Temporal and noninvasive monitoring of inflammatory-cell infiltration to myocardial infarction sites using micrometer-sized iron oxide particles

2009 ◽  
Vol 63 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Yidong Yang ◽  
Yuhui Yang ◽  
Nathan Yanasak ◽  
Autumn Schumacher ◽  
Tom C.-C. Hu
Keyword(s):  
Myocardial Infarction ◽  
Iron Oxide ◽  
Inflammatory Cell ◽  
Noninvasive Monitoring ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Iron Oxide Particles ◽  
Oxide Particles

scholarly journals Assessment of cell infiltration in myocardial infarction: A dose-dependent study using micrometer-sized iron oxide particles

2011 ◽  
Vol 66 (5) ◽  
pp. 1353-1361 ◽  
Author(s):  
Yidong Yang ◽  
Jimei Liu ◽  
Yuhui Yang ◽  
Sang Hyun Cho ◽  
Tom C.-C. Hu
Keyword(s):  
Myocardial Infarction ◽  
Iron Oxide ◽  
Cell Infiltration ◽  
Iron Oxide Particles ◽  
Oxide Particles ◽  
Dose Dependent

scholarly journals Inhibition of the lncRNA Mirt1 Attenuates Acute Myocardial Infarction by Suppressing NF-κB Activation

2017 ◽  
Vol 42 (3) ◽  
pp. 1153-1164 ◽  
Author(s):  
Xiangrao Li ◽  
Jian Zhou ◽  
Kai Huang
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Inflammatory Cell ◽  
Cultured Cells ◽  
Cardiac Fibroblasts ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration ◽  
Inflammatory Factors ◽  
Cardiac Functions

Background/Aims: The expression of a novel lncRNA, myocardial infarction associated transcript 1(Mirt1), has been shown to be upregulated in acute myocardial infarction (AMI). However, the role of Mirt1 in AMI is not clear. Methods: In this study, we analyzed the level of Mirt1 in cardiomyocytes and cardiac fibroblasts in AMI mice. Moreover, adenovirus mediated knockdown of Mirt1 was employed to clarify its roles in AMI mice or cultured cardiac fibroblasts. The cardiac functions and infarct size of AMI mice were examined, and tissues and cultured cells were collected and processed for histology and biochemical examination. Results: We demonstrated that Mirt1 was mainly expressed in cardiac fibroblasts, and that knockdown of Mirt1 improved cardiac functions, decreased cardiomyocytes apoptosis and attenuated inflammatory cell infiltration in vivo. Furthermore, knockdown of Mirt1 in cardiac fibroblasts not only attenuated the apoptosis of cardiomyocytes, but also suppressed the migration of macrophages under hypoxia in vitro. NF-κB signaling pathway, activated under hypoxia, was also inhibited by Mirt1 knockdown in fibroblasts. Conclusions: Knockdown of Mirt1 attenuates AMI injury presumably by decreasing cardiomyocytes apoptosis and reducing inflammatory cell infiltration. These effects could be attributed, at least partly, to inhibition of the NF-κB pathway, resulting in decreased expression of inflammatory factors.

TH-D-201C-04: Quantification of Cellular Response in Myocardial Infarction Using Iron Oxide Particles-Enhanced MRI

2010 ◽  
Vol 37 (6Part8) ◽  
pp. 3469-3470
Author(s):  
Y Yang ◽  
J Liu ◽  
Y Yang ◽  
X Shi ◽  
W Hill ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Iron Oxide ◽  
Cellular Response ◽  
Iron Oxide Particles ◽  
Enhanced Mri ◽  
Oxide Particles

A Case of Bullous Amyloidosis Associated with an Inflammatory Cell Infiltration and Prominent Pruritus

2008 ◽  
Vol 70 (3) ◽  
pp. 269-273
Author(s):  
Taisuke KAMIYAMA ◽  
Yoshihiro KAWAGUCHI ◽  
Masami SASAKI ◽  
Masamichi SATOU ◽  
Kumiko MIURA ◽  
...  
Keyword(s):  
Inflammatory Cell ◽  
Inflammatory Cell Infiltration ◽  
Cell Infiltration
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