Nitric Oxide Synthase Induces Macrophage Death by Apoptosis

Sarih, M’hammed; Souvannavong, Vongthip; Adam, Arlette

doi:10.1006/bbrc.1993.1246

Cited by 337 publications

(164 citation statements)

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“…It has been reported that NO mediates cell death of activated macrophages (Sarih et al, 1993;Hortelano et Fig. 6.…”

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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“…It has been reported that NO mediates cell death of activated macrophages (Sarih et al, 1993;Hortelano et Fig. 6.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐13 and ‐4 induce death of activated microglia

Yang¹,

Park²,

Sohn³

et al. 2002

Glia

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“…However, LPS activation of macrophages primed with con A, IFN-γ, IFN-γ, bovine viral diarrhea virus, or herpesvirus-1 causes macrophage apoptosis [15][16][17][18]20]. We examined the effect of LPS on the viability of macrophages primed with Salmonella typhimurium (MOI of 5:1) or type 5 adenovirus (Ad5) (MOI of 10:1).…”

Section: Lps Induces Cell Death In Primed Macrophagesmentioning

confidence: 99%

“…Treatment of macrophages with zVAD did not cause any morphological change of these cells [20]. We examined the expression of a number of different genes including p53 and Rb that may be related to cell death and cell differentiation in RAW264.7 cells.…”

Section: Mef2c Is Activated In Primed Macrophagesmentioning

confidence: 99%

“…IFN-γ is clearly not the only factor that can prime macrophages to become sensitive to LPS-induced cell killing [17,20]. For example, LPS was reported to cause cell death of conA or IFN-γ primed macrophages and to enhance cell death induced by the Yersinia baccillus [17,20,21].…”

Section: Introductionmentioning

confidence: 99%

“…For example, LPS was reported to cause cell death of conA or IFN-γ primed macrophages and to enhance cell death induced by the Yersinia baccillus [17,20,21]. Intriguingly, it was found that zVAD and boc-D, pan-caspase inhibitors that inhibit apoptosis in many different cells, not only had no inhibitory effect on LPS-induced apoptosis in INF-γ primed macrophages but also by themselves induced susceptibility to LPS-induced cell death in macrophages [22].…”

Section: Introductionmentioning

confidence: 99%

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MEF2C mediates the activation induced cell death (AICD) of macrophages

Wei

2006

Cell Res

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Activation-induced cell death (AICD) of immune cells is widely believed to be crucial for the regulation of immune responses. Although macrophage apoptosis has been observed under a variety of pathological conditions, questions as to whether there is AICD of macrophages and how macrophage life span is regulated have not been well addressed. AICD in macrophages requires two signals. One is cell activation triggered by LPS or other bacterial components. The other is an event that exists in AICD-susceptible (primed) but not unsusceptible (resting) macrophages. Here we show that RAW264.7 cell is susceptible to LPS stimulation when it is primed with Salmonella typhimurium, type 5 adenovirus (Ad5) or IFN-g. We found that the stability of the transcription factor MEF2C is increased in primed RAW264.7 cell. Transfection of a dominant negative form of MEF2C protects primed macrophage from cell death triggered by LPS. Our data demonstrate that the increase of MEF2C protein stability is a key factor in the AICD of macrophage.

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