Mitochondrial and cellular heme-dependent proteins as targets for the bioactive function of the heme oxygenase/carbon monoxide system.
ABSTRACT The toxic effect of high concentrations of CO gas in living organisms is coherently typified at biochemical levels by the high affinity of CO for hemoglobin and cytochromes, heme-dependent proteins that are indispensable for oxygen transport and mitochondrial respiration. However, the basal production of CO during heme degradation and the ability of heme oxygenase-1 (HO-1) to increase CO availability pose the question of how this gaseous molecule interacts with metal centers within the intracellular milieu to serve as one of the most unconventional signaling mediators. Emerging evidence indicates that the diverse and multifaceted beneficial effects exerted by "low concentrations" of CO cannot be explained solely by the activation of classic prototypic targets (i.e., guanylate cyclase/potassium channels) but entails the dynamic and concerted activation/inhibition of a group of CO-responsive proteins. As the complexity of the temporal and spatial action of CO is progressively being appreciated, this review aims to (a) highlight the current knowledge on certain metal-containing proteins that interact directly with CO; (b) analyze the latest notions on their functional role in response to CO; and finally (c) propose a rational view on the mode these CO targets may interrelate with and be regulated by the HO/CO pathway.
- SourceAvailable from: Lian Li[Show abstract] [Hide abstract]
ABSTRACT: Heat shock protein 32 (Hsp32)/ heme oxygenase-1 (HO-1) is believed to represent a key enzyme for the protection of cells against stress. The anti-apoptotic effect of Hsp32/HO-1 has been attributed to its product carbon monoxide (CO) in many types of cells; however, whether the anti-apoptotic mechanism plays a role in Sertoli cells is not yet clear. We hypothesize that Hsp32/HO-1 and CO generated from Hsp32/HO-1 provide survival advantages in Sertoli cells by preventing apoptosis under heat exposure. Therefore, the aim of our investigations was to identify the possible roles of Hsp32/HO-1 in hyperthermia stress Sertoli cells. After treatment of cultured mouse Sertoli cells with hyperthermia or/and Hsp32/HO-1 activator Hemin, we evaluated apoptosis by annexin V-FITC and caspase-3 activation. In addition, we analyzed the Hsp32/HO-1-derived CO contents in cultured media and cyclic guanosine monophosphate (cGMP) production by enzyme-linked immunosorbent assay (ELISA). The results showed that the hyperthermia induced Sertoli cells apoptosis, while preincubation with Hemin suppressed Sertoli cell apoptosis induced by hyperthermia treatment. Hyperthermia or/and Hemin increase Hsp32/HO-1 gene expression and the production of CO which, in turn, stimulates the generation of cGMP. Taken together, our results suggest that Hsp32/HO-1 is a protective factor in heat-stressed Sertoli cells, and that CO generated from Hsp32/HO-1 is involved in the anti-apoptotic pathway.Cell Biology International 01/2014; 38(1). DOI:10.1002/cbin.10177 · 1.64 Impact Factor
Conference Paper: An integrated digital Y/C separator for S-VHS VCR[Show abstract] [Hide abstract]
ABSTRACT: A digital adaptive Y/C separator LSI for S-VHS VCR is described. The LSI 1.3-μm rule, two 8-bit DACs (digital-to-analog converters) and an 8-kb line memory. To reduce the chip size, adaptive Y/C separation is done with a one-line memory and a multipurpose filter. Technologies used to realize the Y/C separator are: (1) noncorrelation detection using a one-line memory; (2) technology to reduce the bandwidth for noncorrelation detection; and (3) use of the soft-mix method. This LSI also operates as a dynamic comb filter and a dropout compensator in the playback modeCustom Integrated Circuits Conference, 1989., Proceedings of the IEEE 1989; 06/1989
Article: Changing faces of heme oxygenases.Antioxidants and Redox Signaling 01/2008; 9(12):2043-7. DOI:10.1089/ars.2007.1833 · 7.67 Impact Factor