Nitrogen oxide‐induced autoprotection in isolated rat hepatocytes

Kim, Young‐Myeong; Bergonia, Hector A.; Lancaster, Jack R.

doi:10.1016/0014-5793(95)01115-u

Cited by 197 publications

(118 citation statements)

References 41 publications

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“…For example, activated RAW264.7 cells are more resistant to NO than inactivated cells (Okada et al, 1998), and LPS-activated BV-2 cells are resistant to NO toxicity while inactivated BV-2 cells are vulnerable (Sugaya et al, 1997). The susceptibility of activated macrophages to NO might be decreased because bacteria and LPS can stimulate expression of self-defenserelated genes in macrophages, such as Bcl-xL, metallothionein, and heat shock protein 70 (Kim et al, 1995;Bellmann et al, 1996;Okada et al, 1998). Based on those reports and our present data, it may be that the antiactivation cytokines IL-13 and IL-4 inhibit the expression of certain self-defense-related genes induced by microglial activators, which in turn leads to microglial cell death.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐13 and ‐4 induce death of activated microglia

Yang¹,

Park²,

Sohn³

et al. 2002

Glia

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When the brain suffers injury, microglia migrate to the damaged sites and become activated. These activated microglia are not detected several days later and the mechanisms underlying their disappearance are not well characterized. In this study, we demonstrate that interleukin (IL)-13, an anti-inflammatory cytokine, selectively induces cell death of activated microglia in vitro. Cell death was detected 4 days after the coaddition of IL-13 with any one of the microglial activators, lipopolysaccharide (LPS), ganglioside, or thrombin. This cell death occurred in a time-dependent manner. LPS, ganglioside, thrombin, or IL-13 alone did not induce cell death. Among antiinflammatory cytokines, IL-4 mimicked the effect of IL-13, while TGF-␤ did not. Cells treated with IL-13 plus LPS, or IL-13 plus ganglioside, showed the characteristics of apoptosis when analyzed by electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Electron micrographs also showed microglia engulfing neighboring dead cells. We propose that IL-13 and IL-4 induce death of activated microglia, and that this process is important for prevention of chronic inflammation that can cause tissue damage. GLIA 38:273-280, 2002.

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Section: Discussionmentioning

confidence: 99%

Interleukin‐13 and ‐4 induce death of activated microglia

Yang¹,

Park²,

Sohn³

et al. 2002

Glia

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“…It has been postulated that the mechanism for enhanced radiosensitivity by NO is presumably due to the rapid reaction between radiation-induced carbon centre radicals on DNA with NO thereby 'fixing' the damage (Howard-Flanders, 1957). It is known that the Experimental Therapeutics exposure of cells to low concentrations of NO can result in protection against challenges from subsequent higher concentrations (Kim et al, 1995). Therefore, the adaptation of hypoxic cells to spontaneous short-term NO release, such as by NO donor agents, may be different to those seen in cells that are exposed to low and sustained levels of NO generated endogenously during tumour growth.…”

Section: Discussionmentioning

confidence: 99%

17β-Oestradiol treatment modulates nitric oxide synthase activity in MDA231 tumour with implications on growth and radiation response

et al. 2002

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The putative oestrogen receptor negative human breast cancer cell line MDA231, when grown as tumours in mice continually receiving 17b-oestradiol, showed substantially increased growth rate when compared to control animals. Further, we observed that 17b-oestradiol treatment could both increase the growth rate of established MDA231 tumours as well as decreasing the time taken for initiating tumour growth. We have also demonstrated that this increase in growth rate is accompanied by a four-fold increase in nitric oxide synthase activity, which was predominantly the inducible form. Inducible-nitric oxide synthase expression in these tumours was confirmed by immunohistochemical analysis and appeared localized primarily in areas between viable and necrotic regions of the tumour (an area that is presumably hypoxic). Prophylactic treatment with the nitric oxide synthase inhibitor nitro-L-arginine methyl ester resulted in significant reduction in this apparent 17b-oestradiol-mediated growth promoting effect. Tumours derived from mice receiving 17b-oestradiol-treatment were characterized by a significantly lower fraction of perfused blood vessels and an indication of an increased hypoxic fraction. Consistent with these observations, 17b-oestradiol-treated tumours were less radio-responsive compared to control tumours when treated with a single radiation dose of 15 Gy. Our data suggests that long-term treatment with oestrogen could significantly alter the tumour oxygenation status during breast tumour progression, thus affecting response to radiotherapy.

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“…Studies using low doses of NO donors demonstrated that NO directly acts as an antioxidant (Chang et al, 1996;Joshi et al, 1999;Kim et al, 1995;Wink et al, 1993). Therefore, we hypothesized that the vasculopathy induced by L-NMMA may be due to increased ROS, suggesting a common pathway with hyperglycemia.…”

Section: No Depletion Increases Ros Production: a Common Pathway In Vmentioning

confidence: 97%

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

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Nitric oxide (NO) has been demonstrated to mediate events during ovulation,pregnancy, blastocyst invasion and preimplantation embryogenesis. However,less is known about the role of NO during postimplantation development. Therefore, in this study, we explored the effects of NO during vascular development of the murine yolk sac, which begins shortly after implantation. Establishment of the vitelline circulation is crucial for normal embryonic growth and development. Moreover, functional inactivation of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during this period leads to embryonic defects/lethality, as this structure is vital for transport, metabolism and induction of vascular development. In this study, we describe the temporally/spatially regulated distribution of nitric oxide synthase (NOS) isoforms during the three stages of yolk sac vascular development (blood island formation, primary capillary plexus formation and vessel maturation/remodeling) and found NOS expression patterns were diametrically opposed. To pharmacologically manipulate vascular development,an established in vitro system of whole murine embryo culture was employed. During blood island formation, the endoderm produced NO and inhibition of NO(L-NMMA) at this stage resulted in developmental arrest at the primary plexus stage and vasculopathy. Furthermore, administration of a NO donor did not cause abnormal vascular development; however, exogenous NO correlated with increased eNOS and decreased iNOS protein levels. Additionally, a known environmental insult (high glucose) that produces reactive oxygen species(ROS) and induces vasculopathy also altered eNOS/iNOS distribution and induced NO production during yolk sac vascular development. However, administration of a NO donor rescued the high glucose induced vasculopathy, restored the eNOS/iNOS distribution and decreased ROS production. These data suggest that NO acts as an endoderm-derived factor that modulates normal yolk sac vascular development, and decreased NO bioavailability and NO-mediated sequela may underlie high glucose induced vasculopathy.

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Nitrogen oxide‐induced autoprotection in isolated rat hepatocytes

Cited by 197 publications

References 41 publications

Interleukin‐13 and ‐4 induce death of activated microglia

Interleukin‐13 and ‐4 induce death of activated microglia

17β-Oestradiol treatment modulates nitric oxide synthase activity in MDA231 tumour with implications on growth and radiation response

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

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