Molecular mechanism of apoptosis and cell cycle arrest in G1 phase in HepG2 cells infected with Klebsiella pneumoniae

• Main Authors: Pei Ying Yang, 楊佩穎
• Other Authors: J. H. Wu
• Format: Others
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/39515702690553416674

碩士 === 長庚大學 === 生物醫學研究所 === 99 === Klebsiella pneumoniae（KP）, a gram-negative bacterium, normal intestinal microflora, usually causes nosocomial infection. In Taiwan. KP infection causes severe liver abscess, especially in patients with diabetes mellitus. Many researches indicate that cells execute apoptosis and necrosis during bacterial infection, and furthermore influence the cell cycle. But the molecular mechanism is still not clear in KP. Previous study in our laboratory found that chromatin condensation, DNA fragmentation and accumulation sub-G1 phase in KP infected HepG2 cells. My results demonstrated that cell viability decreased during KP infection, flowcytometry data showed increased PS exposure, ATP analysis showed that ATP concentration was dramatically decreased after 4 hours KP infection. Apoptosis：The AIF and Endo G were released from mitochondria and translocated to nucleus post-infection. Cyt C also released from mitochondria. Bad, Apaf-1 and m-Calpain were increasd post KP infection. Caspase-9 and Caspase-7 activation, PARP inactivation and α-fodrin cleavage, DFF40 increase and DFF45 decrease were observed during KP infection. Cell cycle molecules including Cyclin D1, Cyclin D2, p-Rb and E2F were decreased during KP infection. Moreover, p-p53 was increased post KP infection. Our data suggest that the KP infection causes HepG2 cells to undergo early apoptosis and late necrosis, and the decrease in the molecules involved in the G1 checkpoint contributes the cell cycle arrest in G1 phase.