Control of nitric oxide production by endogenous TGF‐β1 and systemic nitric oxide in retinal pigment epithelial cells and peritoneal macrophages
Control of nitric oxide production by endogenous TGF‐β1 and systemic nitric oxide in retinal pigment epithelial cells and peritoneal macrophages
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视网膜色素上皮细胞和腹膜巨噬细胞中内源性TGF-β1和全身一氧化氮对一氧化氮产生的控制
DOI：
10.1002/jlb.60.2.261
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发表时间：
1996
影响因子：
5.5
通讯作者：
J. Sparrow
中科院分区：
文献类型：
--
作者：
Y. Vodovotz;J. Letterio;A. Geiser;Louis Chester;A. Roberts;J. Sparrow
体内和体外实验均表明，转化生长因子-β1（TGF-β1）可抑制诱导型一氧化氮合酶（iNOS）的表达。在这项研究中，我们使用来自TGF-β1缺失（TGF-β1-/-）小鼠或年龄匹配的野生型（TGF-β1 +/+）或杂合型（TGF-β 1 +/-）同窝仔的细胞，体外检查了外源性和内源性TGF-β1对视网膜色素上皮（RPE）细胞和常驻腹膜巨噬细胞的影响。来自TGF-β1-/-小鼠和TGF-β1 +/+同窝仔的RPE细胞产生NO，并且仅在用干扰素-γ（IFN-γ）和细菌脂多糖（LPS）处理后对iNOS蛋白呈免疫细胞化学阳性;然而，来自TGF-β1-/-小鼠的RPE细胞产生的NO比来自TGF-β1 +/+小鼠的细胞多40%。相反，TGF-β1 +/+和TGF-β1-/-小鼠的常驻腹腔巨噬细胞在没有刺激和没有可检测的NO产生的情况下表达iNOS蛋白。导致TGF-β1 +/+中的NO. Macrophages的可检测水平小鼠产生NO的方式似乎与获得细胞的小鼠的血清NO2-和NO3-含量成反比;在TGF-β1 +/-或TGF-β1-/-小鼠中不存在这种相关性。用外源性TGF-β1处理来自TGF-β1 +/+和TGF-β1-/-小鼠的RPE细胞或巨噬细胞可降低iNOS蛋白和NO的产生。这些发现证明了内源性TGF-β1在将全身NO产生与巨噬细胞NO产生偶联中的新作用，并证明了内源性和外源性TGF-β1可以不同地抑制NO产生。J.利瓦克60：261-270; 1996.
Both in vivo and in vitro experiments demonstrate that transforming growth factor‐β1 (TGF‐β1) suppresses expression of the inducible form of nitric oxide synthase (iNOS). In this study, we examined the effects of exogenous and endogenous TGF‐β1 on retinal pigment epithelial (RPE) cells and resident peritoneal macrophages ex vivo using cells from TGF‐β1 null (TGF‐β1 ‐/‐) mice or age‐matched wild‐type (TGF‐β1 +/+) or heterozygous (TGF‐β1 +/‐) littermates. RPE cells from both TGF‐β1 ‐/‐ mice and TGF‐β1 +/+ littermates produced NO and were immunocytochemically positive for iNOS protein only following treatment with interferon‐γ (IFN‐γ) and bacterial lipopolysaccharide (LPS); however, RPE cells from TGF‐β1 ‐/‐ mice produced 40% more NO than cells from TGF‐β1 +/+ mice. In contrast, resident peritoneal macrophages from both TGF‐β1 +/+ and TGF‐β1 ‐/‐ mice expressed iNOS protein without stimulation and in the absence of detectable production of NO. The expression of iNOS was increased by treatment with IFN‐γ, resulting in detectable levels of NO. Macrophages from TGF‐β1 +/+ mice appeared to produce NO in a manner inversely proportional to the serum content of NO2 ‐ and NO3 ‐ of the mice from which the cells were obtained; no such correlation existed in TGF‐β1 +/‐ or TGF‐β1 ‐/‐ mice. Treatment of RPE cells or macrophages from both TGF‐β1 +/+ and TGF‐β1 ‐/‐ mice with exogenous TGF‐β1 decreased both iNOS protein and NO production. These findings demonstrate a novel role of endogenous TGF‐β1 in coupling systemic NO production to the production of NO by macrophages, and demonstrate that endogenous and exogenous TGF‐β1 can act differently to suppress NO production. J. Leukoc. Biol. 60: 261–270; 1996.
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转化生长因子-β1缺失小鼠。
DOI：
--
发表时间：
1995
期刊：
The American journal of pathology
影响因子：
--
作者：
Kulkarni,AB;Ward,JM;Yaswen,L;Mackall,CL;Bauer,SR;Huh,CG;Gress,RE;Karlsson,S
通讯作者：
Karlsson,S
影响因子：
4.4
作者：
D. Stuehr;M. Marletta
通讯作者：
D. Stuehr;M. Marletta
影响因子：
4.4
作者：
C. Mills;J. Shearer;R. Evans;M. Caldwell
通讯作者：
C. Mills;J. Shearer;R. Evans;M. Caldwell
影响因子：
4.4
作者：
J. Albina;C. Mills;W. Henry;M. Caldwell
通讯作者：
J. Albina;C. Mills;W. Henry;M. Caldwell
DOI：
10.1073/pnas.84.17.6020
发表时间：
1987-09-01
影响因子：
11.1
作者：
ASSOIAN, RK;FLEURDELYS, BE;SPORN, MB
通讯作者：
SPORN, MB