Uses
pulmonary function, gene expression, healing and repair process, differentiation, extracellular matrix production, growth factor and cytokine activation, actin reorganization, synthesis of type II collagen, elastin, and proteoglycans, airway remodeling, pharmaceutical development
General Description
HLF provide an excellent model system to study many aspects of human pulmonary function and pathophysiology.
HLF have been utilized in a number of research publications, for example to:
- Demonstrate differential gene expression patterns between fetal and adult lung fibroblasts, in particular showing that fetal fibroblasts express higher level of TGF-β receptor interacting protein 1 (TRIP-1) and consequently are less able to contract collagen than adult lung fibroblasts, leading to better healing of acute injuries in very immature lungs compared to higher levels of fibrosis observed in older patients (Navarro, 2009), and additionally discover that TRIP-1 regulates lung fibroblast/myofibroblast trans-differentiation (Nyp, 2014)
- Show that angiotensin II promotes lung fibrosis by activating expression of IL-4, IL-7, and PDGF-D increasing the extracellular matrix formation, and that this process can be blocked by angiotensin receptor inhibitor candesartan (Okada, 2009)
- Determine that phosphorylation of C/EBPβ contributes to lung fibrosis (Buck, 2011)
- Demonstrate that increased tissue rigidity activates toll-like receptor 2 and NF-κB in lung fibroblasts and induces expression of cytokines, CXCL1-3, IL-8 and TNF-α (Zheng, 2011)
- Demonstrate that 2-ethoxyestradiol, a non-estrogenic estradiol metabolite analog, inhibits cell growth and retards the progression of pulmonary fibrosis and hypertension (Tofovic, 2008, 2009)
- Identify the hypoxia-induced ROS/RhoA–ROCK dependent actin reorganization as a mediator of myofibroblast transformation and collagen synthesis in lung fibrosis (Ni, 2013)
