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玛丽女王大学Thomas Iskratsch招聘2022生物方向CSC博士
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玛丽女王大学Dr Thomas Iskratsch, Prof Julien Gautrot and Dr Helena Azevedo 课题组招聘CSC博士，有意者可以直接联系Iskratsch老师（t.iskratsch@qmul.ac.uk）。 研究内容：详见下文英文部分 课题组老师主页： Dr Thomas Iskratsch：https://www.sems.qmul.ac.uk/staff/t.iskratsch Prof Julien Gautrot：https://www.sems.qmul.ac.uk/staff/j.gautrot Dr Helena Azevedo： https://www.sems.qmul.ac.uk/staff/h.azevedo 申请截至日期：2022年一月25日，优先联系导师的同学会优先考虑。 申请者背景要求：具有项目相关学科的硕士学位（生物工程、细胞生物学、生物物理学或生物材料）并且对项目研究内容感兴趣。 Project title: Intima-on-a-chip to investigate the role of glycosaminoglycans in atherosclerosis Project description: Atherosclerosis, if untreated, is the dominant underlying cause of cardiovascular disease. Development of new therapies is hindered by the still limited understanding of complex mechanisms of atherosclerotic onset and progression. Vascular smooth muscle cells (VSMCs) play a central role in the progression of atherosclerosis. After migrating into the intima, they remodel the extracellular matrix (ECM) and especially secrete proteoglycans (PGs) that affect ECM mechanics and VSMC mechanosensing. Based on our pilot data, we hypothesize a deleterious feed forward loop: after initial pathological events, VSMCs secrete PGs. Their glycosaminoglycan (GAG) chains affect the ECM mechanics and additionally influence mechanosignalling leading to a spiraling disease progression. We have previously set up experimental systems that build the foundation for this work (Swiatlowska et al, BioRxiv, 2021) but details about the involvement of GAGs are elusive. Here we will develop 2D and 3D in vitro models to enable the study of the role of GAGs in VSMC phenotypic switching in detail. The Objectives include: 1) Identification which proteoglycan (domains) and GAG receptors are modulating VSMC mechanosensing on 2D functionalised surfaces; 2) development of a strategy for co-presentation of integrin ligands and GAGs in 3D and perform characterisation of the 3D hydrogels (intima-on-a-chip); 3) Analysis of VSMC phenotype and function in 3D intima-on-a-chip and 4) Analysis of the modulation of VSMC phenotype and function after inhibition of GAG receptors. |
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