Transmembrane emp24 domain proteins in development and disease.

Aber, Rachel; Chan, Wesley; Mugisha, Sevane; Jerome-Majewska, Loydie A.

doi:10.1017/s0016672319000090

Cited by 44 publications

(51 citation statements)

References 90 publications

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“…Therefore, in fibroblasts cultured in 3D, we observed a UV-induced increase in the expression of VDAC and the complete elimination of this effect following treatment of the cells with rutin and ascorbic acid. However, the role of TMED following UVA irradiation is still unclear; the downregulation of this protein by rutin and ascorbic acid may prevent metabolic dysfunctions [ 67 ].…”

Section: Discussionmentioning

confidence: 99%

Natural Exogenous Antioxidant Defense against Changes in Human Skin Fibroblast Proteome Disturbed by UVA Radiation

Gęgotek

Domingues

2020

Oxidative Medicine and Cellular Longevity

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Daily exposure of the skin to UVA radiation causes oxidative modifications to cellular components and biomolecules. These include proteins involved in the metabolism and cytoprotection of fibroblasts, and their modification can contribute to the disruption of cell function and the development of skin disorders. Therefore, there remains a need for highly active cytoprotective compounds with antioxidant properties. The purpose of this study was to investigate the effect of ascorbic acid on the activity of rutin against UVA-induced changes in the proteome of human fibroblasts. All analyses were carried out on fibroblasts cultured in a three-dimensional system exposed to UVA radiation and incubated with rutin and ascorbic acid. Their proteomic profile was analyzed using nano-HPLC, which revealed 150 proteins whose expression was significantly altered between treatment conditions. UVA radiation led to changes in the expression of 82 proteins. However, some of these changes were mitigated by rutin and ascorbic acid separately (23 and 25 proteins, respectively) and rutin and ascorbic acid together (23 proteins). UVA radiation has led to the upregulation of proteins involved in gene expression, catalytic processes and antioxidant pathways, and downregulation of proteins with binding activity. Nevertheless, rutin and ascorbic acid used separately or together have countered these changes to varying degrees. Moreover, rutin and ascorbic acid stimulated fibroblasts irradiated by UVA to increase the expression of the signalling molecules responsible for the opening of the transmembrane channels. In the context of the results obtained, the observed cytoprotective effect of the cooperation of rutin and ascorbic acid results not only from the overlapping properties of the compounds. The effect of rutin alone is probably inhibited by its limited bioavailability. Therefore, its interaction with ascorbic acid increases membrane penetration and improves the cytoprotective effect on skin fibroblasts.

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Section: Discussionmentioning

confidence: 99%

Natural Exogenous Antioxidant Defense against Changes in Human Skin Fibroblast Proteome Disturbed by UVA Radiation

Gęgotek

Domingues

2020

Oxidative Medicine and Cellular Longevity

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“…In the endoplasmic reticulum (ER), the conserved cysteine of Wnts is palmitoylated by Porcupine to a lipid-bound form that is also an active form [ 80 ]. The ER-to-Golgi trafficking of Wnts is mediated by the p24 protein family (such as TMED2/CHOp24, TMED4/éclair, and TMED5/opossum) [ 81 – 83 ]. Then, lipid-modified Wnts are transported by GPR177 (also known as Wntless/Evenness/Interrupted/Sprinter) [ 84 – 87 ] in an endosome-dependent manner [ 88 – 90 ] and secreted into the extracellular matrix using exosomes as potent carriers [ 10 , 91 – 93 ].…”

Section: Introductionmentioning

confidence: 99%

Wnt signaling in breast cancer: biological mechanisms, challenges and opportunities

et al. 2020

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Wnt signaling is a highly conserved signaling pathway that plays a critical role in controlling embryonic and organ development, as well as cancer progression. Genome-wide sequencing and gene expression profile analyses have demonstrated that Wnt signaling is involved mainly in the processes of breast cancer proliferation and metastasis. The most recent studies have indicated that Wnt signaling is also crucial in breast cancer immune microenvironment regulation, stemness maintenance, therapeutic resistance, phenotype shaping, etc. Wnt/β-Catenin, Wnt–planar cell polarity (PCP), and Wnt–Ca2+ signaling are three well-established Wnt signaling pathways that share overlapping components and play different roles in breast cancer progression. In this review, we summarize the main findings concerning the relationship between Wnt signaling and breast cancer and provide an overview of existing mechanisms, challenges, and potential opportunities for advancing the therapy and diagnosis of breast cancer.

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“…In addition to aforementioned genes, the coding gene for transmembrane emp24 domain-containing protein 4 ( TMED4 ) was downregulated in SARS-CoV infection. TMED4 can interact with interleukin-1 receptor-like 1 so the production of proinflammatory cytokines including IL-6 and IL-8 was induced [ 63 ]. Another downregulated gene in the SARS-CoV infection was transmembrane protein 184A ( TMEM184A ), which was necessary for heparin responses in endothelial cells and vascular smooth muscle cells with interruption effect on the anti-inflammatory responses of endothelial cells to heparin [ 64 ].…”

Section: Discussionmentioning

confidence: 99%

Expansion of Single Cell Transcriptomics Data of SARS-CoV Infection in Human Bronchial Epithelial Cells to COVID-19

et al. 2020

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Background Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 19 (COVID-19) that was emerged as a new member of coronaviruses since December 2019 in Wuhan, China and then after was spread in all continentals. Since SARS-CoV-2 has shown about 77.5% similarity to SARS-CoV, the transcriptome and immunological regulations of SARS-CoV-2 was expected to have high percentage of overlap with SARS-CoV. Results In this study, we applied the single cell transcriptomics data of human bronchial epithelial cells (2B4 cell line) infected with SARS-CoV, which was annotated in the Expression Atlas database to expand this data to COVID-19. In addition, we employed system biology methods including gene ontology (GO) and Reactome pathway analyses to define functional genes and pathways in the infected cells with SARS-CoV. The transcriptomics analysis on the Expression Atlas database revealed that most genes from infected 2B4 cell line with SARS-CoV were downregulated leading to immune system hyperactivation, induction of signaling pathways, and consequently a cytokine storm. In addition, GO:0016192 (vesicle-mediated transport), GO:0006886 (intracellular protein transport), and GO:0006888 (ER to Golgi vesicle-mediated transport) were shown as top three GOs in the ontology network of infected cells with SARS-CoV. Meanwhile, R-HAS-6807070 (phosphatase and tensin homolog or PTEN regulation) showed the highest association with other Reactome pathways in the network of infected cells with SARS-CoV. PTEN plays a critical role in the activation of dendritic cells, B- and T-cells, and secretion of proinflammatory cytokines, which cooperates with downregulated genes in the promotion of cytokine storm in the COVID-19 patients. Conclusions Based on the high similarity percentage of the transcriptome of SARS-CoV with SARS-CoV-2, the data of immunological regulations, signaling pathways, and proinflammatory cytokines in SARS-CoV infection can be expanded to COVID-19 to have a valid platform for future pharmaceutical and vaccine studies.

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Transmembrane emp24 domain proteins in development and disease.

Cited by 44 publications

References 90 publications

Natural Exogenous Antioxidant Defense against Changes in Human Skin Fibroblast Proteome Disturbed by UVA Radiation

Natural Exogenous Antioxidant Defense against Changes in Human Skin Fibroblast Proteome Disturbed by UVA Radiation

Wnt signaling in breast cancer: biological mechanisms, challenges and opportunities

Expansion of Single Cell Transcriptomics Data of SARS-CoV Infection in Human Bronchial Epithelial Cells to COVID-19

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