Adaptive Immune Responses in Human Atherosclerosis

Lee, Silvia; Bartlett, Benjamin; Dwivedi, Girish

doi:10.3390/ijms21239322

Cited by 20 publications

(14 citation statements)

References 113 publications

(151 reference statements)

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“…Mononuclear cells and cytokines also playing a critical role from the initial stages of atherosclerosis. 14 , 15 However, questions like whether the increasing SUA related inflammation could independently induce atherosclerosis, what are the underlying mechanisms, and whether HUA should be treated to prevent the development of atherosclerosis need to be further investigated.…”

Section: Introductionmentioning

confidence: 99%

High Level of Serum Uric Acid induced Monocyte Inflammation is Related to Coronary Calcium Deposition in the Middle-Aged and Elder Population of China: A five-year Prospective Cohort Study

Wang¹,

Liu²,

Qi³

et al. 2022

JIR

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Background Serum uric acid (SUA) is suspected to be associated with atherosclerosis and calcium deposition in atherosclerosis is known to related poor prognosis, yet there is no cohort study on the aged in China. We aimed to investigate the relationships between SUA levels and coronary calcium deposition in the middle-aged and elderly populations in China. Methods A total of 326 participants between the ages of 50 and 85 who had undergone a coronary CT scan in 2015 at the Huadong Hospital Affiliated to Fudan University (Shanghai, China) were included in this study. Univariate and multivariate binary logistic regression was performed to analyze the correlation between SUA levels and coronary artery calcium score (CACS). The changes in CACS during a five-year follow-up were analyzed through Kaplan–Meier survival and binary cox regression analysis. An observational study was done on another 104 asymptomatic middle-aged and elderly patients to compare relative mRNA expressions of proinflammatory factors in peripheral blood mononuclear cells (PBMCs) from 104 subjects. Results Based on the first year of follow-up data analysis, the elevation of SUA levels ( P <0.001) is an independent risk factor for the increase of CACS after coordinating the confounding factors. According to five-year follow-up data, cox regression analysis proved that SUA was a risk factor for CACS (HR =5.86, P <0.001). The mRNA expression of IL-6 and CXCL8 in the HUA and HUA patients with CAC (HUA-CAC) groups was significantly higher than that in the normal control (NC) and coronary calcium deposition (CAC) groups. Conclusion Taken together, the findings in this study indicate that high SUA levels ( P <0.001) are an independent risk factor for CACS and elevated SUA levels increase the risk of developing coronary calcium deposition among middle-aged and old people in the Chinese population, which may be related to an increase of pro-inflammatory cytokines in the PBMCs.

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Section: Introductionmentioning

confidence: 99%

High Level of Serum Uric Acid induced Monocyte Inflammation is Related to Coronary Calcium Deposition in the Middle-Aged and Elder Population of China: A five-year Prospective Cohort Study

Wang¹,

Liu²,

Qi³

et al. 2022

JIR

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“…AS is a persistent inflammatory condition that is started by the deposition as well as accumulation of low-density lipoproteins in the artery wall 19 . In spite of tremendous advances in both basic and scientific study, is still among the leading reasons for death in the world 20 .…”

Section: Discussionmentioning

confidence: 99%

Myricetin ameliorates ox-LDL-induced HUVECs apoptosis and inflammation via lncRNA GAS5 upregulating the expression of miR-29a-3p

Bai

Liu

Chen

et al. 2021

Sci Rep

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Oxidized low-density lipoprotein (ox-LDL)-induced endothelial cell dysfunction is a significant event in the progression of atherosclerosis. Even Myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. HUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 assay, flow cytometry, quantitative real-time polymerase chain reaction and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization and RNA immunoprecipitation assay. Myr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further reduce the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signalling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. Myr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis.

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“…AS is a persistent in ammatory condition that is started by the deposition as well as accumulation of low-density lipoproteins in the artery wall [19]. In spite of excellent advances in both basic and scienti c study, is still among the leading reasons for death in the world [20].…”

Section: Discussionmentioning

confidence: 99%

Myricetin Ameliorates Ox-LDL-induced HUVECs Apoptosis and Inﬂammation via lncRNA GAS5 Upregulating the Expression of miR-29a-3p

Bai

Chen

Jiang

et al. 2020

Preprint

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BackgroundOxidized low-density lipoprotein (ox-LDL)-induced an endothelial cell dysfunction is a significant event in the progression of atherosclerosis[1]. Even myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. MethodsHUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization (FISH) and RNA immunoprecipitation (RIP) assay. ResultsMyr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further resuced the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signaling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. ConclusionMyr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis.

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Adaptive Immune Responses in Human Atherosclerosis

Cited by 20 publications

References 113 publications

High Level of Serum Uric Acid induced Monocyte Inflammation is Related to Coronary Calcium Deposition in the Middle-Aged and Elder Population of China: A five-year Prospective Cohort Study

High Level of Serum Uric Acid induced Monocyte Inflammation is Related to Coronary Calcium Deposition in the Middle-Aged and Elder Population of China: A five-year Prospective Cohort Study

Myricetin ameliorates ox-LDL-induced HUVECs apoptosis and inflammation via lncRNA GAS5 upregulating the expression of miR-29a-3p

Myricetin Ameliorates Ox-LDL-induced HUVECs Apoptosis and Inﬂammation via lncRNA GAS5 Upregulating the Expression of miR-29a-3p

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