2024年8月14日 · When stimulated with pro-inflammatory cytokines, MSCs lacking CUL4B display enhanced immunosuppressive capacity, which is mediated by the elevated inducible nitric oxide synthase (iNOS). TGF-β...

随后发现tnf-α和ifn-γ联合刺激bmscs，诱导mscs表达inos产生的no反过来也能诱导mscs的凋亡。 这些实验研究的数据结果表明， NO作为血管舒张的小分子，能诱导淋巴细胞和BMSCs的凋亡，损伤免疫系统和机体的修复能力 。

2012年3月16日 · When inducible nitric oxide synthase (iNOS) production was inhibited or genetically ablated, MSCs strongly enhance T-cell proliferation in vitro and the delayed-type hypersensitivity response...

2008年2月7日 · Our most definitive proof of the central role of NO is that iNOS-deficient MSCs lack immunosuppressive capability. Various studies have shown that MSCs expanded ex vivo preferentially home to sites of tissue damage, where they enhance wound healing, support tissue regeneration, restore the bone marrow microenvironment following damage by ...

To resolve this predicament, we developed a novel strategy to humanize murine MSCs by incorporating the human IDO gene into MSCs derived from mice lacking the iNOS gene (iNOS −/−). These IDO-expressing mouse MSC transfectants (MSC-IDO) provide a unique opportunity to study the role of human IDO without interference from iNOS.

2013年8月26日 · We have demonstrated that p53 deficiency allows enhanced upregulation of iNOS expression and NO production in MSCs. NO has long been acknowledged as an important factor in tumor growth for...

2018年6月14日 · In the presence of proinflammatory cytokines, MSCs facilitate high expression of inducible NO synthase (iNOS), which stimulates the secretion of NO, giving rise to inhibition of T-cell proliferation .

究其原因，主要是低水平的炎症因子不足以诱导mscs表达高水平inos或ido发挥免疫抑制作用，反而会在mscs分泌大量趋化因子的作用下招募淋巴细胞至其周围，加剧炎症反应。

2020年9月25日 · Our results showed that 1-h LPS exposure induced a MSC1 phenotype. Indeed, MSCs-LPS1h expressed low levels of NO/iNOS and decreased immunosuppressive capacity in vitro without therapeutic effect in the EAE model.

2014年3月1日 · To address this issue, we established a novel humanized system to model human MSCs, using murine iNOS (-/-) MSCs that constitutively or inducibly express an ectopic human IDO gene.