scholarly journals A novel transcription factor inhibitor, SP100030, inhibits cytokine gene expression, but not airway eosinophilia or hyperresponsiveness in sensitized and allergen-exposed rat

2001 ◽  
Vol 134 (5) ◽  
pp. 1029-1036 ◽  
Author(s):  
Tung-Jung Huang ◽  
Ian M Adcock ◽  
K Fan Chung
2021 ◽  
Vol 4 (4) ◽  
pp. e202000803
Author(s):  
Min Xie ◽  
Ren Hui Chia ◽  
Dan Li ◽  
Fanny Xueting Teo ◽  
Christian Krueger ◽  
...  

Hepatocytes and liver-resident macrophages known as Kupffer cells (KCs) are key cell types involved in liver fibrosis. The transcription factor c-Jun plays a fundamental role in regulating hepatocyte and macrophage functions. We have examined c-Jun’s role in the functional interaction of these cells during liver fibrosis induced by carbon tetrachloride. While hepatocyte-specific c-jun deletion led to increased fibrosis, the opposite outcome was observed when c-jun was deleted in both hepatocytes and KCs. Molecular analyses revealed compromised cytokine gene expression as the apical event related to the phenotype. Yet, purified hepatocytes from both mouse cohorts showed similar defects in cytokine gene expression. However, we noted increased macrophage infiltration in the absence of c-Jun in hepatocytes, which when chemically depleted, reversed the phenotype. Consistently, c-jun deletion in KCs alone also led to reduced fibrosis and cytokine gene expression. By contrast, c-jun deletion in hepatocytes and KCs did not affect the resolution phase after fibrotic injury. These data together demonstrate a pro-fibrogenic role for c-Jun in hepatocytes and KCs that functionally interact to regulate liver fibrosis.


Immunology ◽  
1998 ◽  
Vol 95 (2) ◽  
pp. 242-247 ◽  
Author(s):  
WICHER ◽  
SCAROZZA ◽  
RAMSINGH ◽  
WICHER

2009 ◽  
Vol 50 (3) ◽  
pp. 322 ◽  
Author(s):  
Choong-Gu Lee ◽  
Anupama Sahoo ◽  
Sin-Hyeog Im

2015 ◽  
Vol 23 (3) ◽  
pp. 617-626 ◽  
Author(s):  
Nophar Geifman ◽  
Sanchita Bhattacharya ◽  
Atul J Butte

Abstract Objective Cytokines play a central role in both health and disease, modulating immune responses and acting as diagnostic markers and therapeutic targets. This work takes a systems-level approach for integration and examination of immune patterns, such as cytokine gene expression with information from biomedical literature, and applies it in the context of disease, with the objective of identifying potentially useful relationships and areas for future research. Results We present herein the integration and analysis of immune-related knowledge, namely, information derived from biomedical literature and gene expression arrays. Cytokine-disease associations were captured from over 2.4 million PubMed records, in the form of Medical Subject Headings descriptor co-occurrences, as well as from gene expression arrays. Clustering of cytokine-disease co-occurrences from biomedical literature is shown to reflect current medical knowledge as well as potentially novel relationships between diseases. A correlation analysis of cytokine gene expression in a variety of diseases revealed compelling relationships. Finally, a novel analysis comparing cytokine gene expression in different diseases to parallel associations captured from the biomedical literature was used to examine which associations are interesting for further investigation. Discussion We demonstrate the usefulness of capturing Medical Subject Headings descriptor co-occurrences from biomedical publications in the generation of valid and potentially useful hypotheses. Furthermore, integrating and comparing descriptor co-occurrences with gene expression data was shown to be useful in detecting new, potentially fruitful, and unaddressed areas of research. Conclusion Using integrated large-scale data captured from the scientific literature and experimental data, a better understanding of the immune mechanisms underlying disease can be achieved and applied to research.


1994 ◽  
Vol 68 (6) ◽  
pp. 293-298 ◽  
Author(s):  
F. H. M. Cluitmans ◽  
B. H. J. Esendam ◽  
J. E. Landegent ◽  
R. Willemze ◽  
J. H. F. Falkenburg

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