Amyloid-beta peptide fragments p3 and p4 induce pro-inflammatory cytokine and chemokine production in vitro and in vivo

2001 ◽  
Vol 77 (1) ◽  
pp. 304-317 ◽  
Author(s):  
Ann Marie Szczepanik ◽  
David Rampe ◽  
Garth E. Ringheim
Keyword(s):  
Amyloid Beta ◽  
Inflammatory Cytokine ◽  
Amyloid Beta Peptide ◽  
Peptide Fragments ◽  
Chemokine Production ◽  
Beta Peptide

In vitro reconstitution of a cell-like environment using liposomes for amyloid beta peptide aggregation and its propagation

2013 ◽  
Vol 49 (55) ◽  
pp. 6119 ◽  
Author(s):  
Abhijit Saha ◽  
Goutam Mondal ◽  
Atanu Biswas ◽  
Indrani Chakraborty ◽  
Batakrishna Jana ◽  
...  
Keyword(s):  
Amyloid Beta ◽  
Amyloid Beta Peptide ◽  
Peptide Aggregation ◽  
In Vitro Reconstitution ◽  
Beta Peptide ◽  
A Cell

scholarly journals MicroRNA-155 Promotes Atherosclerosis Inflammation via Targeting SOCS1

2015 ◽  
Vol 36 (4) ◽  
pp. 1371-1381 ◽  
Author(s):  
Yang Yang ◽  
Lixia Yang ◽  
Xing Liang ◽  
Guofu Zhu
Keyword(s):  
Functional Role ◽  
Inflammatory Cytokine ◽  
Activity Levels ◽  
Chemokine Production ◽  
Arterial Walls ◽  
Atherosclerosis Progression ◽  
Pathophysiological Process ◽  
Expression And Activity

Aims: Accumulating evidence suggests that atherosclerotic progression depends on persistent and chronic inflammation in the arterial walls. MicroRNA-155 is reportedly involved in cardiovascular disease and has been implicated as a pro-inflammation regulator. Although some researchers have focused on microRNA-155 as an atherosclerosis regulator, the mechanisms by which microRNA-155 functions as a putative pro-atherosclerosis microRNA are largely unknown. This study aims to analyze microRNA-155's effects on atherosclerotic inflammation and to explore its mechanism. Methods: MicroRNA-155's effects on atherosclerotic inflammation were observed along with the expression and activity levels of SOCS1, STAT3 and NF-κB though microRNA-155 inhibition or overexpression. Results: Highly expressions of microRNA-155 in oxLDL-stimulated macrophages and atherosclerosis mice were inversely correlated with SOCS1 expression. Ectopic microRNA-155 overexpression significantly promoted inflammatory cytokine and chemokine production and atherosclerosis progression. We then observed microRNA-155's functional role in the atherosclerotic pathophysiological process in vivo and in vitro. The observation revealed that by enhancing STAT3 and NF-κB signaling and facilitating immune inflammation by targeting SOCS1, microRNA-155 plays a promotable role in atherosclerosis progression. Conclusions: microRNA-155 works as a promoter in the atherosclerotic procession. Its mechanism may include enhancing inflammatory response in atherosclerosis by increasing STAT3 and NF-κB signaling via targeting SOCS1.

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