Upregulated fractalkine levels in Chinese patients with lupus nephritis

You, Yun; Qin, Yueqiu; Lin, Xu; Yang, Fafen; Wang, Junjie; Fang, Yuan; Sooranna, Suren R.; Pinhu, Liao

doi:10.1016/j.cyto.2018.01.027

Cited by 12 publications

(15 citation statements)

References 30 publications

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“…In Chinese patients with IgAN, plasma CX3CL1 levels were associated with renal function, proteinuria, and histologic changes [136]. Furthermore, they suggest a possible role in the pathogenesis and activity of lupus nephritis [137]. However, a study on mice showed that CX3CR1 inhibition in hypertension could promote hypertensive renal injury [138].…”

Section: Cx3c Subfamilymentioning

confidence: 99%

Review on Inflammation Markers in Chronic Kidney Disease

et al. 2021

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Chronic kidney disease (CKD) is one of the major health problems of the modern age. It represents an important public health challenge with an ever-lasting rising prevalence, which reached almost 700 million by the year 2017. Therefore, it is very important to identify patients at risk for CKD development and discover risk factors that cause the progression of the disease. Several studies have tackled this conundrum in recent years, novel markers have been identified, and new insights into the pathogenesis of CKD have been gained. This review summarizes the evidence on markers of inflammation and their role in the development and progression of CKD. It will focus primarily on cytokines, chemokines, and cell adhesion molecules. Nevertheless, further large, multicenter studies are needed to establish the role of these markers and confirm possible treatment options in everyday clinical practice.

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Section: Cx3c Subfamilymentioning

confidence: 99%

Review on Inflammation Markers in Chronic Kidney Disease

et al. 2021

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“…FKN binding to its unique receptor, CX3CR1, can promote hypertensive interstitial fibrosis in the kidney (48). In our previous studies, we have verified that FKN positively correlated with LN (42), especially in patients with active LN and those with renal damage (49). Other studies have also reported that FKN is involved in the development of glomerulopathy in humans, including crescentic glomerulonephritis (50).…”

Section: Discussionmentioning

confidence: 55%

“…We previously found that in LN, FKN expression is significantly higher than that in peripheral blood mononuclear cells and serum from healthy controls. Notably, there is a positive correlation between FKN and the pathogenesis and activity of LN (42). In addition, our other findings showed that FKN expression levels were upregulated in HK-2 cells after stimulation with lipopolysaccharide and that as the level of FKN expression decreased, kidney function improved and kidney lesions decreased (32).…”

Section: Discussionmentioning

confidence: 99%

FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis

Senouthai

Wang

et al. 2019

Front. Immunol.

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Fractalkine (FKN), also known as chemokine (C-X3-C motif) ligand 1, constitutes an intriguing chemokine with a documented role in the development of numerous inflammatory diseases including autoimmune disease. Specifically, it has been reported that FKN is involved in the disease progression of lupus nephritis (LN). The epithelial-mesenchymal transition (EMT) plays a significant role in the formation of tubulointerstitial lesions (TIL), which are increasingly recognized as a hallmark of tissue fibrogenesis after injury. However, the correlation between FKN and EMT or TIL in LN has not been determined. To investigate the potential role of FKN in EMT and TIL, MRL lymphoproliferation (MRL/lpr) strain mice were treated with an anti-FKN antibody, recombinant-FKN chemokine domain, or isotype antibody. Our results revealed that treatment with the anti-FKN antibody improved EMT, TIL, and renal function in MRL/lpr mice, along with inhibiting activation of the Wnt/β-catenin signaling pathway. In contrast, administration of the recombinant-FKN chemokine domain had the opposite effect. Furthermore, to further explore the roles of FKN in EMT, we assessed the levels of EMT markers in FKN-depleted or overexpressing human proximal tubule epithelial HK-2 cells. Our results provide the first evidence that the E-cadherin level was upregulated, whereas α-SMA and vimentin expression was downregulated in FKN-depleted HK-2 cells. In contrast, overexpression of FKN in HK-2 cells enhanced EMT. In addition, inhibition of the Wnt/β-catenin pathway by XAV939 negated the effect of FKN overexpression, whereas activation of the Wnt/β-catenin pathway by Ang II impaired the effect of the FKN knockout on EMT in HK-2 cells. Together, our data indicate that FKN plays essential roles in the EMT progression and development of TIL in MRL/lpr mice, most likely through activation of the Wnt/β-catenin signaling pathway.

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“…Chemokine FKN adheres to immune cells in the process of in ammation and preferentially induce the migration of cytotoxic effector lymphocytes. This migration of cytotoxic effector lymphocytes positively correlates with the activity of in ammatory diseases [22][23][24]. Recent studies focused on the therapeutic strategy of FKN in in ammatory diseases.…”

Section: Discussionmentioning

confidence: 91%

Fractalkine Aggravates LPS-induced Macrophage Activation and Acute Kidney Injury via Wnt/β-catenin Signaling Pathway

Gong

Jiang

Pan

et al. 2021

Preprint

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Background: Fractalkine（CX3CL1, FKN），a CX3C gene sequence inflammatory chemokine, has been found to have pro-inflammatory and pro-adhesion effects. Macrophages are immune cells with a critical role in regulate inflammatory response. The imbalance of M1/M2 macrophage polarization can lead to aggravated inflammation. This study takes an attempt to investigate the mechanisms through which FKN regulates the macrophage activation and the acute kidney injury (AKI) involved in the inflammatory response induced by lipopolysaccharide (LPS) by using FKN-knockout (FKN-KO) mice and cultured macrophages.Results: In this study, we found that FKN and Wnt/β-catenin signaling have a positive interaction in macrophages. FKN-overexpression inhibited LPS-induced macrophage apoptosis. However, it enhanced the cell viability and transformed them into M2 type. The effects of FKN-overexpression were accelerated by activation of Wnt/β-catenin signaling. In the in vivo experiments, FKN deficiency suppressed the macrophage activation and reduced AKI induced by LPS. Inhibition of Wnt/β-catenin signaling and FKN deficiency further mitigated the pathologic process of AKI. Conclusions: We provide a novel mechanism underlying activation of macrophage in LPS-induced AKI. The positive interaction between FKN and Wnt/β-catenin signaling pathway may be the therapeutic target in kidney injury.

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Upregulated fractalkine levels in Chinese patients with lupus nephritis

Cited by 12 publications

References 30 publications

Review on Inflammation Markers in Chronic Kidney Disease

Review on Inflammation Markers in Chronic Kidney Disease

FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/β-Catenin Pathway in a Murine Model of Lupus Nephritis

Fractalkine Aggravates LPS-induced Macrophage Activation and Acute Kidney Injury via Wnt/β-catenin Signaling Pathway

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