Loss of fatty acid binding protein 3 ameliorates lipopolysaccharide-induced inflammation and endothelial dysfunction

Nguyen, Hien; Bu, Shuhan; Nikfarjam, Sepideh; Rasheed, Berk; Michels, David; Singh, Aman; Singh, Shweta; Marszal, Caroline; McGuire, John J.; Feng, Qingping; Frisbee, Jefferson C.; Qadura, Mohammad; Singh, Krishna K.

doi:10.1016/j.jbc.2023.102921

Cited by 8 publications

(6 citation statements)

References 112 publications

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“…Inhibition of FABP3 restored PGPC-induced ferroptosis and PGPC-impaired endothelium-dependent vasodilation, demonstrating that PGPC induces ferroptosis by increasing FABP3 expression. Recent studies showed that the loss of FABP3 improves lipopolysaccharide-induced inflammation and endothelial dysfunction, also supporting our findings ( 53 ). Indeed, we found that PGPC inhibited both GSH and GPX4 expression, and FABP3 silencing reversed the PGPC-inhibited GSH and GPX4 expression.…”

Section: Discussionsupporting

confidence: 92%

The oxidized phospholipid PGPC impairs endothelial function by promoting endothelial cell ferroptosis via FABP3

Chen,

Gao,

Liu

et al. 2024

Journal of Lipid Research

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Section: Discussionsupporting

confidence: 92%

The oxidized phospholipid PGPC impairs endothelial function by promoting endothelial cell ferroptosis via FABP3

Chen,

Gao,

Liu

et al. 2024

Journal of Lipid Research

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“…Recently it was also shown to possess immune properties, potentiating B-cell-mediated effects [55]. Macrophages, myeloid dendritic cells, and endothelial cells appeared to be capable of FABP-3 production in pro-inflammatory conditions, typical for atherosclerosis [56,57]. In these circumstances, the effects of FABP-3 on the endothelium were detrimental: exogenous FABP-3 increased LPS-induced inflammation, while silencing of FABP-3 in endothelial cell culture promoted protective, anti-inflammatory, and pro-angiogenic effects [57].…”

Section: Discussionmentioning

confidence: 99%

“…Macrophages, myeloid dendritic cells, and endothelial cells appeared to be capable of FABP-3 production in pro-inflammatory conditions, typical for atherosclerosis [56,57]. In these circumstances, the effects of FABP-3 on the endothelium were detrimental: exogenous FABP-3 increased LPS-induced inflammation, while silencing of FABP-3 in endothelial cell culture promoted protective, anti-inflammatory, and pro-angiogenic effects [57]. FABP-3 also played a role in cholesterol uptake by macrophages and in the formation of foam cells, thus exhibiting pro-atherogenic effects [58].…”

Section: Discussionmentioning

confidence: 99%

Intermediate Monocytes and Circulating Endothelial Cells: Interplay with Severity of Atherosclerosis in Patients with Coronary Artery Disease and Type 2 Diabetes Mellitus

Kologrivova,

Suslova,

Koshelskaya

et al. 2023

Biomedicines

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The aim was to investigate the association of monocyte heterogeneity and presence of circulating endothelial cells with the severity of coronary atherosclerosis in patients with coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM). We recruited 62 patients with CAD, including 22 patients with DM2. The severity of atherosclerosis was evaluated using Gensini Score. Numbers of classical (CD14++CD16–), intermediate (CD14++CD16+), and non-classical (CD14+CD16++) monocyte subsets; circulating endothelial progenitor cells; and the presence of circulating endothelial cells were evaluated. Counts and frequencies of intermediate monocytes, but not glycaemia parameters, were associated with the severity of atherosclerosis in diabetic CAD patients (rs = 0.689; p = 0.001 and rs = 0.632; p = 0.002, respectively). Frequency of Tie2+ cells was lower in classical than in non-classical monocytes in CAD patients (p = 0.007), while in patients with association of CAD and T2DM, differences between Tie2+ monocytes subsets disappeared (p = 0.080). Circulating endothelial cells were determined in 100% of CAD+T2DM patients, and counts of CD14++CD16+ monocytes and concentration of TGF-β predicted the presence of circulating endothelial cells (sensitivity 92.3%; specificity 90.9%; AUC = 0.930). Thus, intermediate monocytes represent one of the key determinants of the appearance of circulating endothelial cells in all the patients with CAD, but are associated with the severity of atherosclerosis only in patients with association of CAD and T2DM.

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“…Upon physical and chemical stresses, such as hemodynamic, metabolic, oxidative, or infectious stresses, the injured ECs undergo reversible endothelial activation, favoring a state of increased permeability, pro-inflammation, thrombosis, and vasoconstriction [109]. Endothelial activation notably involves the secretion of inflammatory cytokines, growth factors, and coagulative factors from ECs that upregulate inflammation, angiogenesis, and thrombosis [110,111]. Prolonged or more severe endothelial activation can introduce irreversible injuries, upon which ECs sustain endothelial dysfunction and malfunction in regulating vascular homeostasis.…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Different Mechanisms in Doxorubicin-Induced Cardiomyopathy: Impact of BRCA1 and BRCA2 Mutations

Nguyen,

Frisbee,

Singh

2024

Hearts

Self Cite

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Germline mutations in Breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) cause breast, ovarian, and other cancers, and the chemotherapeutic drug doxorubicin (Dox) is widely used to treat these cancers. However, Dox use is limited by the latent induction of severe cardiotoxicity known as Dox-induced cardiomyopathy, for which there are no specific treatments currently available. Dox is administered into the systemic circulation, where it readily translocates into sub-cellular compartments and disrupts the integrity of DNA. Accumulating evidence indicates that oxidative stress, DNA damage, inflammation, and apoptosis all play a central role in Dox-induced cardiomyopathy. The BRCA1 and BRCA2 proteins are distinct as they perform crucial yet separate roles in the homologous recombination repair of DNA double-strand breaks, thereby maintaining genomic integrity. Additionally, both BRCA1 and BRCA2 mitigate oxidative stress and apoptosis in both cardiomyocytes and endothelial cells. Accordingly, BRCA1 and BRCA2 are essential regulators of pathways that are central to the development of cardiomyopathy induced by Doxorubicin. Despite extensive investigations, there exists a gap in knowledge about the role of BRCA1 and BRCA2 in Doxorubicin-induced cardiomyopathy. Here, we review the previous findings and associations about the expected role and associated mechanisms of BRCA1 and 2 in Dox-induced cardiomyopathy and future perspectives.

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Loss of fatty acid binding protein 3 ameliorates lipopolysaccharide-induced inflammation and endothelial dysfunction

Cited by 8 publications

References 112 publications

The oxidized phospholipid PGPC impairs endothelial function by promoting endothelial cell ferroptosis via FABP3

The oxidized phospholipid PGPC impairs endothelial function by promoting endothelial cell ferroptosis via FABP3

Intermediate Monocytes and Circulating Endothelial Cells: Interplay with Severity of Atherosclerosis in Patients with Coronary Artery Disease and Type 2 Diabetes Mellitus

Different Mechanisms in Doxorubicin-Induced Cardiomyopathy: Impact of BRCA1 and BRCA2 Mutations

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