Toll-like receptor 9 prevents cardiac rupture after myocardial infarction in mice independently of inflammation

Omiya, Shigemiki; Omori, Yosuke; Taneike, Manabu; Protti, Andrea; Yamaguchi, Osamu; Akira, Shizuo; Shah, Ajay M.; Nishida, Keiya; Otsu, Kinya

doi:10.1152/ajpheart.00481.2016

Cited by 40 publications

(47 citation statements)

References 34 publications

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“…Complete remission (CR) was defined by bone marrow blasts < 5% durable for at least 28 days, absence of blasts with Auer rods, absence of extramedullary disease, absolute neutrophil count > 1.0 × 10 9 /L, platelet count > 100 × 9 /L, and independence of red cell transfusions. Partial remission (PR) was defined by all hematologic criteria of CR, decreased bone marrow blast percentage from 5 to 25% and decreased pretreatment bone marrow blast percentage by at least 50%.…”

Section: Clinical Outcomes and Survival Analysismentioning

confidence: 99%

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Toll-like receptor 9 negatively related to clinical outcome of AML patients

Al-Kahiry

Dammag

Abdelsalam

et al. 2020

J Egypt Natl Canc Inst

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Background: Acute myeloid leukemia (AML) can modulate toll-like receptor-9 (TLR9) expression and activation. This study was conducted to elucidate the expression of TLR9 in AML patients and its relation to the prognosis of the disease. Results: The study included 40 newly diagnosed AML patients managed in the hospital in addition to 20 sex and age matched normal volunteers as control. TLR9 expression assay was conducted on peripheral blood samples of AML cases before the start of treatment as well as the controls by immunophenotyping. TLR9 expression was ranging from 0.10 to 2.40% in AML patients with higher expression among the control, ranging from 0.94 to 8.25%. The median TLR9 expression in AML patients was significantly lower with advanced cytogenetic risk score. It is not significantly differing in relation to patients' sex, age group, and FAB type of AML. However, significant lower median expression was found in relation to clinical outcome. TLR9 expression ≤ 1% showed lower median overall survival time when compared to those with > 1% expression. Conclusion: This study concluded that AML patients express TLR9 in leukemic cells with very low percentage. This expression was negatively related to the clinical outcome.

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Section: Clinical Outcomes and Survival Analysismentioning

confidence: 99%

“…It can trigger signaling cascades for a pro-inflammatory cytokine response [6,7]. Cancer and tissue damage can modulate TLR9 expression and activation [8,9].…”

Section: Introductionmentioning

confidence: 99%

Toll-like receptor 9 negatively related to clinical outcome of AML patients

Al-Kahiry

Dammag

Abdelsalam

et al. 2020

J Egypt Natl Canc Inst

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“…A, Bioinformatics software predicted the binding sites between miR-7 and Smad2 3′UTR. 40 In this study, we determined the NETs promoted TLR9 signalling pathway in LFs, and TLR9 knockdown suppressed the proliferation of LF and their differentiation into MF. C, miR-7 mimic decreased mRNA level of Smad2, and miR-7 inhibitor up-regulated mRNA level of Smad2.…”

Section: Discussionmentioning

confidence: 96%

Neutrophil extracellular traps activate lung fibroblast to induce polymyositis‐related interstitial lung diseases via TLR9‐miR‐7‐Smad2 pathway

Zhang

Jia

Zhang

et al. 2019

J Cellular Molecular Medi

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| INTRODUC TI ONPolymyositis (PM) is the common disease of idiopathic inflammatory myopathy that affects skeletal muscle, lung, heart, joints, etc. 1 Interstitial lung diseases (ILDs) is the most common complication which seriously affects the prognosis of PM patients. 2 A retrospective study showed the morbidity rate was 48.9% in patients with PM/dermatomyositis (DM)-related ILD in Chinese Han population. 3 Another study reported the mortality rate was 47.1% in myositis patients with ILD. 4 Based on the high morbidity and mortality rates, finding effective preventive and therapeutic methods is important for improving prognosis of patients with PM-related ILD. Interstitial lung diseases AbstractExcessive neutrophil extracellular trap (NET) formation may contribute to polymyositis (PM)-associated interstitial lung diseases (ILD), but the underlying mechanism is not fully revealed. In this study, we found that NET accelerated the progression of ILD and promoted pulmonary fibrosis (PF) in vivo. miR-7 expression was downregulated in lung tissue of PM group than control group, and NETs further decreased miR-7 expression. TLR9 and Smad2 were up-regulated in lung tissue of PM group than control group, and NETs further increased TLR9 and Smad2 expressions. In vitro experiments showed that PMA-treated NETs accelerated the proliferation of LF and their differentiation into myofibroblast (MF), whereas DNase I decreased the promotion effect of NETs. Neutrophil extracellular trap components myeloperoxidase (MPO) and histone 3 also promoted the proliferation and differentiation of LF. In addition, we demonstrated that TLR9 involved in the regulation of NETs on LF proliferation and differentiation, and confirmed the interaction between miR-7 and Smad2 in LF. Finally, miR-7-Smad2 pathway was confirmed to be involved in the regulation of TLR9 on LF proliferation and differentiation. Therefore, NETs promote PM-related ILD, and TLR9-miR-7-Smad2 signalling pathway is involved in the proliferation of LFs and their differentiation into MFs. K E Y W O R D Sdifferentiation, interstitial lung diseases, lung fibroblast, myofibroblast, neutrophil extracellular traps, polymyositis

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“…Both inhibitions of LXR-RXR complex formation and ABCA1 activation promote HDL and LDL accumulation in the plasma, which increases OS and inflammation through ox-LDL/PI3K/MAPK/NF-κB pathway. Ultimately, these abnormalities lead to ECs adhesion molecules overexpression, macrophage foam cell formation, intima media IMT and AS plaque development [ [53] , [54] , [55] , [56] ] ( Fig. 1 A1–2).…”

Section: Abnormalities In Dna and Histone In Asmentioning

confidence: 99%

Molecular mechanisms and genetic regulation in atherosclerosis

Jackson

Regine

Subrata

et al. 2018

IJC Heart & Vasculature

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Atherosclerosis (AS) manifested by lipid accumulation, extracellular matrix protein deposition, and calcification in the intima and media of the large to medium size arteries promoting arterial stiffness and reduction of elasticity. It has been accepted that AS leads to increased morbidity and mortality worldwide. Recent studies indicated that genetic abnormalities play an important role in the development of AS. Specific genetic mutation and histone modification have been found to induce AS formation. Furthermore, specific RNAs such as microRNAs and circular RNAs have been identified to play a crucial role in the progression of AS. Nevertheless, the mechanisms by which genetic mutation, DNA and histone modification, microRNAs and circular RNA induce AS still remain elusive. This review describes specific mechanisms and pathways through which genetic mutation, DNA and histone modification, microRNAs and circular RNA instigate AS. This review further provides a therapeutic strategic direction for the treatment of AS targeting genetic mechanisms.

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Toll-like receptor 9 prevents cardiac rupture after myocardial infarction in mice independently of inflammation

Cited by 40 publications

References 34 publications

Toll-like receptor 9 negatively related to clinical outcome of AML patients

Toll-like receptor 9 negatively related to clinical outcome of AML patients

Neutrophil extracellular traps activate lung fibroblast to induce polymyositis‐related interstitial lung diseases via TLR9‐miR‐7‐Smad2 pathway

Molecular mechanisms and genetic regulation in atherosclerosis

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