Apoliporotein L3 interferes with endothelial tube formation via regulation of ERK1/2, FAK and Akt signaling pathway

Khalil, Alia; Poelvoorde, Philippe; Fayyad‐Kazan, Mohammad; Rousseau, Alexandre Fontaine; Nuyens, Vincent; Uzureau, Sophie; Biston, Patrick; El-Makhour, Yolla; Badran, Bassam; Antwerpen, Pierre Van; Boudjeltia, Karim Zouaoui; Vanhamme, Luc

doi:10.1016/j.atherosclerosis.2018.10.023

Cited by 9 publications

(12 citation statements)

References 47 publications

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“…Endothelial function decreases during PE, and endothelial dysfunction is a characteristic of atherosclerosis. ApoL3, as a regulator of MAPK and FAK signaling in endothelial cells, has been shown to be involved in angiogenesis in vitro (Khalil et al, 2018). Increased ApoL3 in PE may be a compensatory response to endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Serum proteins differentially expressed in early- and late-onset preeclampsia assessed using iTRAQ proteomics and bioinformatics analyses

Feng

Qin

et al. 2020

PeerJ

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Background Preeclampsia remains a serious disorder that puts at risk the lives of perinatal mothers and infants worldwide. This study assessed potential pathogenic mechanisms underlying preeclampsia by investigating differentially expressed proteins (DEPs) in the serum of patients with early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) compared with healthy pregnant women. Methods Blood samples were collected from four women with EOPE, four women with LOPE, and eight women with normal pregnancies, with four women providing control samples for each preeclampsia group. Serum proteins were identified by isobaric tags for relative and absolute quantitation combined with liquid chromatography–tandem mass spectrometry. Serum proteins with differences in their levels compared with control groups of at least 1.2 fold-changes and that were also statistically significantly different between the groups at P < 0.05 were further analyzed. Bioinformatics analyses, including gene ontology and Kyoto Encyclopedia of Genes and Genomes signaling pathway analyses, were used to determine the key proteins and signaling pathways associated with the development of PE and to determine those DEPs that differed between women with EOPE and those with LOPE. Key protein identified by mass spectrometry was verified by enzyme linked immunosorbent assay (ELISA). Results Compared with serum samples from healthy pregnant women, those from women with EOPE displayed 70 proteins that were differentially expressed with significance. Among them, 51 proteins were significantly upregulated and 19 proteins were significantly downregulated. In serum samples from women with LOPE, 24 DEPs were identified , with 10 proteins significantly upregulated and 14 proteins significantly downregulated compared with healthy pregnant women. Bioinformatics analyses indicated that DEPs in both the EOPE and LOPE groups were associated with abnormalities in the activation of the coagulation cascade and complement system as well as with lipid metabolism. In addition, 19 DEPs in the EOPE group were closely related to placental development or invasion of tumor cells. Downregulationof pregnancy-specific beta-1-glycoprotein 9 (PSG9) in the LOPE group was confirmed by ELISA. Conclusion The pathogenesis of EOPE and LOPE appeared to be associated with coagulation cascade activation, lipid metabolism, and complement activation. However, the pathogenesis of EOPE also involved processes associated with greater placental injury. This study provided several new proteins in the serum which may be valuable for clinical diagnosis of EOPE and LOPE, and offered potential mechanisms underpinning the development of these disorders.

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Section: Discussionmentioning

confidence: 99%

Serum proteins differentially expressed in early- and late-onset preeclampsia assessed using iTRAQ proteomics and bioinformatics analyses

Feng

Qin

et al. 2020

PeerJ

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“…Pintus et al reported that activation of the PKC/Raf/MEK/ERK pathway could regulate blood lipid levels and increase the risk of atherosclerosis by increasing the expression of native LDL and E2F-1. 32 The activation of ERK1/2 plays an important role in this pathway 33,34 and inhibition of ERK1/2 activation can inhibit the phosphorylation of MAPK, thereby regulating cell proliferation and migration. In addition, the activation of ERK1/2 can increase the expression of the downstream nuclear transcription factor NF-κB and the cell cycle proteins, such as Cyclin D1, which leads to a change in cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

<p>Inhibitory Effect of Curcumin on Artery Restenosis Following Carotid Endarterectomy and Its Associated Mechanism in vitro and in vivo</p>

Zhang

Yang

et al. 2020

DDDT

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Objective: The present study aimed to assess the effect of curcumin (Cur) on carotid artery restenosis following carotid endarterectomy (CEA) and its associated mechanism in vivo and in vitro. Methods: Ang II was used to induce excessive proliferation of rabbit aortic smooth muscle cells (CCC-SMC-1) in order to establish a hemadostenosis cell model. Similarly, the animal model of carotid artery restenosis was established by carotid artery gas drying injury combined with high-fat feed prior to CEA. CCC-SMC-1 cells and animals were treated by Cur and its effects on neointimal hyperplasia, inflammation and oxidative stress were detected and observed. The proteins that were associated with the Raf/MEK/ERK pathway were detected in cells and rabbit carotid artery tissues. Results: Cur inhibited the proliferation of smooth muscle cells and neointimal formation and reduced the inflammation and oxidative stress indices. Concomitantly, Cur reduced the phosphorylation of the Raf/MEK/ERK pathway proteins. Conclusion: Cur could inhibit carotid restenosis following CEA by inhibiting the activation of the Raf/MEK/ERK pathway.

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“…Recently, Gaudet et al [31] reported that IFN-γinduced APOL3 was a potent bactericidal agent protecting multiple non-immune barrier cell types against infection. Besides, the phenotype of APOL3 KO podocytes exhibits striking similarities to that resulting from cancer metastasis, with strong reduction of cellular adherence and increase in cell motility [27]. In cancer, the APOL3-controlled NCS-1 is known to promote motility, metastatic spread and survival of cancer cells [32,33].…”

Section: Discussionmentioning

confidence: 99%

“…As an apolipoprotein, APOL3 was reported in many cell types, such as endothelial cells [27], podocyte [28], neurones [29], trypanosomes [30]. Recently, Gaudet et al [31] reported that IFN-γinduced APOL3 was a potent bactericidal agent protecting multiple non-immune barrier cell types against infection.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein L3 enhances CD8+ T cell antitumor immunity of colorectal cancer by promoting LDHA-mediated ferroptosis

Lv¹,

Tang²,

Xu³

et al. 2023

Int. J. Biol. Sci.

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Aim: Colorectal cancer (CRC) is the leading cause of cancer associated death worldwide and immune checkpoint blockade therapy only benefit a small set of CRC patients. Tumor ferroptosis of CRC reflected immune-activation in our previous findings. Understanding the mechanisms underlying how to bolster CD8+ T cells function through ferroptosis in CRC tumor microenvironment (TME) will greatly benefit cancer immunotherapy. Methods: Genes between ferroptosis and CD8+ T cell function in CRC were screened through Cox, WGCNA and differential expression analysis. Immunohistochemistry and Immunofluorescence analysis were performed. Co-immunoprecipitation were performed to determine protein-protein interaction, mRNA level was determined by qRT-PCR. RSL3 was used to induce ferroptosis, and ferroptosis levels were evaluated by measuring Transmission Electron Microscope analysis, MDA, Fe 2+ level and cell viability. Results: We screened APOL3 as the significant modulator for ferroptosis-related CD8+ infiltration in CRC. Next, by in vitro and in vivo, we found that increased APOL3 expression was positively correlated with sensitivity to ferroptosis and antitumor ability of CD8+ T cells. Next, we demonstrated that APOL3 can binds LDHA and promote its ubiquitylation-related degradation. Then, based on in vivo analysis and tumor specimen, we discovered the APOL3-LDHA axis can facilitate the tumor ferroptosis and cytotoxic ability of CD8+ T cells through increased IFNγ and decreased lactic acid concentration. Conclusion:The present study demonstrated that APOL3 promotes ferroptosis and immunotherapy in colorectal cancer cells. The present work provides us with a novel target to overcome drug resistance to ferroptosis and immunotherapy.

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Apoliporotein L3 interferes with endothelial tube formation via regulation of ERK1/2, FAK and Akt signaling pathway

Cited by 9 publications

References 47 publications

Serum proteins differentially expressed in early- and late-onset preeclampsia assessed using iTRAQ proteomics and bioinformatics analyses

Serum proteins differentially expressed in early- and late-onset preeclampsia assessed using iTRAQ proteomics and bioinformatics analyses

<p>Inhibitory Effect of Curcumin on Artery Restenosis Following Carotid Endarterectomy and Its Associated Mechanism in vitro and in vivo</p>

Apolipoprotein L3 enhances CD8+ T cell antitumor immunity of colorectal cancer by promoting LDHA-mediated ferroptosis

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