Transcriptional expression of CXCL10 and STAT1 in lupus nephritis and the intervention effect of triptolide

Shi, Dongliang; Li, Yan; Shi, Xiaomei; Yao, Min; Wu, Dan; Zheng, Yuhui; Lin, Qing; Yang, Yinghong

doi:10.1007/s10067-022-06400-y

Cited by 8 publications

(7 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cxcl10 expression can be induced by the transcription factor Stat1, the major Stat protein activated by IFNγ. 25 Consistent with this concept, Stat1 activation, as determined by phosphorylated Stat1 (p-Stat1), was decreased in RvD1-treated MASH livers ( Fig. 3B ).…”

Section: Resultssupporting

confidence: 78%

Therapeutic Activity of Resolvin D1 (RvD1) in Murine MASH

Navarro-Corcuera,

Zhu,

et al. 2024

Preprint

View full text Add to dashboard Cite

Background and Aims: Recent studies have highlighted the beneficial effect of resolvin D1 (RvD1), a DHA-derived specialized pro-resolving mediator, on metabolic dysfunction-associated steatohepatitis (MASH), but the underlying mechanisms are not well understood. Our study aims to determine the mechanism by which RvD1 protects against MASH progression. Methods: RvD1 was administered to mice with experimental MASH, followed by bulk and single-cell RNA sequencing analysis. Primary cells including bone marrow-derived macrophages (BMDMs), Kupffer cells, T cells, and primary hepatocytes were isolated to elucidate the effect of RvD1 on inflammation, cell death, and fibrosis regression genes. Results: Hepatic tissue levels of RvD1 were decreased in murine and human MASH, likely due to an expansion of pro-inflammatory M1-like macrophages with diminished ability to produce RvD1. Administering RvD1 reduced inflammation, cell death, and liver fibrosis. Mechanistically, RvD1 reduced inflammation by suppressing the Stat1-Cxcl10 signaling pathway in macrophages and prevented hepatocyte death by alleviating ER stress-mediated apoptosis. Moreover, RvD1 induced Mmp2 and decreased Acta2 expression in hepatic stellate cells (HSCs), and promoted Mmp9 and Mmp12 expression in macrophages, leading to fibrosis regression in MASH. Conclusions: RvD1 reduces Stat1-mediated inflammation, mitigates ER stress-induced apoptosis, and promotes MMP-mediated fibrosis regression in MASH. This study highlights the therapeutic potential of RvD1 to treat MASH.

show abstract

Section: Resultssupporting

confidence: 78%

Therapeutic Activity of Resolvin D1 (RvD1) in Murine MASH

Navarro-Corcuera,

Zhu,

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…Glomerular mesangial cells treated with IFNγ induced production of CXCL10, whereas triptolide-stimulated glomerular mesangial cells showed less production of CXCL10. 39 It is known that biglycan is a proteoglycan of extracellular matrix and can stimulate the generation of Th1/Th17 chemoattractant CXCL10 in macrophages, neutrophils. In biglycan gene deficient (biglycan −/− ) MRL/lpr mice, there were less Th1 and Th17 cells in periglomerular/interstitial and perivascular areas in kidneys, and there were less renal levels of IFNγ and IL-17 in the biglycan −/− MRL/lpr mice.…”

Section: Fli-1 and Lupus Developmentmentioning

confidence: 99%

“…Since expression of CXCL10 was elevated both from SLE having or having not LN, lupus mice models, methods to suppressing expression, function of CXCL10 may help to control SLE development. Glomerular mesangial cells treated with IFNγ induced production of CXCL10, whereas triptolide‐stimulated glomerular mesangial cells showed less production of CXCL10 39 . It is known that biglycan is a proteoglycan of extracellular matrix and can stimulate the generation of Th1/Th17 chemoattractant CXCL10 in macrophages, neutrophils.…”

Section: Cxcl10 and Sle/lnmentioning

confidence: 99%

Targeting Fli‐1 and chemokine axis CXCL10/CXCL13/CXCR3 in systemic lupus erythematosus and lupus nephritis

Zhu

2024

Int J of Rheum Dis

View full text Add to dashboard Cite

Fli‐1 is a critical factor involved in hematopoietic stem cells, vascular endothelial cells apoptosis, and differentiation. Similarly, Fli‐1 regulates immune cell proliferation and differentiation, such as T cells, B cells, and monocytes. Regarding T/B cell dysfunction, SLE including LN is recognized to be associated with abnormal expression and function of Fli‐1. Moreover, three ligands of Fli‐1 including CXCL10 (C‐X‐C motif chemokine ligand 10), CXCR3 (C‐X‐C motif chemokine receptor 3), CXCL13 are widely discussed in SLE/LN. In this comprehensive review, we not only discussed Fli‐1 within SLE/LN pathogenesis, but also discussed the effects of CXCL10, CXCR3, and CXCL13 on SLE/LN development. Furthermore, we discussed how Fli‐1 regulates CXCL10, CXCR3, and CXCL13, and then involved in lupus development. It is possible that the Fli‐1 axis might be a potential target in SLE and LN.

show abstract

“…Table 6 summarizes the presumable applications of ncRNAs (miRs, lncRNAs and circRNAs) as novel potential therapeutic strategies for LN in the future. • IFN-γ-induced JAK/STAT signaling and CXCL10 expression [167] II Modulation of complement levels [169] or complement factor B level [170] III Targeting proinflammatory cytokines or growth factors by microRNAs…”

Section: Molecular Mechanisms For Other Unique Ncrna Inhibitors In Th...mentioning

confidence: 99%

Decipher the Immunopathological Mechanisms and Set Up Potential Therapeutic Strategies for Patients with Lupus Nephritis

Tsai

Shen

et al. 2023

IJMS

View full text Add to dashboard Cite

Lupus nephritis (LN) is one of the most severe complications in patients with systemic lupus erythematosus (SLE). Traditionally, LN is regarded as an immune complex (IC) deposition disease led by dsDNA–anti-dsDNA-complement interactions in the subendothelial and/or subepithelial basement membrane of glomeruli to cause inflammation. The activated complements in the IC act as chemoattractants to chemically attract both innate and adaptive immune cells to the kidney tissues, causing inflammatory reactions. However, recent investigations have unveiled that not only the infiltrating immune-related cells, but resident kidney cells, including glomerular mesangial cells, podocytes, macrophage-like cells, tubular epithelial cells and endothelial cells, may also actively participate in the inflammatory and immunological reactions in the kidney. Furthermore, the adaptive immune cells that are infiltrated are genetically restricted to autoimmune predilection. The autoantibodies commonly found in SLE, including anti-dsDNA, are cross-reacting with not only a broad spectrum of chromatin substances, but also extracellular matrix components, including α-actinin, annexin II, laminin, collagen III and IV, and heparan sulfate proteoglycan. Besides, the glycosylation on the Fab portion of IgG anti-dsDNA antibodies can also affect the pathogenic properties of the autoantibodies in that α-2,6-sialylation alleviates, whereas fucosylation aggravates their nephritogenic activity. Some of the coexisting autoantibodies, including anti-cardiolipin, anti-C1q, anti-ribosomal P autoantibodies, may also enhance the pathogenic role of anti-dsDNA antibodies. In clinical practice, the identification of useful biomarkers for diagnosing, monitoring, and following up on LN is quite important for its treatments. The development of a more specific therapeutic strategy to target the pathogenic factors of LN is also critical. We will discuss these issues in detail in the present article.

show abstract

Transcriptional expression of CXCL10 and STAT1 in lupus nephritis and the intervention effect of triptolide

Cited by 8 publications

References 43 publications

Therapeutic Activity of Resolvin D1 (RvD1) in Murine MASH

Therapeutic Activity of Resolvin D1 (RvD1) in Murine MASH

Targeting Fli‐1 and chemokine axis CXCL10/CXCL13/CXCR3 in systemic lupus erythematosus and lupus nephritis

Decipher the Immunopathological Mechanisms and Set Up Potential Therapeutic Strategies for Patients with Lupus Nephritis

Contact Info

Product

Resources

About