Notch, BMP and WNT/β-catenin network is impaired in endothelial cells of the patients with thoracic aortic aneurysm

Kostina, Aleksandra; Björk, Hanna; Ignatieva, Elena; Irtyuga, Olga; Uspensky, Vladimir; Semenova, Daria; Maleki, Shohreh; Tomilin, Alexey; Моисеева, О. М.; Franco‐Cereceda, Anders; Гордеев, М. Л.; Faggian, Giuseppe; Kostareva, Anna; Eriksson, Per; Malashicheva, Anna

doi:10.1016/j.atherosclerosissup.2018.08.002

Cited by 23 publications

(14 citation statements)

References 29 publications

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“…Hyperexpression of oncogenic miRNAs or genetic loss of anti-tumor miRNAs is demonstrated to be associated with human cancer and function as drivers of metastasis and tumor growth in mouse models (6). Previous studies revealed that glioblastoma (7) and colon cancer cells (8) are known to have miR-338-3p serve critical roles, an aberrant miRNA that are commonly seen as a pivotal player in a variety of different types of cancer, including renal cell carcinoma (9), myeloma (10), GH-producing pituitary adenomas (11), and non-small cell lung cancer (12). miR-338-3p could lead to attenuation of multiple biological behaviors including proliferation, invasion and migration though targeting the 3′untranslated region (UTR) of mRNA (13).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑338‑3p suppresses cell proliferation, migration and invasion in human malignant melanoma by targeting MACC1

Zhang¹,

Li²,

Wang³

et al. 2019

Exp Ther Med

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Malignant melanoma (MM) is the most aggressive form of skin cancer originating from melanocytes with increased proliferative and metastatic ability. Previous studies have revealed that microRNA-338-3p (miR-338-3p) functions as a tumor suppressor in several types of cancer, including cervical cancer, renal cell carcinoma and thyroid cancer. However, the function and mechanism underlying the action of miR-383-3p in MM remain unclear. In the study, aberrant downregulation of miR-338-3p was observed in 60 pairs of MM and adjacent non-tumor tissue using quantitative polymerase chain reaction assay. Decreased miR-383-3p expression was associated with advanced clinical stage (P<0.05) and lymph node metastasis (P<0.001). The overexpression of miR-338-3p in A375 and G361 cells suppressed cell proliferation and migration using MTT, colony formation, wound healing and transwell assays. Mechanistically, MACC1 was identified as a direct target for miR-338-3p using bioinformatics prediction and dual-luciferase assays. Furthermore, MACC1 expression was significantly increased and inversely correlated with the levels of miR-338-3p in MM tissues. More importantly, restoration of MACC1 resulted in reversed the inhibitory effects of miR-338-3p overexpression on MM cells by altering the expression levels of PCNA and epithelial-mesenchymal transition (EMT)-associated proteins. These results suggest that miR-338-3p functions as a novel tumor suppressor, at least in part, via targeting MACC1 and suggest that miR-338-3p may serve as a potential target for treatment of MM patients.

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Section: Introductionmentioning

confidence: 99%

MicroRNA‑338‑3p suppresses cell proliferation, migration and invasion in human malignant melanoma by targeting MACC1

Zhang¹,

Li²,

Wang³

et al. 2019

Exp Ther Med

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“…Dysregulation of the TGF-β and BMP signaling pathway, previously described for TAA patients [8,[60][61][62], was also shown for AAA patients in our IPA analysis. While we found most components of the TGF-β signaling pathway significantly upregulated, most components of the BMP-pathway were downregulated in AAA compared to AOD.…”

Section: Discussionsupporting

confidence: 85%

Inflammation and TGF-β Signaling Differ between Abdominal Aneurysms and Occlusive Disease

IJpma

Riet

Luijtgaarden

et al. 2019

JCDD

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Abdominal aortic aneurysms (AAA), are usually asymptomatic until rupture causes fatal bleeding, posing a major vascular health problem. AAAs are associated with advanced age, male gender, and cardiovascular risk factors (e.g. hypertension and smoking). Strikingly, AAA and AOD (arterial occlusive disease) patients have a similar atherosclerotic burden, yet develop either arterial dilatation or occlusion, respectively. The molecular mechanisms underlying this diversion are yet unknown. As this knowledge could improve AAA treatment strategies, we aimed to identify genes and signaling pathways involved. We compared RNA expression profiles of abdominal aortic AAA and AOD patient samples. Based on differential gene expression profiles, we selected a gene set that could serve as blood biomarker or as pharmacological intervention target for AAA. In this AAA gene list we identified previously AAA-associated genes COL11A1, ADIPOQ, and LPL, thus validating our approach as well as novel genes; CXCL13, SLC7A5, FDC-SP not previously linked to aneurysmal disease. Pathway analysis revealed overrepresentation of significantly altered immune-related pathways between AAA and AOD. Additionally, we found bone morphogenetic protein (BMP) signaling inhibition simultaneous with activation of transforming growth factor β (TGF-β) signaling associated with AAA. Concluding our gene expression profiling approach identifies novel genes and an interplay between BMP and TGF-β signaling regulation specifically for AAA.

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“…Namely, 293T cells were transfected with envelope-encoding pMD2.G (2.5 μg), packaging psPAX2 (7.5 μg), and either pHAGE2-tetO-miniCMV-hOct4-F2A-hKlf4-IRES-hSox2-E2A-hcMyc-W-loxP (OKSM), FUW-M2rtTA (hereafter rtTA), or EnvΔR-IRES-tdTomato plasmids (10 μg) by polyethylenimine hydrochloride (PEI 40 kDa, 40 μg) transfection method [32,33]. Lentiviruses in cell culture supernatant were collected and processed, as described elsewhere [33,34,35,36].…”

Section: Methodsmentioning

confidence: 99%

Transfer of Synthetic Human Chromosome into Human Induced Pluripotent Stem Cells for Biomedical Applications

Sinenko

Skvortsova

Liskovykh

et al. 2018

Cells

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AlphoidtetO-type human artificial chromosome (HAC) has been recently synthetized as a novel class of gene delivery vectors for induced pluripotent stem cell (iPSC)-based tissue replacement therapeutic approach. This HAC vector was designed to deliver copies of genes into patients with genetic diseases caused by the loss of a particular gene function. The alphoidtetO-HAC vector has been successfully transferred into murine embryonic stem cells (ESCs) and maintained stably as an independent chromosome during the proliferation and differentiation of these cells. Human ESCs and iPSCs have significant differences in culturing conditions and pluripotency state in comparison with the murine naïve-type ESCs and iPSCs. To date, transferring alphoidtetO-HAC vector into human iPSCs (hiPSCs) remains a challenging task. In this study, we performed the microcell-mediated chromosome transfer (MMCT) of alphoidtetO-HAC expressing the green fluorescent protein into newly generated hiPSCs. We used a recently modified MMCT method that employs an envelope protein of amphotropic murine leukemia virus as a targeting cell fusion agent. Our data provide evidence that a totally artificial vector, alphoidtetO-HAC, can be transferred and maintained in human iPSCs as an independent autonomous chromosome without affecting pluripotent properties of the cells. These data also open new perspectives for implementing alphoidtetO-HAC as a gene therapy tool in future biomedical applications.

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Notch, BMP and WNT/β-catenin network is impaired in endothelial cells of the patients with thoracic aortic aneurysm

Cited by 23 publications

References 29 publications

MicroRNA‑338‑3p suppresses cell proliferation, migration and invasion in human malignant melanoma by targeting MACC1

MicroRNA‑338‑3p suppresses cell proliferation, migration and invasion in human malignant melanoma by targeting MACC1

Inflammation and TGF-β Signaling Differ between Abdominal Aneurysms and Occlusive Disease

Transfer of Synthetic Human Chromosome into Human Induced Pluripotent Stem Cells for Biomedical Applications

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