Haem Oxygenase-1 And Apoptosis

Cell proliferation, differentiation, apoptosis and senescence is the most important life activity of cell. They are contect and refrain each other. The apoptosis was stimulied by many kinds singles of surround environment, and the cell spontaneous death by gene regulatory. This is an important role in cell proliferation, differentiationand many pathogenesis.It is an important balanceable factor in lives grow up. Apoptosis is a way to automatically end life process by initiatively by gene regulatory. Apoptosis is key role in multiple cell biology's normally individual grow up keeping self-balanceable and rejecting interferon of surround environment . Living being clean no more requirement cell ,but no inflammation. In the tissures of mature ripe individual apoptosis can cell's naturally renew, clean be infected with pathogen. In other hand ,the disproportion of apoptosis include mistake stimuli or getting disease by inhibit. HO-1 is a heat-shock protein that is induced by stressful stimuli. Acting in concert with cytochrone P450 reductase (CPR) and biliverdin reductase. HO-1 converts haem into bilirubin, carbon monoxide and iron, but these three products are toxic. Thus,HO-1 has a protect function in the cellular response to stress, when serum deprivation induce cell apoptosis. HO-1 is sufficient to protect cells from toxicity elicited by serum deprivation, protect intracellular proteins from denaturation. Studies the important role of HO-1 in cell apoptosis, we can understand affect factor of apoptosis. Protecting cell normally apoptosis, elicting no necessary senescence factor make living being normally and healthly lived. We use primary cultures of from HO-1 fibroblasts and their wild-type littermates fibroblasts CPR-293 and HO1/CPR-293 cell lines. Inducing cellular stress by serum deprivation, staurosprine treatment or etoposide treatment and physiological stressors.1,Induce cell apoptosis by serum deprivationSerum deprivation is a widely used model of cellular stress that is associated with depletion of growth factors and nutrients, and many elicit cell death through oxidative stress and subsequent apoptosis. We compared wild-type and HO-1-1- cell following serum deprivation. Before serum deprivation, wild-type and HO-1-1-cells showed similar nuclear morphology and a low rate of spontaneous apoptosis as detected by staining with Hoechst 33258. However, following serum deprivation, most nuclei from HO-1-1-cells were smalland condensed, DNA ladder formation, whereas nuclei from wild-type cells remained normal. This showed HO-1 is a cytoprotective in cell apoptosis.We treated wild-type and HO1 cell with staurosporine or etoposide for 4-24h and monitored cell death by DNA fragmentation using agarose-gel electrophoresis. After 20h of treatment with either staurosporine or etoposide, we observed large DNA fragments in HO-1-1- cells but not in wild-type cells. These date indicate that HO-1 is necessary to protect cells from apoptotic cell death. Particularly in response to serum deprivation.2,Physiological stressors induce apoptosis To minic HO-1 induction in the absence of the induction of other proteins, we generated cell lines . Showing stable overexpression of either CPR alone or HO-1 and CPR together, as CPR co-expression is required to achieve maximal increase in HO-1 enzymatic activity. After 4 days of serum deprivation, CPR-293 cells exhibited substantial nuclear condensation and fragmentation DNA laddering but HO-1/CPR-293 cells was not apparent. Thus HO-1 expression is sufficient to protect cells from serum deprivation-induced apoptosis.In the experiment, we used primary cultures of from HO-1 fibroblasts and their wild-type littermates fibroblasts CPR-293 cell and HO!/CPR-293 cell by serum deprivation, staurosporine treatment or etoposide treatment and physiological stress induce cellular stress to induce cell apoptosis. In the condition most nucleir from HO-1-1- cell were small and condensed DNA ladder formation than wild-type cells. The results showed HO-1...