Thesis
Investigation of Non-Muscle Myosin II Genes Expression During Lung Development and Homeostasis in Lung Injury Model
Lung is vital to the intricate maintenance of oxygen and carbon dioxide exchange which is regulated
by specialised cell lineages. This regulation involves tight coordination of epithelial cells regulated by
Non-Muscle Myosin II (NM II). Although adult lung cells are typically quiescent, Acute Lung Injury
(ALI) may disturb the homeostasis and cause loss of airway epithelial layer. This will compromise NM
II isoform expression which was believed to be crucial in the regeneration process. It is believed that
isoforms which share functional redundancy may be able to compensate for each other loss.
Therefore, this study aims to investigate the expression of NM II paralog genes (Myh9, Myh10,
Myh14) in developmental and impaired homeostatic conditions as an initial study to elucidate NM II
compensatory mechanisms through localisation and quantification analysis. Results obtained showed
that NM II paralog genes were expressed in specific cells and were upregulated in the alveolar stage.
This suggests that NM II genes might play an important role in inhibiting cell migration during the
alveolar stage. Meanwhile, in the regeneration phase, Myh9 and Myh14 were downregulated
suggesting that epithelial cell migration was prioritised. Myh10 also displayed a compensatory
mechanism in AT2 cells. Further study utilising gene specific knockout mice were recommended to
further elucidate NM II paralog genes compensatory mechanisms. Overall, the exploration of NM II
paralog gene dynamics in lung injury and regeneration offers promising avenues for improving lung
health and disease management.
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