MECP2 is upregulated in alveolar type 2 cells when exposed to cigarette smoke extract.

Sietsma, Mart (2022) MECP2 is upregulated in alveolar type 2 cells when exposed to cigarette smoke extract. Bachelor's Research Project (period 2b), Biology.

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Abstract

Idiopathic Pulmonary Fibrosis is a chronic inflammatory disease which is associated with high levels of collagen accumulation in the lungs which causes lung tissue to stiffen up and thicken. There is not yet enough evidence to support a conclusive cause for the disease hence the term ‘idiopathic’. What is known is that myofibroblasts, which are differentiated from fibroblasts, produce these excessive amounts of collagen when the lung tissue is damaged by for example cigarette smoke and it is known that cigarette also plays a role in altering expression levels of certain genes in alveolar lung cells(6). In a previous study by Biao Hu(2) et al., the role of the MECP2 gene was elucidated to be playing an important regulatory role in this differentiation process. The MECP2 gene is expressed in the lung epithelial cells and regulates alpha smooth muscle actin which drives fibroblasts differentiation(2). In this study, alveolar type 2 cells were tested for MECP2 expression under different levels of cigarette smoke exposure. A SA-β-gal activity staining was done to find out the proportion of cells that went senescent after the cigarette smoke exposure at different levels. Following up was a qPCR to measure the expression level of MECP2 in these cells. The data found in this study point towards the conclusion that expression of MECP2 is upregulated at higher concentrations of smoke exposure to a certain point where cells were dying off and could not express anything anymore.

Item Type:	Thesis (Bachelor's Research Project (period 2b))
Supervisor name:	Burgess, J.K.
Degree programme:	Biology
Thesis type:	Bachelor's Research Project (period 2b)
Language:	English
Date Deposited:	27 Jun 2022 12:46
Last Modified:	27 Jun 2022 12:46
URI:	https://fse.studenttheses.ub.rug.nl/id/eprint/27414

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