scholarly journals Use of Perfluorochemical Liquid Allows Earlier Detection of Gene Expression and Use of Less Vector in Normal Lung and Enhances Gene Expression in Acutely Injured Lung

2001 ◽  
Vol 3 (5) ◽  
pp. 734-745 ◽  
Author(s):  
Daniel J. Weiss ◽  
Laura Bonneau ◽  
Denny Liggitt
Keyword(s):  
Gene Expression ◽  
Normal Lung ◽  
Injured Lung

scholarly journals Progesterone Aggravates Lung Fibrosis in a Mouse Model of Systemic Sclerosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Fatemeh Vafashoar ◽  
Kazem Mousavizadeh ◽  
Hadi Poormoghim ◽  
Amir Haghighi ◽  
Salar Pashangzadeh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Systemic Sclerosis ◽  
Serum Level ◽  
Mouse Model ◽  
Autoimmune Diseases ◽  
Lung Fibrosis ◽  
Normal Lung ◽  
Related Factors ◽  
Progesterone Treatment ◽  
Injured Lung

BackgroundGender-related factors have explained the higher prevalence of autoimmune diseases in women. Sex hormones play a key role in the immune system and parenchymal cells function; therefore, these hormones can be important in the pathogenesis of autoimmune diseases as a risk or beneficial factor. Lung fibrosis is the main cause of mortality in systemic sclerosis, a female predominant autoimmune disease. The objective of this study was to examine the effect of progesterone on lung fibrosis in a mouse model of systemic sclerosis.MethodsMice with bleomycin-induced lung fibrosis treated with progesterone subcutaneously for 21 and 28 days. Blood was collected for hormone and cytokine measurement at the end of treatment then, skin and lung tissues were harvested for histological assessment, gene expression, cytokine, hydroxyproline, and gelatinase measurement.ResultsTrichrome staining and hydroxyproline measurements showed that progesterone treatment increased the content of collagen in fibrotic and normal lung tissues. Progesterone increased α-SMA (P < 0.01), TGF- β (P < 0.05) and decreased MMP9 (P < 0.05) in fibrotic lung tissues. Also progesterone treatment decreased the gene expression of Col1a2 (P <0.05), Ctgf (P <01), End1 (0.001) in bleomycin- injured lung tissues. The serum level of TNF-α was decreased, but the serum level of cortisol was increased by progesterone treatment in fibrotic mice (P< 0.05).ConclusionOur results showed that progesterone aggravates lung fibrosis in a mouse model of systemic sclerosis.

scholarly journals Functions and clinical significance of KLRG1 in the development of lung adenocarcinoma and immunotherapy

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xiaodong Yang ◽  
Yuexin Zheng ◽  
Zhihai Han ◽  
Xiliang Zhang
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Killer Cell ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Normal Lung ◽  
Using Data ◽  
Low Expression

Abstract Background As a marker of differentiation, Killer cell lectin like receptor G1 (KLRG1) plays an inhibitory role in human NK cells and T cells. However, its clinical role remains inexplicit. This work intended to investigate the predictive ability of KLRG1 on the efficacy of immune-checkpoint inhibitor in the treatment of lung adenocarcinoma (LUAD), as well as contribute to the possible molecular mechanisms of KLRG1 on LUAD development. Methods Using data from the Gene Expression Omnibus, the Cancer Genome Atlas and the Genotype-Tissue Expression, we compared the expression of KLRG1 and its related genes Bruton tyrosine kinase (BTK), C-C motif chemokine receptor 2 (CCR2), Scm polycomb group protein like 4 (SCML4) in LUAD and normal lung tissues. We also established stable LUAD cell lines with KLRG1 gene knockdown and investigated the effect of KLRG1 knockdown on tumor cell proliferation. We further studied the prognostic value of the four factors in terms of overall survival (OS) in LUAD. Using data from the Gene Expression Omnibus, we further investigated the expression of KLRG1 in the patients with different responses after immunotherapy. Results The expression of KLRG1, BTK, CCR2 and SCML4 was significantly downregulated in LUAD tissues compared to normal controls. Knockdown of KLRG1 promoted the proliferation of A549 and H1299 tumor cells. And low expression of these four factors was associated with unfavorable overall survival in patients with LUAD. Furthermore, low expression of KLRG1 also correlated with poor responses to immunotherapy in LUAD patients. Conclusion Based on these findings, we inferred that KLRG1 had significant correlation with immunotherapy response. Meanwhile, KLRG1, BTK, CCR2 and SCML4 might serve as valuable prognostic biomarkers in LUAD.

Hypoxia downregulates tropoelastin gene expression in rat lung fibroblasts by pretranslational mechanisms

1999 ◽  
Vol 277 (3) ◽  
pp. L566-L572 ◽  
Author(s):  
John L. Berk ◽  
Nima Massoomi ◽  
Christine Hatch ◽  
Ronald H. Goldstein
Keyword(s):  
Gene Expression ◽  
Gene Transcription ◽  
Actinomycin D ◽  
Lung Fibroblasts ◽  
Mrna Levels ◽  
Rat Lung ◽  
Cell Toxicity ◽  
Chromium Release ◽  
Injured Lung ◽  
Isolated Rat Lung

Elastolytic lung injury disrupts cell barriers, flooding alveoli and producing regional hypoxia. Abnormal O2 tensions may alter repair of damaged elastin fibers. To determine the effect of hypoxia on extravascular elastin formation, we isolated rat lung fibroblasts and cultured them under a variety of O2 conditions. Hypoxia downregulated tropoelastin mRNA in a dose- and time-related fashion while upregulating glyceraldehyde-3-phosphate dehydrogenase mRNA levels. The changes in tropoelastin gene expression were not due to cell toxicity as measured by chromium release and cell proliferation studies. Neither cycloheximide nor actinomycin D abrogated this effect. Hypoxia induced early decreases in tropoelastin mRNA stability; minor suppression of gene transcription occurred later. When returned to 21% O2, tropoelastin mRNA recovered to control levels in part by upregulating tropoelastin gene transcription. Taken together, these data indicate that hypoxia regulates tropoelastin gene expression and may alter repair of acutely injured lung.

scholarly journals The Marine Dinoflagellate Alexandrium minutum Activates a Mitophagic Pathway in Human Lung Cancer Cells

Marine Drugs ◽  
2018 ◽  
Vol 16 (12) ◽  
pp. 502 ◽  
Author(s):  
Christian Galasso ◽  
Genoveffa Nuzzo ◽  
Christophe Brunet ◽  
Adrianna Ianora ◽  
Angela Sardo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Water Soluble ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Normal Lung ◽  
Alexandrium Minutum ◽  
Human Lung Cancer Cells

Marine dinoflagellates are a valuable source of bioactive molecules. Many species produce cytotoxic compounds and some of these compounds have also been investigated for their anticancer potential. Here, we report the first investigation of the toxic dinoflagellate Alexandrium minutum as source of water-soluble compounds with antiproliferative activity against human lung cancer cells. A multi-step enrichment of the phenol–water extract yielded a bioactive fraction with specific antiproliferative effect (IC50 = 0.4 µg·mL−1) against the human lung adenocarcinoma cells (A549 cell line). Preliminary characterization of this material suggested the presence of glycoprotein with molecular weight above 20 kDa. Interestingly, this fraction did not exhibit any cytotoxicity against human normal lung fibroblasts (WI38). Differential gene expression analysis in A549 cancer cells suggested that the active fraction induces specific cell death, triggered by mitochondrial autophagy (mitophagy). In agreement with the cell viability results, gene expression data also showed that no mitophagic event was activated in normal cells WI38.

T cell receptor variable beta-gene expression in the normal lung and in active pulmonary sarcoidosis

CHEST Journal ◽  
1993 ◽  
Vol 103 (2) ◽  
pp. 78S-78
Author(s):  
J. D. Forman ◽  
R. F. Silver ◽  
J. T. Klein ◽  
E. J. Britt ◽  
P. P. Scott ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Pulmonary Sarcoidosis ◽  
Normal Lung ◽  
Beta Gene

scholarly journals Prediction of the gene expression in normal lung tissue by the gene expression in blood

2015 ◽  
Vol 8 (1) ◽  
Author(s):  
Justin W. Halloran ◽  
Dakai Zhu ◽  
David C. Qian ◽  
Jinyoung Byun ◽  
Olga Y. Gorlova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Tissue ◽  
Normal Lung Tissue ◽  
Normal Lung

Differences in gene expression levels between early and later stages of human lung development are opposite to those between normal lung tissue and non-small lung cell carcinoma

Lung Cancer ◽  
2008 ◽  
Vol 62 (1) ◽  
pp. 23-34 ◽  
Author(s):  
Eugene P. Kopantzev ◽  
Galina S. Monastyrskaya ◽  
Tatyana V. Vinogradova ◽  
Marina V. Zinovyeva ◽  
Marya B. Kostina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Carcinoma ◽  
Lung Tissue ◽  
Lung Development ◽  
Human Lung ◽  
Normal Lung Tissue ◽  
Normal Lung ◽  
Expression Levels ◽  
Gene Expression Levels

scholarly journals A Hint on the COVID-19 Risk: Population Disparities in Gene Expression of Three Receptors of SARS-CoV

2020 ◽  
Author(s):  
Guoshuai Cai ◽  
Xiang Cui ◽  
Xia Zhu ◽  
Jun Zhou
Keyword(s):  
Gene Expression ◽  
Bronchial Epithelium ◽  
Cell Types ◽  
Normal Lung ◽  
Alveolar Type ◽  
Significant Difference ◽  
Former Smokers ◽  
Novel Coronavirus ◽  
Gender Groups ◽  
Different Cell Types

The current spreading novel coronavirus SARS-CoV-2 is highly infectious and pathogenic and has attracted global attention. Recent studies have found that SARS-CoV-2 and SARS-CoV share around 80% of homology and use the same cell entry receptor, ACE2. These inspired us to study other receptors of SARS-CoV, which may be used for SARS-CoV-2 binding as well. In this study, we screened the gene expression of three receptors (ACE2, DC-SIGN and L-SIGN) in four datasets of normal lung tissue from lung adenocarcinoma patients and two single-cell RNA sequencing datasets from normal lung and bronchial epithelial cells separately. No significant difference in gene expression of these three receptors were found between gender groups (male vs female). We found higher gene expression of DC-SIGN in elder with age>60 and higher gene expression of L-SIGN in Caucasian than Asian. Similar to ACE2, we observed significantly higher DC-SIGN gene expression in the lungs of smokers, especially former smokers. However, smokers upregulate ACE2 and DC-SIGN gene expression in different cell types. In the whole lung, ACE2 is actively expressed in remodeled Alveolar Type II cells of former smokers, while DC-SIGN is largely expressed in monocytes of former smokers and dendritic cells of current smokers. In bronchial epithelium, no obvious gene expression of DC-SIGN and L-SIGN was observed while ACE2 was found to be actively expressed in goblet cells of current smokers and club cells of non-smokers. In conclusion, our findings may indicate that smokers, especially former smokers, and people over 60 have higher risk and are more susceptible to SARS-CoV-2 infection. Also, this study provides hints on possible SARS-CoV-2 pathogenicity mechanisms in lung infection.

scholarly journals Functions and Clinical Significance of KLRG1 in the Development of Lung Adenocarcinoma and Immunotherapy

2020 ◽  
Author(s):  
Xiaodong Yang ◽  
Yuexin Zheng ◽  
Zhihai Han ◽  
xiliang zhang
Keyword(s):  
Gene Expression ◽  
Overall Survival ◽  
Lung Adenocarcinoma ◽  
Killer Cell ◽  
Gene Expression Omnibus ◽  
The Cancer Genome Atlas ◽  
Prognostic Biomarkers ◽  
Normal Lung ◽  
Using Data ◽  
Low Expression

Abstract Background. As a marker of differentiation, Killer cell lectin like receptor G1 (KLRG1) plays an inhibitory role in human NK cells and T cells. However, its clinical role remains inexplicit. This work intended to investigate the predictive ability of KLRG1 in lung adenocarcinoma (LUAD) after immune-checkpoint inhibitor therapy, as well as to explore the role of a possible KLRG1 molecular mechanism on LUAD development.Methods. Using data from the Gene Expression Omnibus, the Cancer Genome Atlas and the Genotype-Tissue Expression, we compared the expression of KLRG1 and its related genes Bruton tyrosine kinase (BTK), C-C motif chemokine receptor 2 (CCR2), Scm polycomb group protein like 4 (SCML4) in LUAD and normal lung tissues. We further established a stable LUAD cell line with KLRG1 knockdown and investigate the effect of KLRG1 knockdown on tumor cell proliferation. We also studied the prognostic value of the four factors in terms of overall survival (OS) in LUAD. Using data from the Gene Expression Omnibus, we further investigated the expression of KLRG1 in the patients with different responses after immunotherapy.Results. The expression of KLRG1, BTK, CCR2 and SCML4 was significantly downregulated in LUAD tissues compared to normal controls. Knockdown of KLRG1 promoted the proliferation of A549 tumor cells. And low expression of these four factors was all associated with unfavorable overall survival in patients with LUAD. Furthermore, low expression of KLRG1 also correlated with poor responses in LUAD patients after immunotherapy.Conclusion. Based on these findings, we infer that KLRG1 had significant correlation with immunotherapy response. Meanwhile, KLRG1, BTK, CCR2 and SCML4 might serve as valuable prognostic biomarkers in LUAD. Key pointsKLRG1 inhibits the progress of LUAD.KLRG1 had significant correlation with immunotherapy response.KLRG1, BTK, CCR2 and SCML4 might serve as valuable prognostic biomarkers in LUAD.

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