Increased MMP12 mRNA expression in induced sputum was correlated with airway eosinophilic inflammation in asthma patients: evidence from bioinformatic analysis and experiment verification

Gene ◽  
2021 ◽  
pp. 145896
Author(s):  
Lijuan Du ◽  
Fengjia Chen ◽  
Changyi Xu ◽  
Weiping Tan ◽  
Jia Shi ◽  
...  
2006 ◽  
Vol 117 (2) ◽  
pp. S200 ◽  
Author(s):  
K. Kowal ◽  
S. Zukowski ◽  
O. Kowal-Bielecka ◽  
L.M. DuBuske ◽  
A. Bodzenta-Lukaszyk

2019 ◽  
Vol 2019 ◽  
pp. 1-15
Author(s):  
Mingfu Tong ◽  
Wenquan Lu ◽  
Hao Liu ◽  
Jian Wu ◽  
Mingzuo Jiang ◽  
...  

Background. Metallothioneins (MTs) family comprises many isoforms, most of which are frequently dysregulated in a wide range of cancers. However, the expression pattern and exact role of each distinct MT family isoform which contributes to tumorigenesis, progression, and drug resistance of gastric cancer (GC) are still unclear. Methods. Publicly available databases including Oncomine, Gene Expression Profiling Interactive Analysis (GEPIA), Kaplan-Meier plotter, SurvExpress, MethHC, cBioportal, and GeneMANIA were accessed to perform an integrated bioinformatic analysis and try to detect fundamental relationships between each MT family member and GC. Results. Bioinformatic data indicated that the mRNA expression of all MT family members was almost lowly expressed in GC compared with normal gastric tissue (P<0.05), and patients with reduced mRNA expression of each individual MT member had inconsistent prognostic value (OS, FP, PPS), which depended on the individual isoform of MT. A negative correlation between the methylation in promoter region of majority of MT members and their mRNA expression was detected from MethHC database (p<0.001). Data downloaded from TCGA revealed that MTs were rarely mutated in GC patients and MT2A was frequently regulated by other three genes (FOS, JUN, SP1) in GC patients. Conclusion. MTs were nearly downregulated, and distinct type of MT harbored different prognostic role in GC patients. Methylation in gene promoter region of MTs partially contributed to their reduced expression in GC. Our comprehensive analyses from multiple independent databases may further lead researches to explore MT-targeting reagents or potential diagnostic and prognostic markers for GC patients.


2011 ◽  
Vol 16 (6) ◽  
pp. 673-673 ◽  
Author(s):  
Changchun Hou ◽  
Haijin Zhao ◽  
Wenjun Li ◽  
Zhenyu Liang ◽  
Dan Zhang ◽  
...  

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Hugo Cornelis van Woerden ◽  
Clive Gregory ◽  
Richard Brown ◽  
Julian Roberto Marchesi ◽  
Bastiaan Hoogendoorn ◽  
...  

1999 ◽  
Vol 93 (3) ◽  
pp. 183-189 ◽  
Author(s):  
P.Tarodo De La Fuente ◽  
M. Romagnoli ◽  
L. Carlsson ◽  
P. Godard ◽  
J. Bousquet ◽  
...  

2016 ◽  
Vol 137 (2) ◽  
pp. AB392
Author(s):  
Lucyna Mastalerz ◽  
Maria Ignacak ◽  
Michal Buczek ◽  
Aleksandra Cholewa ◽  
Natalia Celejewska-Wojcik ◽  
...  

2011 ◽  
Vol 110 (5) ◽  
pp. 1256-1263 ◽  
Author(s):  
Jin-jing Zou ◽  
Ya-dong Gao ◽  
Shuang Geng ◽  
Jiong Yang

Hyperplasia of airway smooth muscle cells (ASMCs) is a characteristic change of chronic asthma patients. However, the underlying mechanisms that trigger this process are not yet completely understood. Store-operated Ca2+ (SOC) entry (SOCE) occurs in response to the intracellular sarcoplasma reticulum (SR)/endoplasmic reticulum (ER) Ca2+ store depletion. SOCE plays an important role in regulating Ca2+ signaling and cellular responses of ASMCs. Stromal interaction molecule (STIM)1 has been proposed as an ER/SR Ca2+ sensor and translocates to the ER underneath the plasma membrane upon depletion of the ER Ca2+ store, where it interacts with Orai1, the molecular component of SOC channels, and brings about SOCE. STIM1 and Orai1 have been proved to mediate SOCE of ASMCs. In this study, we investigated whether STIM1/Orai1-mediated SOCE is involved in rat ASMC proliferation. We found that SOCE was upregulated during ASMC proliferation accompanied by a mild increase of STIM1 and a significant increase of Orai1 mRNA expression, whereas the proliferation of ASMCs was partially inhibited by the SOC channel blockers SKF-96365, NiCl2, and BTP-2. Suppressing the mRNA expression of STIM1 or Orai1 with specific short hairpin RNA resulted in the attenuation of SOCE and ASMC proliferation. Moreover, after knockdown of STIM1 or Orai1, the SOC channel blocker SKF-96365 had no inhibitory effect on the proliferation of ASMCs anymore. These results suggested that STIM1/Orai1-mediated SOCE is involved in ASMC proliferation.


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