LINC00240/miR-155 axis regulates function of trophoblasts and M2 macrophage polarization via modulating oxidative stress-induced pyroptosis in preeclampsia

Wu, Haiying; liu, Kan; Zhang, Jingli

doi:10.1186/s10020-022-00531-3

Cited by 11 publications

(6 citation statements)

References 79 publications

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“…A direct association between LINC00240 and miR-155-5p was identified in this study, and miR-155-5p functioned as a downstream molecule of LINC00240 to mediate Th9 differentiation. Interestingly, a more recent study has demonstrated that LINC00240 binds to miR-155-5p directly, and LINC00240/miR-155-5p/Nrf2 axis contributes to the pathogenesis of preeclampsia [32], indicating the diverse function of LINC00240/miR-155-5p axis in different diseases.…”

Section: Discussionmentioning

confidence: 99%

Role of LINC00240 on T-helper 9 differentiation in Allergic Rhinitis through influencing DNMT1-dependent methylation of PU.1

Liu,

Jiang,

Liu

et al. 2023

Preprint

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Background Allergic rhinitis (AR) is a common allergic disease with increasing prevalence globally. However, the molecular mechanism underlying AR pathogenesis remains largely undefined. Methods Samples of peripheral blood and nasal mucosa from patients with AR, as well as the ovalbumin-induced AR mice model was obtained. qRT-PCR and western blot were used to detect the expression of LINC00240, miR-155-5p, PU.1 and other key molecules. ELISA assay and flow cytometry were employed to evaluate the secretion of IL-9 and T-helper 9 (Th9) cell ratio, respectively. Bioinformatics analysis, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP) and luciferase reporter assays were employed to further elucidate the regulatory network of LINC00240/miR-155-5p/DNMT1. The methylation of PU.1 promoter was assessed by methylation-specific PCR (MSP). This signaling axis was finally confirmed in the AR mice model. Results LINC00240 was downregulated, while miR-155-5p and PU.1 were upregulated in the peripheral blood and nasal mucosa of AR patients, as well as in the AR mice. This was accompanied with the increased ratio of Th9 cells and elevated IL-9 secretion. Mechanistically, LINC00240 served as a miR-155-5p sponge, and DNMT1 was a target of miR-155-5p. In addition, DNMT1 mediated the methylation of PU.1 promoter. In vivo studies verified that LINC00240 mitigated AR progression, possibly via miR-155-5p/DNMT1/PU.1-dependent Th9 differentiation. Conclusion In summary, the involvement of LINC00240 in AR pathogenesis is closely associated with Th9 differentiation through modulating DNMT1-dependent methylation of PU.1 by sponging miR-155-5p.

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Section: Discussionmentioning

confidence: 99%

Role of LINC00240 on T-helper 9 differentiation in Allergic Rhinitis through influencing DNMT1-dependent methylation of PU.1

Liu,

Jiang,

Liu

et al. 2023

Preprint

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“…Pyroptosis, another cell death pathway, has been observed in primary human trophoblasts under pathophysiological condition [ 42 ]. Enhanced oxidative stress or NLRP3-inflammasome-activation-induced pyroptosis inhibit trophoblast cell proliferation, migration and invasion in both in vitro and in vivo models of preeclampsia [ 62 , 63 ] (Fig. 2B ).…”

Section: Involvement Of Rcd At the Maternal-fetal Interface In Pregnancymentioning

confidence: 99%

“…Oxidative stress-induced pyroptosis inhibited M2 macrophage polarization [ 62 ]. In women experiencing spontaneous preterm labor, decidual macrophages undergo pyroptosis, as evidenced by the presence of active caspase-1, GSDMD and mature IL-1β [ 82 ].…”

Section: Involvement Of Rcd At the Maternal-fetal Interface In Pregnancymentioning

confidence: 99%

The regulated cell death at the maternal-fetal interface: beneficial or detrimental?

Chen,

Zheng

2024

Cell Death Discov.

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Regulated cell death (RCD) plays a fundamental role in placental development and tissue homeostasis. Placental development relies upon effective implantation and invasion of the maternal decidua by the trophoblast and an immune tolerant environment maintained by various cells at the maternal-fetal interface. Although cell death in the placenta can affect fetal development and even cause pregnancy-related diseases, accumulating evidence has revealed that several regulated cell death were found at the maternal-fetal interface under physiological or pathological conditions, the exact types of cell death and the precise molecular mechanisms remain elusive. In this review, we summarized the apoptosis, necroptosis and autophagy play both promoting and inhibiting roles in the differentiation, invasion of trophoblast, remodeling of the uterine spiral artery and decidualization, whereas ferroptosis and pyroptosis have adverse effects. RCD serves as a mode of communication between different cells to better maintain the maternal-fetal interface microenvironment. Maintaining the balance of RCD at the maternal-fetal interface is of utmost importance for the development of the placenta, establishment of an immune microenvironment, and prevention of pregnancy disorders. In addition, we also revealed an association between abnormal expression of key molecules in different types of RCD and pregnancy-related diseases, which may yield significant insights into the pathogenesis and treatment of pregnancy-related complications.

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“…On the contrary, LINC00240 is lowlyexpressed in the placenta tissues of PE patients. The downregulated LINC00240 aggravates oxidative stress-induced pyroptosis through increasing miR-155 and reducing Nrf2 expression, and LINC00240 overexpression mitigates the pyroptotic death of trophoblasts (58). Additionally, the lowlyexpressed miR-520c-3p is observed in the placental tissues of PE patients and H/R-treated trophoblasts, and melatonin may suppress trophoblasts pyroptosis via modulating miR-520c-3p/SETD7 axis (93).…”

Section: The Role Of Pyroptosis In Trophoblastsmentioning

confidence: 99%

Pyroptosis-triggered pathogenesis: New insights on antiphospholipid syndrome

Tan

Liu

et al. 2023

Front. Immunol.

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APS (antiphospholipid syndrome) is a systematic autoimmune disease presenting with the high levels of aPLs (antiphospholipid antibodies). These autoantibodies are involved in various clinical manifestations, mainly including arterial or venous thrombosis formation, proinflammatory response, and recurrent pregnant loss. Pyroptosis is a form of lytic programmed cell death, and it aggravates autoimmune diseases progression via activating NOD-like receptors, especially the NLRP3 inflammasome and its downstream inflammatory factors IL (interleukin)-1β and IL-18. However, the underlying mechanisms of pyroptosis-induced APS progression remain to be elucidated. ECs (endothelial cells), monocytes, platelets, trophoblasts, and neutrophils are prominent participants in APS development. Of significance, pyroptosis of APS-related cells leads to the excessive release of proinflammatory and prothrombotic factors, which are the primary contributors to APOs (adverse pregnancy outcomes), thrombosis formation, and autoimmune dysfunction in APS. Furthermore, pyroptosis-associated medicines have made encouraging advancements in attenuating inflammation and thrombosis. Given the potential of pyroptosis in regulating APS development, this review would systematically expound the molecular mechanisms of pyroptosis, and elaborate the role of pyroptosis-mediated cellular effects in APS progression. Lastly, the prospective therapeutic approaches for APS would be proposed based on the regulation of pyroptosis.

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LINC00240/miR-155 axis regulates function of trophoblasts and M2 macrophage polarization via modulating oxidative stress-induced pyroptosis in preeclampsia

Cited by 11 publications

References 79 publications

Role of LINC00240 on T-helper 9 differentiation in Allergic Rhinitis through influencing DNMT1-dependent methylation of PU.1

Role of LINC00240 on T-helper 9 differentiation in Allergic Rhinitis through influencing DNMT1-dependent methylation of PU.1

The regulated cell death at the maternal-fetal interface: beneficial or detrimental?

Pyroptosis-triggered pathogenesis: New insights on antiphospholipid syndrome

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