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33. c-Abl antagonizes the YAP oncogenic function.

Author

Keshet, R, Adler, J, Ricardo Lax, I, Shanzer, M, Porat, Z, Reuven, N, and Shaul, Y

Subjects
ONCOGENES, CANCER genes, DNA damage, PHOSPHORYLATION, TRANSCRIPTION factors, CELL transformation
Abstract

YES-associated protein (YAP) is a central transcription coactivator that functions as an oncogene in a number of experimental systems. However, under DNA damage, YAP activates pro-apoptotic genes in conjunction with p73. This program switching is mediated by c-Abl (Abelson murine leukemia viral oncogene) via phosphorylation of YAP at the Y357 residue (pY357). YAP as an oncogene coactivates the TEAD (transcriptional enhancer activator domain) family transcription factors. Here we asked whether c-Abl regulates the YAP-TEAD functional module. We found that DNA damage, through c-Abl activation, specifically depressed YAP-TEAD-induced transcription. Remarkably, c-Abl counteracts YAP-induced transformation by interfering with the YAP-TEAD transcriptional program. c-Abl induced TEAD1 phosphorylation, but the YAP-TEAD complex remained unaffected. In contrast, TEAD coactivation was compromised by phosphomimetic YAP Y357E mutation but not Y357F, as demonstrated at the level of reporter genes and endogenous TEAD target genes. Furthermore, YAP Y357E also severely compromised the role of YAP in cell transformation, migration, anchorage-independent growth, and epithelial-to-mesenchymal transition (EMT) in human mammary MCF10A cells. These results suggest that YAP pY357 lost TEAD transcription activation function. Our results demonstrate that YAP pY357 inactivates YAP oncogenic function and establish a role for YAP Y357 phosphorylation in cell-fate decision. [ABSTRACT FROM AUTHOR]

Published
2015
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39. Co-expression of fibulin-5 and VEGF165increases long-term patency of synthetic vascular grafts seeded with autologous endothelial cells

Author

Preis, M, Schneiderman, J, Koren, B, Ben-Yosef, Y, Levin-Ashkenazi, D, Shapiro, S, Cohen, T, Blich, M, Israeli-Amit, M, Sarnatzki, Y, Gershtein, D, Shofti, R, Lewis, B S, Shaul, Y, and Flugelman, M Y

Abstract

Small caliber synthetic vascular grafts are commonly used for bypass surgery and dialysis access sites but have high failure rates because of neointima formation and thrombosis. Seeding synthetic grafts with endothelial cells (ECs) provides a biocompatible surface that may prevent graft failure. However, EC detachment following exposure to blood flow still remains a major obstacle in the development of biosynthetic grafts. We tested the hypothesis that induced expression by the seeded EC, of vascular endothelial growth factor165(VEGF165) and of fibulin-5, an extracellular matrix glycoprotein that has a crucial role in elastin fiber organization and increase EC adherence to surfaces, may improve long-term graft patency. Autologous ECs were isolated from venous segments, and were transduced with retroviral vectors expressing fibulin-5 and VEGF165. The modified cells were seeded on expanded polytetrafluoroethylene (ePTFE) grafts and implanted in a large animal model. Three months after transplantation, all grafts seeded with modified EC were patent on a selective angiography, whereas only a third of the control grafts were patent. Similar results were shown at 6 months. Thus, seeding ePTFE vascular grafts with genetically modified EC improved long-term small caliber graft patency. The biosynthetic grafts may provide a novel therapeutic modality for patients with peripheral vascular disease and patients requiring vascular access for hemodialysis.

Published
2016
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43. Pleurisy Can Cause Chest Wall Tenderness: A Case Report

Author

Shaul Yaari, Elchanan Juravel, Murad Daana, and Samuel Noam Heyman

Subjects
pulmonary embolism, chest pain, pleura, symptoms, physical examination, Medicine
Abstract

Stab-like localized chest pain, aggravated by breathing, is compatible with pleuritic pain or with aching related to chest wall abnormalities. Local tenderness inflicted by palpation helps to differentiate pleuritic from musculoskeletal chest pain and serves as a principal accessory manoeuvre in the algorithm of chest pain evaluation. Herein, we report the case of a 27-year-old patient with pulmonary thromboembolism and right lower lobe consolidation/atelectasis. The patient presented with right-sided chest pain, radiating to the shoulder, related to pleural irritation, yet associated with confounding intense chest wall tenderness and guarding, also involving the costovertebral angle. We propose that spinal reflex-related chest wall tenderness was involved, similar to peritoneal signs evoked by irritation of the parietal peritoneum. This case report illustrates that localized chest wall tenderness and guarding, triggered by palpation, may not serve as unequivocal indicators of musculoskeletal pain, and could be unrecognized features of pleuritic chest pain also.

Published
2020
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