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首页> 外文期刊>American Journal of Physiology >Gp91phox contributes to NADPH oxidase activity in aortic fibroblasts but not smooth muscle cells.
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Gp91phox contributes to NADPH oxidase activity in aortic fibroblasts but not smooth muscle cells.

机译：Gp91phox有助于主动脉成纤维细胞中的NADPH氧化酶活性，但不影响平滑肌细胞。

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摘要

Reactive oxygen species (ROS) derived from vascular NADPH oxidase are important in normal and pathological regulation of vessel growth and function. Cell-specific differences in expression and function of the catalytic subunit of NADPH oxidase may contribute to differences in vascular cell response to NADPH oxidase activation. We examined the functional expression of gp91phox on NADPH oxidase activity in vascular smooth muscle cells (SMC) and fibroblasts (FB). As measured by dihydroethidium fluorescence in situ, superoxide (O2-*) levels were greater in adventitial cells compared with medial SMC in wild-type aorta. In contrast, there was no difference in O2-* levels between adventitial cells and medial SMC in aorta from gp91phox-deficient (gp91phox KO) mice. Adventitial-derived FB and medial SMC were isolated from the aorta of wild-type and gp91phox KO mice and grown in culture. Consistent with the observations in situ, basal and stimulated ROS levels were reduced in FB isolated from aorta of gp91phox KO compared with FB from wild-type aorta, whereas ROS levels were similar in SMC derived from gp91phox KO and wild-type aorta. There were no differences in expression of superoxide dismutase between gp91phox KO and wild-type FB to account for these observations. Because gp91phox is associated with membranes, we examined NADPH-stimulated O2-. production in membrane-enriched fractions of cell lysate. As measured by chemiluminescence, NADPH oxidase activity was markedly greater in wild-type FB compared with gp91phox KO FB but did not differ among the SMCs. Confirming functional expression of gp91phox in FB, antisense to gp91phox decreased ROS levels in wild-type FB. Finally, deficiency of gp91phox did not alter expression of the gp91phox homolog NOX4 in isolated FB. We conclude that the neutrophil subunit gp91phox contributes to NADPH oxidase function in vascular FB, but not SMC.
机译：源自血管NADPH氧化酶的活性氧（ROS）在正常和病理性调节血管生长和功能中很重要。 NADPH氧化酶催化亚基表达和功能的细胞特异性差异可能会导致血管细胞对NADPH氧化酶激活的反应差异。我们检查了gp91phox在血管平滑肌细胞（SMC）和成纤维细胞（FB）中对NADPH氧化酶活性的功能性表达。通过原位二氢乙啶荧光测定，与野生型主动脉中的SMC相比，外膜细胞中的超氧化物（O2- *）水平更高。相反，来自gp91phox缺陷型（gp91phox KO）小鼠的主动脉外膜细胞与内侧SMC之间的O2- *水平没有差异。从野生型和gp91phox KO小鼠的主动脉中分离出Adventitive来源的FB和内侧SMC，并使其在培养物中生长。与原位观察结果一致，与野生型主动脉的FB相比，gp91phox KO主动脉分离的FB的基础和受刺激的ROS水平降低，而源自gp91phox KO和野生型主动脉的SMC的ROS水平相似。 gp91phox KO和野生型FB之间的超氧化物歧化酶表达没有差异，以解释这些观察结果。因为gp91phox与膜相关，所以我们检查了NADPH刺激的O2-。在细胞裂解液的膜富集级分中进行生产。通过化学发光测定，与gp91phox KO FB相比，野生型FB中的NADPH氧化酶活性明显更高，但在SMC之间没有差异。证实了gp91phox在FB中的功能性表达，反义于gp91phox降低了野生型FB中的ROS水平。最后，gp91phox的缺乏不会改变分离的FB中gp91phox同源NOX4的表达。我们得出结论，嗜中性粒细胞亚基gp91phox有助于血管性FB中的NADPH氧化酶功能，但不促进SMC。

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