Lung Inflammation And Inflammatory Gene Expression In Response To Endotoxemia Are Attenuated In Bone Marrow Chimera Mice With Functionally Inactive PU.1

Author(s):  
MANJULA KARPURAPU ◽  
Xuerong Wang ◽  
Jing Deng ◽  
Hyesuk Park ◽  
Lei Xiao ◽  
...  
Biomedicines ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 1432
Author(s):  
Dabin Jeong ◽  
Wan-Kyu Ko ◽  
Seong-Jun Kim ◽  
Gong-Ho Han ◽  
Daye Lee ◽  
...  

The purpose of this study is to elucidate the anti-inflammatory effect of lobeglitazone (LOBE) in lipopolysaccharide (LPS)-induced bone-marrow derived macrophages (BMDMs). We induced nitric oxide (NO) production and pro-inflammatory gene expression through LPS treatment in BMDMs. The changes of NO release and expression of pro-inflammatory mediators by LOBE were assessed via NO quantification assay and a real-time quantitative polymerase chain reaction (RT-qPCR), respectively. In addition, the regulatory effect of LOBE on activation of mitogen-activated protein kinase (MAPK) signaling pathway was investigated by measuring the phosphorylation state of extracellular regulatory protein (ERK) and c-Jun N-terminal kinase (JNK) proteins by Western blot. Our results show that LOBE significantly reduced LPS-induced NO production and pro-inflammatory gene expression of interleukin-1β (IL-1β), IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and monocyte chemoattractant protein-1 (MCP-1). Moreover, LOBE reduced phosphorylation levels of ERK and JNK of MAPK signaling pathway. In conclusion, LOBE exerts an anti-inflammatory effect in LPS-induced BMDMs by suppression of NO production and pro-inflammatory gene expression, and this effect is potentially through inhibition of the MARK signaling pathway.


2017 ◽  
Vol 178 (1) ◽  
Author(s):  
A.G. Ortega‐Loayza ◽  
W.H. Nugent ◽  
O.M. Lucero ◽  
S.L. Washington ◽  
J.R. Nunley ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Diego Guerrieri ◽  
Luis Re ◽  
Jorgelina Petroni ◽  
Nella Ambrosi ◽  
Roxana E. Pilotti ◽  
...  

Background.Delayed graft function (DGF) remains an important problem after kidney transplantation and reduced long-term graft survival of the transplanted organ. The aim of the present study was to determine if the development of DGF was associated with a specific pattern of inflammatory gene expression in expanded criteria of deceased donor kidney transplantation. Also, we explored the presence of correlations between DGF risk factors and the profile that was found.Methods.Seven days after kidney transplant, a cDNA microarray was performed on biopsies of graft from patients with and without DGF. Data was confirmed by real-time PCR. Correlations were performed between inflammatory gene expression and clinical risk factors.Results.From a total of 84 genes analyzed, 58 genes were upregulated while only 1 gene was downregulated in patients with DGF compared with no DGF (P=0.01). The most relevant genes fold changes observed was IFNA1, IL-10, IL-1F7, IL-1R1, HMOX-1, and TGF-β. The results were confirmed for IFNA1, IL-1R1, HMOX-1 and TGF-β. A correlation was observed between TGF-β, donor age, and preablation creatinine, but not body mass index (BMI). Also, TGF-βshowed an association with recipient age, while IFNA1 correlated with recipient BMI. Furthermore, TGF-β, IFNA1 and HMOX-1 correlated with several posttransplant kidney function markers, such as diuresis, ultrasound Doppler, and glycemia.Conclusions.Overall, the present study shows that DGF is associated with inflammatory markers, which are correlated with donor and recipient DGF risk factors.


2006 ◽  
Vol 49 (1) ◽  
pp. 62-71 ◽  
Author(s):  
Chun-Jung Chen ◽  
Yen-Chuan Ou ◽  
Shih-Yi Lin ◽  
Su-Lan Liao ◽  
Shih-Yun Chen ◽  
...  

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