scholarly journals Targeted Therapy of Atherosclerosis Vulnerable Plaque By ROS-Scavenging Nanoparticles And MR/Fluorescence Dual-Modality Imaging Tracing

Author(s):  
Yue Dai ◽  
Xuan Sha ◽  
Xiaoxi Song ◽  
Xiuli Zhang ◽  
Mengyuan Xing ◽  
...  

Abstract Background: Cardiovascular diseases are currently the leading cause of death and disability worldwide, and the key pathological basis is atherosclerosis (AS). Especially, the rupture of vulnerable plaques is the main cause of acute cardiovascular and cerebrovascular events such as myocardial infarction and stroke. Thus, the early identifying and therapy of vulnerable plaques are necessary. Results: In this study, we developed a novel multimodal imaging platform (GPRD) based on Gd doped Prussian blue (GPB) and rhodamine (Rd) to specifically target and identify the vulnerable plaques with the help of dextran sulfate (DS), one of the excellent ligands of scavenger receptor class A (SR-A). It is more important that the nano-enzyme capacity of GPRD NPs realized the elimination of the excessive production of ROS in cells, and the following reduction of ROS-induced oxidative stress, inflammation, apoptosis, and the formation of macrophage-derived foam cells, presenting an inhibition of plaque progress eventually. Conclusions: The ROS-scavenging multimodal imaging nanoprobe provided a new avenue for the diagnosis and treatment of AS vulnerable plaques.

2021 ◽  
Author(s):  
Yi Li ◽  
Feng Peng ◽  
Xiangyun Tan ◽  
Jin Wang ◽  
Yeqing Xu

Abstract Background Colorectal cancer (CRC) exhibits high risks of morbidity and mortality. Objective To investigate the effect of scavenger receptor class A member 5 (SCRAR5) on CRC and its mechanism on modulation of cancer development. Methods The SCRAR5 expression in four kinds of CRC cell lines (SW620, SW480, HT29, and HCT116) was measured by quantitative PCR and western blotting, respectively. The effects of SCRAR5 abnormal expression on cell proliferation, apoptosis, and migration were analyzed by CCK-8 assay, EdU assay, colony-forming assay, flow cytometry assay, Transwell assay and wound healing assay, respectively. Meanwhile, the involvements of PI3K/AKT/mTOR pathway with the role of SCRAR5 were investigated by western blotting. Afterwards, the in vivo effects of SCRAR5 abnormal expression on CRC xenograft mice were finally investigated by evaluating tumor volume, apoptosis and Ki67 expression. Results SCRAR5 was lowly expressed in CRC cell lines, especially SW480 cells. Up-regulation of SCRAR5 significantly promoted cell apoptosis, reduced cell proliferation and migration in SW480 cells. Notably, SCRAR5 overexpression obviously inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Reversely, SCRAR5 silence exhibited promoting effects on HT29 cells. Consistently, in vivo experiments also revealed that SCRAR5 overexpression remarkably suppressed tumor volume and Ki67 expression, as well as promoted cell apoptosis. Conclusions Overall, up-regulating of SCRAR5 obviously inhibited CRC tumor growth in vitro and in vivo, which might be related to PI3K/AKT/mTOR pathway.


2000 ◽  
Vol 164 (9) ◽  
pp. 4861-4867 ◽  
Author(s):  
Nick Platt ◽  
Hiroshi Suzuki ◽  
Tatsuhiko Kodama ◽  
Siamon Gordon

2016 ◽  
Vol 6 (7) ◽  
pp. 567-572
Author(s):  
Aamir Rana ◽  
Syed Sajjad Sattar ◽  
Afshann Shahzad ◽  
Ghulam Muhammad Ali ◽  
Yasir Waheed

Medicine ◽  
2019 ◽  
Vol 98 (40) ◽  
pp. e17471
Author(s):  
Ye Tian ◽  
Kai Zhou ◽  
Jing Hu ◽  
Ming-Feng Shan ◽  
Hong-Jian Chen ◽  
...  

Author(s):  
Takeshi Murakami ◽  
Yoshihiko Yamada ◽  
Takefumi Doi ◽  
Takao Hamakubo ◽  
Tatsuhiko Kodama

2001 ◽  
Vol 280 (4) ◽  
pp. L689-L694 ◽  
Author(s):  
Boris W. Kramer ◽  
Alan H. Jobe ◽  
Machiko Ikegami

Alveolar macrophages are essential for the maintenance of surfactant homeostasis. We asked whether surfactant treatment would change alveolar macrophage number and whether the alveolar macrophage phenotype would become activated or apoptotic when challenged in vivo with exogenous surfactant. Surfactant pool size in mice was increased by repetitive surfactant treatments containing 120 mg/kg (110 μmol/kg) saturated phosphatidylcholine. The number of alveolar macrophages recovered by alveolar lavage decreased after the first dose by 49% and slightly increased after the second and third doses. Up to 28.5% of the macrophages became large and foamy, and their appearance normalized within 12 h. Surfactant treatment did not increase the percent of apoptotic or necrotic cells. The alveolar macrophages were not activated as indicated by no change in expression of CD14, CD16, CD54, CD95, and scavenger receptor class A types I and II after surfactant treatment. Surfactant treatment in healthy mice transiently changed the phenotype of alveolar macrophages to large and foamy without indications of changes in the surface markers characteristic of activation.


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