratinas/sangue , Rim/metabolismo , Rim/patologia , Nefropatias/genética , Nefropatias/fisiopatologia , Falência Renal Crônica/sangue , Túbulos Renais Coletores/metabolismo , Masculino , Camundongos , Camundongos Transgênicos , Junções Íntimas , Uroplaquinas/sangue , Urotélio/metabolismo , Urotélio/patologia
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