scholarly journals Changes in miRNA Gene Expression during Wound Repair in Differentiated Normal Human Bronchial Epithelium

2018 ◽  
Vol 2018 ◽  
pp. 1-8
Author(s):  
Beata Narożna ◽  
Wojciech Langwiński ◽  
Claire Jackson ◽  
Peter M. Lackie ◽  
John W. Holloway ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Profile ◽  
Wound Repair ◽  
Mirna Gene ◽  
Bronchial Epithelium ◽  
Airway Epithelial ◽  
Epithelial Repair ◽  
Mirna Genes ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

Purpose. Airway epithelium acts as a protective barrier against the particles from the inhaled air. Damage to the epithelium may result in loss of the barrier function. Epithelial repair in response to injury requires complex mechanisms, such as microRNA, small noncoding molecules, to regulate the processes involved in wound repair. We aimed to establish if the microRNA gene expression profile is altered during the airway epithelial repair in differentiated cells. Methods. miRNA gene expression profile during the wound closure of differentiated normal human bronchial epithelium (NHBE) from one donor was analysed using quantitative real-time PCR. We have analysed the expression of 754 genes at five time points during a 48-hour period of epithelium repair using TaqMan Low Density Array. Results. We found out that 233 miRNA genes were expressed in normal human bronchial epithelium. Twenty miRNAs were differentially expressed during the wound repair process, but only one (miR-455-3p) showed significance after FDR adjustment (p=0.02). Using STEM, we have identified two clusters of several miRNA genes with similar expression profile. Pathway enrichment analysis showed several significant signaling pathways altered during repair, mainly involved in cell cycle regulation, proliferation, migration, adhesion, and transcription regulation. Conclusions. miRNA expression profile is altered during airway epithelial repair of differentiated cells from one donor in response to mechanical injury in vitro, suggesting their potential role in wound repair.

Effect of San-ao Decoction, a traditional Chinese prescription, on IL-4 treated normal human bronchial epithelium

2010 ◽  
Vol 131 (1) ◽  
pp. 104-109 ◽  
Author(s):  
Yu Li ◽  
Ming-Yan Wang ◽  
Xin-sheng Fan ◽  
Xu Qi ◽  
Yan Chen ◽  
...  
Keyword(s):  
Bronchial Epithelium ◽  
Normal Human Bronchial Epithelium ◽  
Normal Human

scholarly journals Identification of myeloid cells in the human enthesis as the main source of local IL-23 production

2019 ◽  
Vol 78 (7) ◽  
pp. 929-933 ◽  
Author(s):  
Charlie Bridgewood ◽  
Abdulla Watad ◽  
Tobias Russell ◽  
Timothy M Palmer ◽  
Helena Marzo-Ortega ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Cell Population ◽  
Expression Profile ◽  
Myeloid Cells ◽  
Myeloid Cell ◽  
Ccr2 Gene ◽  
Similar Gene Expression Profile ◽  
Normal Human ◽  
Similar Gene

ObjectiveWe investigated whether the normal human spinal enthesis contained resident myeloid cell populations, capable of producing pivotal proinflammatory cytokines including tumour necrosis factor (TNF) and interleukin (IL)-23 and determined whether these could be modified by PDE4 inhibition.MethodsNormal human enthesis soft tissue (ST) and adjacent perientheseal bone (PEB) (n=15) were evaluated using immunohistochemistry (IHC), digested for myeloid cell phenotyping, sorted and stimulated with different adjuvants (lipopolysaccharide and mannan). Stimulated enthesis fractions were analysed for inducible production of spondyloarthropathy disease-relevant mediators (IL-23 full protein, TNF, IL-1β and CCL20). Myeloid populations were also compared with matched blood populations for further mRNA analysis and the effect of PDE4 inhibition was assessed.ResultsA myeloid cell population (CD45+ HLADR+ CD14+ CD11c+) phenotype was isolated from both the ST and adjacent PEB and termed ‘CD14+ myeloid cells’ with tissue localisation confirmed by CD14+ IHC. The CD14− fraction contained a CD123+ HLADR+ CD11c− cell population (plasmacytoid dendritic cells). The CD14+ population was the dominant entheseal producer of IL-23, IL-1β, TNF and CCL20. IL-23 and TNF from the CD14+ population could be downregulated by a PDE4I and other agents (histamine and 8-Bromo-cAMP) which elevate cAMP. Entheseal CD14+ cells had a broadly similar gene expression profile to the corresponding CD14+ population from matched blood but showed significantly lower CCR2 gene expression.ConclusionsThe human enthesis contains a CD14+ myeloid population that produces most of the inducible IL-23, IL-1β, TNF and CCL20. This population has similar gene expression profile to the matched blood CD14+ population.

MicroRNA Expression Analysis in Multiple Myeloma.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1554-1554 ◽  
Author(s):  
Azzah Al Masri ◽  
Tammy Price-Troska ◽  
Marta Chesi ◽  
Tae-Hoon Chung ◽  
Seungchan Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Multiple Myeloma ◽  
Human Plasma ◽  
Expression Analysis ◽  
Mirna Expression ◽  
Plasma Cells ◽  
Normal Human Plasma ◽  
Mirna Genes ◽  
Normal Plasma ◽  
Normal Human

Abstract Introduction: The analysis of what goes awry in a malignant cell has focused primarily on mutations of protein-encoding genes and their regulatory sequences. However, recent work on microRNA (miRNA) has shed light on the possible involvement of miRNA genes in human disease. miRNA are small “noncoding” or “non-messenger” RNAs of about 21–25 nucleotides in length that function as regulators of gene expression essentially by pairing to the mRNA of protein-coding genes to initiate mRNA degradation or repression of translation. We are interested in characterizing miRNA expression profiles in human myeloma cell lines (HMCLs) and myeloma patient samples. Multiple myeloma (MM) is a plasma cell tumor characterized by frequent chromosomal translocations. Materials and methods: The expression of miRNA in HMCLs, primary MM cells (hyperdiploid samples) and normal plasma cells was determined using human microRNA chips. The GenoExporerTM Human microRNA chips were developed by GenoSensor (Tempe, AZ) and the microarray contains 226 human microRNA sequences in addition to control sequences. The DNA oligo probes are synthesized and immobilized on the chips (1”x 3” standard glass microslide). The probes are designed based on the active mature miRNA sequences and some of their flanking sequences. Our analysis included seven myeloma patients (hyperdiploid MM), eight different HMCLs (MM1, 8226 with t(14;16); SKMM2, U266, INA-6 with t(11;14) and H929, KMS11, UTMC-2 with t(4;14)), and eight normal human plasma cells. The normal human plasma cells were collected at Mayo Clinic Rochester from bone samples of patients undergoing orthopedic surgery. For the assay 5–10 μg of total RNA per sample were used at a concentration of 1 μg/μL. The RNA is directly labeled with biotin and used as a target for the on-chip hybridization assays. A streptavidin-Alexa dye is used to stain the hybridized targets and the fluorescent signals are captured and analyzed. The gene signal intensities were normalized to tRNA signal intensity. Results: The primary MM cells and HMCLs displayed a distinctive miRNA expression profile compared with normal plasma cells. Using the GeneSpring 7 (Agilent Technologies, Palo Alto, CA) for gene expression analysis we have identified miRNA genes with significant variation in expression levels between tumor and normal samples including miR-125b, miR-133a, miR1, and miR-124a (p<0.01). Recently defined algorithms were used to identify putative targets for the miRNA genes of interest such as leukemia inhibitory factor (LIF) as targets of miR-125b and Stat3 and angiopoietin-1 precursor as targets of miR-124a (Lewis et al. 2003). Of note, miR-15 and miR-16, previously identified to be downregulated in CLL, were expressed at low levels in some MM patients and HMCLs, but not in the normal plasma cells. Further analysis will be carried out to validate the data from miRNA profiling using northern blot analysis or real-time RT-PCR to measure expression levels of miRNA genes and that of their target genes. Conclusion: Analysis of miRNA expression pattern (along with aCGH and gene expression profiling studies) will undoubtedly refine our understanding of the various genotypic subtypes of multiple myeloma.

Integrative Genomic Approach Identifies Deregulated MicroRNAs in Human Myeloma Cell Lines.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1684-1684
Author(s):  
Marta Lionetti ◽  
Luca Agnelli ◽  
Laura Mosca ◽  
Katia Todoerti ◽  
Domenica Ronchetti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Mirna Expression ◽  
Mirna Gene ◽  
Myeloma Cell ◽  
Host Gene ◽  
Expression Levels ◽  
Mirna Genes ◽  
Genome Wide ◽  
Human Myeloma Cell

Abstract The recent discovery of microRNAs (miRNAs), small noncoding RNAs involved in the regulation of cell cycle, survival, and differentiation programmes, has added a further level of complexity to normal and cancer cell biology. Loss or amplification of miRNA genes by broad cytogenetic abnormalities or minute molecular aberrations has been observed in a variety of human malignancies, with the consequent altered expression of these regulatory genes. Additionally, approximately one third of miRNAs are located within the intronic regions of coding transcription units, and recent evidence indicates that the expression of these miRNAs largely coincides with the transcription of the corresponding host genes. To date, no evidence of deregulated miRNA expression has been reported in multiple myeloma (MM). To provide insights into miRNA biology in MM, we performed an integrative analysis of genome-wide, gene expression and miRNA expression profilings in a panel of 16 human myeloma cell lines (HMCLs). Global miRNA and mRNA expression data were generated on Agilent miRNA microarrays (representing 470 human mature miRNAs) and GeneChip® HG-U133A arrays, respectively, and both quantile-normalized. Genome-wide profiling data were generated on GeneChip® Human Mapping 250K NspI arrays and copy number (CN) values were inferred using the circulary binary segmentation (DNAcopy R Bioconductor package). To measure the correlation between the expression levels of each miRNA and the corresponding CN value or host gene expression, conventional non-parametric analyses were performed (Kendall’s tau and Wilcoxon rank-sum tests). As regards miRNA gene CN, the most frequent alteration identified was represented by gain/amplification (for all miRNA genes investigated, an increased CN was present in at least 3 HMCLs, with an average frequency of 58%), followed by loss (5%) and biallelic deletion (0.3%). Our analysis revealed that 14 different miRNA transcripts (miR-15a, miR-19a, miR-21, miR-22, miR-30d, miR-99b, miR-130b, miR-132, miR-140, miR-185, miR-339, miR-491, miR-503, miR-768-3p) had concordant levels with the inferred CN value of the corresponding miRNA gene. Notably, the identified miRNAs mapped to different genomic regions, some of which are involved in recurrent CN alterations in MM, such as 8q24, 19q13.33, or chromosome arms 13q, 16q, 17p, 17q, 22q, and for some of the miRNAs a role in other types of cancer has already been suggested. As regards intragenic miRNAs, 187 miRNA/host gene pairs were obtained after localizing miRNAs within the absolute 5′ and 3′ regions of genes represented on the HG-U133A arrays; 25 of these showed a significant correlation between miRNA and mRNA levels. Among the most correlated miRNA/hostgene pairs we identified miR-152/COPZ2, miR-342-3p/EVL, miR-335/MEST, miR-25 and miR-106b/MCM7. For some of the identified pairs, miRNA expression levels were validated by means of Q-RT-PCR. In conclusion, we showed that miRNA expression in HMCLs could be affected by the presence of genomic lesions or may correlate with host-gene modulation, suggesting a possible role in the molecular pathogenesis of MM. Our integrative approach represents the basis for further investigations, also in primary tumors, aimed at functionally characterizing specific miRNAs in MM.

scholarly journals Transcriptome Analysis of Pseudomonas aeruginosa after Interaction with Human Airway Epithelial Cells

2004 ◽  
Vol 72 (9) ◽  
pp. 5433-5438 ◽  
Author(s):  
Anders Frisk ◽  
Jill R. Schurr ◽  
Guoshun Wang ◽  
Donna C. Bertucci ◽  
Luis Marrero ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Human Airway ◽  
Normal Human ◽  
Human Airway Epithelial Cells

ABSTRACT The transcriptional profile of Pseudomonas aeruginosa after interactions with primary normal human airway epithelial cells was determined using Affymetrix GeneChip technology. Gene expression profiles indicated that various genes involved in phosphate acquisition and iron scavenging were differentially regulated.

Comprehensive Gene Expression Profile of a Normal Human Liver

2000 ◽  
Vol 269 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Taro Yamashita ◽  
Shin-ichi Hashimoto ◽  
Shuichi Kaneko ◽  
Shigenori Nagai ◽  
Nobuaki Toyoda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Human Liver ◽  
Normal Human Liver ◽  
Normal Human

Airway epithelial wound repair: role of carbohydrate sialyl Lewisx

2006 ◽  
Vol 291 (4) ◽  
pp. L828-L836 ◽  
Author(s):  
Sima Allahverdian ◽  
Kimberly R. Wojcik ◽  
Delbert R. Dorscheid
Keyword(s):  
Epithelial Cells ◽  
Wound Repair ◽  
Rna Extraction ◽  
Cell Interaction ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Epithelial Repair ◽  
Epithelial Migration ◽  
Cell Cell

Epithelial repair is a complex cellular and molecular process, the details of which are still not clearly understood. Plasma membrane glycoconjugates can modulate cell function by altering the function of protein and lipids. Sialyl Lewisx(sLex), a fucose-containing tetrasaccharide, decorates membrane-bound and secreted proteins and mediates cell-cell interaction. In the present study we investigated the role of sLexin airway epithelial repair. Using immunohistochemistry, we showed an increased expression of sLexin areas of damaged bronchial epithelium compared with intact regions. Confluent monolayers of airway epithelial cells were mechanically wounded and allowed to close. Wounded monolayers were photographed for wound closure kinetics, fixed for immunocytochemical studies, or subjected to RNA extraction. Examining the expression of different α1,3-fucosyltransferases (FucT), enzymes that mediate the final step in the synthesis of sLex, we found that FucT-IV was the common gene expressed in all cell lines and primary airway epithelial cells. We demonstrated an increased expression of sLexover time after mechanical injury. Blocking of sLexwith an inhibitory antibody completely prevented epithelial repair. Our data suggest an essential functional role for sLexin epithelial repair. Further studies are necessary to explore the exact mechanism for sLexin mediating cell-cell interaction in bronchial epithelial cells to facilitate epithelial migration and repair.

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