scholarly journals Genetic background-dependent abnormalities of the enteric nervous system and intestinal function in Kif26a-deficient mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yukiko Ohara ◽  
Lisa Fujimura ◽  
Akemi Sakamoto ◽  
Youichi Teratake ◽  
Shuichi Hiraoka ◽  
...  
Keyword(s):  
Genetic Background ◽  
Survival Rates ◽  
Gastrointestinal Diseases ◽  
Negative Regulator ◽  
Enteric Neurons ◽  
Enteric Neuron ◽  
Protein Coding ◽  
Underlying Mechanisms ◽  
Functional Gastrointestinal Diseases ◽  
Deficient Mice

AbstractThe Kif26a protein-coding gene has been identified as a negative regulator of the GDNF-Ret signaling pathway in enteric neurons. The aim of this study was to investigate the influence of genetic background on the phenotype of Kif26a-deficient (KO, −/−) mice. KO mice with both C57BL/6 and BALB/c genetic backgrounds were established. Survival rates and megacolon development were compared between these two strains of KO mice. Functional bowel assessments and enteric neuron histopathology were performed in the deficient mice. KO mice with the BALB/c genetic background survived more than 400 days without evidence of megacolon, while all C57BL/6 KO mice developed megacolon and died within 30 days. Local enteric neuron hyperplasia in the colon and functional bowel abnormalities were observed in BALB/c KO mice. These results indicated that megacolon and enteric neuron hyperplasia in KO mice are influenced by the genetic background. BALB/c KO mice may represent a viable model for functional gastrointestinal diseases such as chronic constipation, facilitating studies on the underlying mechanisms and providing a foundation for the development of treatments.

scholarly journals A Novel Long Non-Coding RNA-01488 Suppressed Metastasis and Tumorigenesis by Inducing miRNAs That Reduce Vimentin Expression and Ubiquitination of Cyclin E

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1504
Author(s):  
Syuan-Ling Lin ◽  
Yang-Hsiang Lin ◽  
Hsiang-Cheng Chi ◽  
Tzu-Kang Lin ◽  
Wei-Jan Chen ◽  
...  
Keyword(s):  
Human Cancer ◽  
Cyclin E ◽  
Survival Rates ◽  
Negative Regulator ◽  
Vimentin Expression ◽  
Protein Coding ◽  
Tumorigenic Activity ◽  
Underlying Mechanisms

Long intergenic non-coding RNAs (lincRNAs) play important roles in human cancer development, including cell differentiation, apoptosis, and tumor progression. However, their underlying mechanisms of action are largely unknown at present. In this study, we focused on a novel suppressor lincRNA that has the potential to inhibit progression of human hepatocellular carcinoma (HCC). Our experiments disclosed long intergenic non-protein coding RNA 1488 (LINC01488) as a key negative regulator of HCC. Clinically, patients with high LINC01488 expression displayed greater survival rates and better prognosis. In vitro and in vivo functional assays showed that LINC01488 overexpression leads to significant suppression of cell proliferation and metastasis in HCC. Furthermore, LINC01488 bound to cyclin E to induce its ubiquitination and reduced expression of vimentin mediated by both miR-124-3p/miR-138-5p. Our results collectively indicate that LINC01488 acts as a tumor suppressor that inhibits metastasis and tumorigenesis in HCC via the miR-124-3p/miR-138-5p/vimentin axis. Furthermore, LINC01488 interacts with and degrades cyclin E, which contributes to its anti-tumorigenic activity. In view of these findings, we propose that enhancement of LINC01488 expression could be effective as a potential therapeutic strategy for HCC.

scholarly journals Propolis Extract and Chitosan Improve Health of Nosema ceranae Infected Giant Honey Bees, Apis dorsata Fabricius, 1793

Pathogens ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 785
Author(s):  
Sanchai Naree ◽  
Rujira Ponkit ◽  
Evada Chotiaroonrat ◽  
Christopher L. Mayack ◽  
Guntima Suwannapong
Keyword(s):  
Honey Bees ◽  
Treatment Options ◽  
Survival Rates ◽  
Nosema Ceranae ◽  
Apis Dorsata ◽  
Propolis Extract ◽  
Bee Health ◽  
Honey Bee Health ◽  
Underlying Mechanisms ◽  
Honey Solution

Nosema ceranae is a large contributing factor to the most recent decline in honey bee health worldwide. Developing new alternative treatments against N. ceranae is particularly pressing because there are few treatment options available and therefore the risk of increased antibiotic resistance is quite high. Recently, natural products have demonstrated to be a promising avenue for finding new effective treatments against N. ceranae. We evaluated the effects of propolis extract of stingless bee, Tetrigona apicalis and chito-oligosaccharide (COS) on giant honey bees, Apis dorsata, experimentally infected with N. ceranae to determine if these treatments could improve the health of the infected individuals. Newly emerged Nosema-free bees were individually inoculated with 106N. ceranae spores per bee. We fed infected and control bees the following treatments consisting of 0%, 50%, propolis extracts, 0 ppm and 0.5 ppm COS in honey solution (w/v). Propolis extracts and COS caused a significant increase in trehalose levels in hemolymph, protein contents, survival rates and acini diameters of the hypopharyngeal glands in infected bees. Our results suggest that propolis and COS could improve the health of infected bees. Further research is needed to determine the underlying mechanisms responsible for the improved health of the infected bees.

scholarly journals Association Between Functional Gastrointestinal Diseases and Exposure to Abuse in Teenagers

2014 ◽  
Vol 60 (5) ◽  
pp. 386-392 ◽  
Author(s):  
N. M. Devanarayana ◽  
S. Rajindrajith ◽  
M. S. Perera ◽  
S. W. Nishanthanie ◽  
A. Karunanayake ◽  
...  
Keyword(s):  
Gastrointestinal Diseases ◽  
Functional Gastrointestinal Diseases

Homeostasis and regeneration of the hematopoietic stem cell pool are altered in SHIP-deficient mice

Blood ◽  
2003 ◽  
Vol 102 (10) ◽  
pp. 3541-3547 ◽  
Author(s):  
Cheryl D. Helgason ◽  
Jennifer Antonchuk ◽  
Caroline Bodner ◽  
R. Keith Humphries
Keyword(s):  
Negative Regulator ◽  
Wild Type Littermate ◽  
Hematopoietic Stem ◽  
Cell Pool ◽  
Multipotent Progenitors ◽  
Important Negative Regulator ◽  
Total Body ◽  
Deficient Mice

AbstractSH2-containing inositol 5-phosphatase (SHIP) is an important negative regulator of cytokine and immune receptor signaling. SHIP-deficient mice have a number of hematopoietic perturbations, including enhanced cytokine responsiveness. Because cytokines play an important role in the maintenance/expansion of the primitive hematopoietic cell pool, we investigated the possibility that SHIP also regulates the properties of cells in these compartments. Primitive hematopoietic cells were evaluated in SHIP-deficient mice and wild-type littermate controls using the colony-forming unit-spleen (CFU-S) and competitive repopulating unit (CRU) assays for multipotent progenitors and long-term lympho-myeloid repopulating cells, respectively. Absence of SHIP was found to affect homeostasis of CFU-S and CRU compartments. Numbers of primitive cells were increased in extramedullary sites such as the spleen of SHIP-deficient mice, although total body numbers were not significantly changed. In vivo cell cycle status of the CRU compartment was further evaluated using 5-fluorouracil (5-FU). SHIP-deficient CRUs were more sensitive to 5-FU killing, indicating a higher proliferative cell fraction. More strikingly, SHIP was found to regulate the ability of primitive cells to regenerate in vivo, as CRU recovery was approximately 30-fold lower in mice that received transplants of SHIP-deficient cells compared with controls. These results support a major role for SHIP in modulating pathways important in homeostasis and regeneration of hematopoietic stem cells, and emphasize the importance of negative cytokine regulation at the earliest stages of hematopoiesis. (Blood. 2003;102:3541-3547)

scholarly journals Genome Size Estimation and Full-Length Transcriptome of Sphingonotus tsinlingensis: Genetic Background of a Drought-Adapted Grasshopper

2021 ◽  
Vol 12 ◽  
Author(s):  
Lu Zhao ◽  
Hang Wang ◽  
Ping Li ◽  
Kuo Sun ◽  
De-Long Guan ◽  
...  
Keyword(s):  
Genome Size ◽  
Genetic Background ◽  
Tandem Repeats ◽  
Full Length ◽  
Arid Environments ◽  
Size Estimation ◽  
Sequencing Data ◽  
Protein Coding ◽  
Grasshopper Species ◽  
Hsp Genes

Sphingonotus Fieber, 1852 (Orthoptera: Acrididae), is a grasshopper genus comprising approximately 170 species, all of which prefer dry environments such as deserts, steppes, and stony benchlands. In this study, we aimed to examine the adaptation of grasshopper species to arid environments. The genome size of Sphingonotus tsinlingensis was estimated using flow cytometry, and the first high-quality full-length transcriptome of this species was produced. The genome size of S. tsinlingensis is approximately 12.8 Gb. Based on 146.98 Gb of PacBio sequencing data, 221.47 Mb full-length transcripts were assembled. Among these, 88,693 non-redundant isoforms were identified with an N50 value of 2,726 bp, which was markedly longer than previous grasshopper transcriptome assemblies. In total, 48,502 protein-coding sequences were identified, and 37,569 were annotated using public gene function databases. Moreover, 36,488 simple tandem repeats, 12,765 long non-coding RNAs, and 414 transcription factors were identified. According to gene functions, 61 cytochrome P450 (CYP450) and 66 heat shock protein (HSP) genes, which may be associated with drought adaptation of S. tsinlingensis, were identified. We compared the transcriptomes of S. tsinlingensis and two other grasshopper species which were less tolerant to drought, namely Mongolotettix japonicus and Gomphocerus licenti. We observed the expression of CYP450 and HSP genes in S. tsinlingensis were higher. We produced the first full-length transcriptome of a Sphingonotus species that has an ultra-large genome. The assembly characteristics were better than those of all known grasshopper transcriptomes. This full-length transcriptome may thus be used to understand the genetic background and evolution of grasshoppers.

scholarly journals Influence of Sex and Genetic Background on Anxiety-Related and Stress-Induced Behaviour of Prodynorphin-Deficient Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e34251 ◽  
Author(s):  
Iris Kastenberger ◽  
Christian Lutsch ◽  
Herbert Herzog ◽  
Christoph Schwarzer
Keyword(s):  
Genetic Background ◽  
Deficient Mice

scholarly journals Toll-Interacting Protein, Tollip, Inhibits IL-13-Mediated Pulmonary Eosinophilic Inflammation in Mice

2018 ◽  
Vol 10 (2) ◽  
pp. 106-118 ◽  
Author(s):  
Yoko Ito ◽  
Niccolette Schaefer ◽  
Amelia Sanchez ◽  
David Francisco ◽  
Rafeul Alam ◽  
...  
Keyword(s):  
Lung Inflammation ◽  
Negative Regulator ◽  
Airflow Limitation ◽  
Eosinophilic Inflammation ◽  
Interacting Protein ◽  
Proinflammatory Responses ◽  
Cytokine Milieu ◽  
Underlying Mechanisms

Toll-interacting protein (Tollip) is a key negative regulator of innate immunity by preventing excessive proinflammatory responses. Tollip genetic variation has been associated with airflow limitation in asthma subjects and Tollip expression. Whether Tollip regulates lung inflammation in a type 2 cytokine milieu (e.g., IL-13) is unclear. Our goal was to determine the in vivo role of Tollip in IL-13-mediated lung eosinophilic inflammation and the underlying mechanisms. Tollip-knockout (KO) and wild-type (WT) mice were inoculated intranasally with recombinant mouse IL-13 protein to examine lung inflammation. To determine how Tollip regulates inflammation, alveolar macrophages and bone marrow-derived macrophages from Tollip KO and WT mice were cultured with or without IL-13 and/or IL-33. IL-13-treated Tollip KO mice significantly increased lung eosinophilic inflammation and eotaxin-2 (CCL24) levels compared with the WT mice. IL-13- treated Tollip KO (vs. WT) macrophages, in the absence and particularly in the presence of IL-33, increased expression of the IL-33 receptor ST2L and CCL24, which was in part dependent on enhanced activation of interleukin (IL)-1 receptor-associated kinase 1 (IRAK1) and signal transducer and activator of transcription 6 (STAT6). Our results suggest that Tollip downregulates IL-13-mediated pulmonary eosinophilia in part through inhibiting the activity of the ST2L/IL-33/IRAK1 axis and STAT6.

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