Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

Ueno-Shuto, Keiko; Kato, Kosuke; Tasaki, Yukihiro; Sato, Miki; Sato, Keizo; Uchida, Yuji; Sakai, Hiroya; Ono, Tomomi; Suico, Mary Ann; Mitsutake, Kazunori; Tokutomi, Naofumi; Kai, Hirofumi; Shuto, Tsuyoshi

doi:10.1074/jbc.m113.532093

Cited by 28 publications

(25 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LPS has also been implicated in the regulation of the expression of certain proteins. For example, LPS negatively regulates single Ig IL-1 receptor-related molecule by inhibiting transcription factor specificity protein 1 (Sp1) binding to the promoter of single Ig IL-1 receptor-related molecule (42). Ye et al (43) demonstrated that LPS increases Sp1-degrading enzyme (LISPDE, a unique trypsin-like serine protease) activity to degrade Sp1 protein.…”

Section: Discussionmentioning

confidence: 99%

A novel role for myeloid cell‐specific neuropilin 1 in mitigating sepsis

et al. 2017

View full text Add to dashboard Cite

Sepsis-typically caused by an uncontrolled and amplified host systemic inflammatory response to microbial infection-is a life-threatening complex clinical disorder and remains a major cause of infection-related deaths in the intensive care unit. Emerging evidence suggests that neuropilin 1 (Nrp1), an originally defined coreceptor for class 3 semaphorins and VEGF, plays important roles in the immune system; however, the function and regulation of macrophage Nrp1 in host immune defense against bacterial infection remain unknown. To address this problem, we generated myeloid cell-specific Nrp1-knockout (Nrp1) mice and applied 2 stringent animal models of sepsis: cecal ligation and puncture as well as intraperitoneal injection of LPS. Here, we reported that myeloid cell-specific Nrp1-deficient mice exhibited enhanced susceptibility to cecal ligation and puncture- and LPS-induced sepsis, which correlated with significantly decreased survival rates and heightened levels of proinflammatory cytokines in both peritoneal lavage and serum. Mechanistically, LPS specifically attenuated the expression of Nrp1 in macrophages, which was mediated by TLR4-NF-κB p50 and -65 pathways. By using isolated primary macrophages, loss of Nrp1 consistently resulted in increased production of proinflammatory cytokines, including iNOS, TNF-α, and IL-6. Together, these findings demonstrate a novel role of macrophage Nrp1 in sepsis.-Dai, X. Okon, I., Liu, Z., Wu, Y., Zhu, H., Song, P., Zou, M.-H. A novel role for myeloid cell-specific neuropilin 1 in mitigating sepsis.

show abstract

Section: Discussionmentioning

confidence: 99%

A novel role for myeloid cell‐specific neuropilin 1 in mitigating sepsis

et al. 2017

View full text Add to dashboard Cite

show abstract

“…TIR8 was also detected in myeloid cells [92,93]. TIR8 expression is, at least partially, under the control of the SP-1 transcription factor, which is inhibited under inflammatory conditions, such as the activation of TLR4/p38 pathway by LPS [94,95]. The molecular mechanisms of action of TIR8 remain unclear, especially regarding its potential ligand(s).…”

Section: Siggir/tir8mentioning

confidence: 94%

“…Specifically, TIR8 deficiency leads to a higher inflammatory response to LPS or IL-1 in vitro and in vivo [91][92][93]95,103,104]. TIR8 is involved in the restriction of inflammation, limiting excessive response to sterile damage or infection, for instance in the kidney [105][106][107] or in the lung [108][109][110][111].…”

Section: Siggir/tir8mentioning

confidence: 99%

The interleukin (IL)-1 cytokine family – Balance between agonists and antagonists in inflammatory diseases

et al. 2015

View full text Add to dashboard Cite

“…Quantitative real-time RT-PCR for mouse Scnn1b (βENaC), Gob5, 18 s ribosomal RNA (18srRNA) was carried out based on the previously established methods63 using the following primer sets; mouse Scnn1b (FW 5′-ATGTGGTTCCTGCTTACGCTG-3′ and RV 5′-GTCCTGGTGGTGTTGCTGTG-3′), mouse Gob5 (FW 5′-CTGTCTTCCTCTTGATCCTCCA-3′ and RV 5′-CGTGGTCTATGGCGATGACG-3′), mouse KC (FW 5′-TGTCAGTGCCTGCAGACCAT-3′ and RV 5′-CCTCGCGACCATTCTTGAGT-3′), mouse Muc5ac (FW 5′-GTGGTTTGACACTGACTTCCC-3′ and RV 5′-CTCCTCTCGGTGACAGAGTCT-3′) and mouse 18srRNA (FW 5′-GTAACCCGTTGAACCCCATT-3′ and RV 5′-CCATCCAATCGGTAGTAGCG-3′). Briefly, total RNA from the mouse lung tissue was isolated using RNAisoPlus (TaKaRa, Japan) and synthesis of cDNA was performed using PrimeScript RT regent kit (TaKaRa, Japan).…”

Section: Methodsmentioning

confidence: 99%

Pharmacological and genetic reappraisals of protease and oxidative stress pathways in a mouse model of obstructive lung diseases

Shuto¹,

Kamei²,

Fujikawa³

et al. 2016

Sci Rep

Self Cite

View full text Add to dashboard Cite

Protease-antiprotease imbalance and oxidative stress are considered to be major pathophysiological hallmarks of severe obstructive lung diseases including chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF), but limited information is available on their direct roles in the regulation of pulmonary phenotypes. Here, we utilized βENaC-transgenic (Tg) mice, the previously established mouse model of severe obstructive lung diseases, to produce lower-mortality but pathophysiologically highly useful mouse model by backcrossing the original line with C57/BL6J mice. C57/BL6J-βENaC-Tg mice showed higher survival rates and key pulmonary abnormalities of COPD/CF, including mucous hypersecretion, inflammatory and emphysematous phenotypes and pulmonary dysfunction. DNA microarray analysis confirmed that protease- and oxidative stress-dependent pathways are activated in the lung tissue of C57/BL6J-βENaC-Tg mice. Treatments of C57/BL6J-βENaC-Tg mice with a serine protease inhibitor ONO-3403, a derivative of camostat methylate (CM), but not CM, and with an anti-oxidant N-acetylcystein significantly improved pulmonary emphysema and dysfunction. Moreover, depletion of a murine endogenous antioxidant vitamin C (VC), by genetic disruption of VC-synthesizing enzyme SMP30 in C57/BL6J-βENaC-Tg mice, exaggerated pulmonary phenotypes. Thus, these assessments clarified that protease-antiprotease imbalance and oxidative stress are critical pathways that exacerbate the pulmonary phenotypes of C57/BL6J-βENaC-Tg mice, consistent with the characteristics of human COPD/CF.

show abstract

Lipopolysaccharide Decreases Single Immunoglobulin Interleukin-1 Receptor-related Molecule (SIGIRR) Expression by Suppressing Specificity Protein 1 (Sp1) via the Toll-like Receptor 4 (TLR4)-p38 Pathway in Monocytes and Neutrophils

Cited by 28 publications

References 30 publications

A novel role for myeloid cell‐specific neuropilin 1 in mitigating sepsis

A novel role for myeloid cell‐specific neuropilin 1 in mitigating sepsis

The interleukin (IL)-1 cytokine family – Balance between agonists and antagonists in inflammatory diseases

Pharmacological and genetic reappraisals of protease and oxidative stress pathways in a mouse model of obstructive lung diseases

Contact Info

Product

Resources

About