dc.contributor.author | Chou, Tzu-wen Joy | |
dc.date.accessioned | 2010-09-14T21:32:57Z | |
dc.date.available | 2010-09-14T21:32:57Z | |
dc.date.issued | 2009 | |
dc.identifier.citation | Chou, T. J. (2009). Establishment of THP-1 Monocytes with Compromised Mitochondrial Functions (Thesis, Master of Science (MSc)). The University of Waikato, Hamilton, New Zealand. Retrieved from https://hdl.handle.net/10289/4569 | en |
dc.identifier.uri | https://hdl.handle.net/10289/4569 | |
dc.description.abstract | The process of inflammation is important for both normal health and in a number of diseases, such as metabolic disorders, autoimmune diseases, and neurodegenerative diseases. Mitochondria are vital for the functioning of all cells. It had been implicated as a key player in inflammatory processes, especially through reactive oxygen species as signals of various immune responses. This study aimed to establish a THP-1 cell line with compromised mitochondrial functions, using antimycin A as a Complex III inhibitor, and to investigate the role of mitochondrial stress, as monitored by the expression of Hsp60, in inflammatory processes. High concentrations of antimycin A (100 and 200 μM) were cytotoxic to THP-1 monocytes that they were rapidly killed within 48 hours of exposure. Lower concentrations of antimycin A (5, 10, 25 and 50 μM) gave growth inhibition effects to THP-1 monocytes. Pyruvate and uridine were used with an intention of rescuing the THP-1 cell growth at lower antimycin A concentrations. The THP-1 monocytes treated with antimycin A with uridine and pyruvate showed more growth compared to the ones without uridine and pyruvate supplement. Yet this difference is insignificant statistically. The expressions of Hsp60 and TNF-α at the mRNA level was monitored using reverse transcriptase polymerase chain reaction. Hsp60 expression from THP-1 monocytes only showed some minor fluctuations in different antimycin A concentrations, regardless of uridine and iii pyruvate supplement, indicating the stress mitochondrial response was unobvious. On the other hand, TNF-α expression was dramatically down-regulated in THP-1 monocytes treated with antimycin A only compared to the untreated control and ones supplemented with uridine and pyruvate. These results suggest that antimycin A may have inhibition effect towards TNF-α expression, and uridine and pyruvate could also have other functions in THP-1 monocytes apart from redox rescue compounds. Yet the mitochondrial stress response shown by Hsp60 induction still remains to be further investigated. | en_NZ |
dc.format.mimetype | application/pdf | |
dc.language.iso | en | |
dc.publisher | The University of Waikato | |
dc.rights | All items in Research Commons are provided for private study and research purposes and are protected by copyright with all rights reserved unless otherwise indicated. | |
dc.subject | THP-1 monocytes | en_NZ |
dc.subject | compromised mitochondrial functions | en_NZ |
dc.subject | cell culture model | en_NZ |
dc.subject | redox rescue | en_NZ |
dc.subject | Hsp60 | en_NZ |
dc.subject | inflammation | en_NZ |
dc.title | Establishment of THP-1 Monocytes with Compromised Mitochondrial Functions | en_NZ |
dc.type | Thesis | |
thesis.degree.discipline | Biological Sciences | |
thesis.degree.grantor | University of Waikato | |
thesis.degree.level | Masters | |
thesis.degree.name | Master of Science (MSc) | en_NZ |
uow.identifier.adt | http://adt.waikato.ac.nz/public/adt-uow20090310.135249/index.html | |
pubs.place-of-publication | Hamilton, New Zealand | en_NZ |