Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway

Liu, Xinnong; Qu, Chengjia; Zhang, Yongbao; Fang, Jie; Teng, Lequn; Zhang, Rujiao; Zhang, Xiangyu; Shen, Chenyang

doi:10.1002/2211-5463.12942

Cited by 5 publications

(4 citation statements)

References 32 publications

(39 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous research has shown that VCAM-1 is closely related to restenosis in venous bridges 36,37 . VCAM-1 belongs to the immunoglobulin superfamily and can be expressed in endothelial cells, smooth muscle cells, and macrophages 38 .…”

Section: Discussionmentioning

confidence: 96%

Bletilla striata Polysaccharide Prevents Restenosis of Vein Graft Through Inhibiting Cell Proliferation in Rat Model

et al. 2020

View full text Add to dashboard Cite

Coronary artery bypass grafting (CABG) is still the most effective method for the treatment of coronary heart disease at present. However, the restenosis of vein grafts following surgery is an important complication of CABG. In this study, Bletilla striata polysaccharide (BSP), which has anti-inflammatory and antiproliferative properties, was used to prevent or delay the proliferation of venous bridge endothelial cells in a rat model. We transplanted the autogenous jugular vein to the rat carotid artery, and wrapped it with BSP. We carried out experiments in 4 groups (with 24 rats in each group): a high-BSP dose group (the HBG group, 10 mg), a low-BSP dose group (the LBG group, 3 mg), a pluronic gel group (the gel group), and a control group. Vein grafts were then harvested after 3, 14, and 28 days. Following transplantation, we used color Doppler ultrasound to assess the patency of the transplanted vein. The grafted veins were stained with hematoxylin and eosin (H&E) and Masson to measure the thickness of the intima and media of the blood vessels. Proliferating cell nuclear antigen (PCNA) and vascular cell adhesion molecule-l (VCAM-1) were assessed in vein grafts by immunohistochemistry and western blotting. We detected a significant reduction in the proliferation of endothelial cells in the BSP group compared with the control group ( P < 0.05). H&E and Masson’s trichrome staining showed that the extent of intimal hyperplasia in transplanted veins from the high BSP group (HBS) (67.42 ± 0.54 µm) and low BSP group (LBS) (120.83 ± 1.87 µm) groups was significantly lower than that in the control group (257.03 ± 2.74 µm, P < 0.05), and that the extent of intimal hyperplasia in the HBS group was lower than that in the LBS group ( P < 0.05). We found that the effect of BSP was dose-dependent, as high-dose BSP had a more significant inhibitory effect on cell proliferation than low-dose BSP ( P < 0.05). The results of immunohistochemistry and western blotting showed that PCNA and VCAM-1 were significantly downregulated in the BSP treatment group on days 14 and 28 ( P < 0.05). BSP inhibits the proliferation of vascular endothelial cells and reduces the expression of VCAM-1, thereby inhibiting the restenosis of graft veins.

show abstract

Section: Discussionmentioning

confidence: 96%

Bletilla striata Polysaccharide Prevents Restenosis of Vein Graft Through Inhibiting Cell Proliferation in Rat Model

et al. 2020

View full text Add to dashboard Cite

show abstract

“…It was found that the expression of CKLF1 and vascular adhesion molecule-1 (VCAM-1) was significantly increased in human carotid plaques compared to controls. Meanwhile, CKLF1 promoted the aggregation of human aortic smooth muscle cells (HASMCs) and monocyte adhesion through the NF-κB/VCAM-1 pathway ( 71 ).…”

Section: Cklf1-related Diseasesmentioning

confidence: 99%

“…Unlike other ligands of CCR4, such as TRAC and MDC, CKLF1 can activate the NF-κB classical signaling pathway involved in disease-causing mechanisms, which may have to do with its specific structure. A study on human amniotic mesenchymal stromal cells showed that CKLF1 mediates monocyte adhesion and smooth muscle cell (SMC) migration through the NF-κB/VCAM-1 pathway and that the use of PDTC, an NF-κB inhibitor, suppressed the CKLF1-induced elevation of VCAM-1 ( 71 ). A mouse MCAO model study showed that CKLF1 binding to CCR4 activated the NF-κB pathway and promoted microglia/macrophage polarization toward the M1 phenotype ( 49 ).…”

Section: Mechanisms Of Cklf1-mediated Pathogenesismentioning

confidence: 99%

Role of chemokine-like factor 1 as an inflammatory marker in diseases

Feng

2023

Front. Immunol.

View full text Add to dashboard Cite

Immunoinflammatory mechanisms have been incrementally found to be involved in the pathogenesis of multiple diseases, with chemokines being the main drivers of immune cell infiltration in the inflammatory response. Chemokine-like factor 1 (CKLF1), a novel chemokine, is highly expressed in the human peripheral blood leukocytes and exerts broad-spectrum chemotactic and pro-proliferative effects by activating multiple downstream signaling pathways upon binding to its functional receptors. Furthermore, the relationship between CKLF1 overexpression and various systemic diseases has been demonstrated in both in vivo and in vitro experiments. In this context, it is promising that clarifying the downstream mechanism of CKLF1 and identifying its upstream regulatory sites can yield new strategies for targeted therapeutics of immunoinflammatory diseases.

show abstract

“…For instance, the findings of a study by Liu et al ( 17 ) suggest that CKLF1 serves an oncogenic role in the tumorigenesis and metastasis of hepatocellular carcinoma. CKLF1 contributes to neointimal hyperplasia via the activation of the NF-κB/vascular cell adhesion molecule 1 signaling pathway ( 18 ). Additionally, Pan et al ( 19 ) proposed that CKLF1 exhibits higher expression in necrotic cartilage tissues compared with normal cartilage tissues.…”

Section: Introductionmentioning

confidence: 99%

CKLF1 interference alleviates IL‑1β‑induced inflammation, apoptosis and degradation of the extracellular matrix in chondrocytes via CCR5

Wang

2023

Exp Ther Med

View full text Add to dashboard Cite

Osteoarthritis (OA) is a type of joint disease with a rising prevalence and incidence among the elderly across the global population. Chemokine-like factor 1 (CKLF1) is a human cytokine, which has been demonstrated to be involved in the progression of multiple human diseases. However, little attention has been paid to the impact of CKLF1 on OA. The present study was designed to identify the role of CKLF1 in OA and to clarify the regulatory mechanism. The expression levels of CKLF1 and its receptor CC chemokine receptor 5 (CCR5) were examined by reverse transcription-quantitative PCR (RT-qPCR) and western blotting. A Cell Counting Kit-8 assay was used to estimate cell viability. The levels and expression of inflammatory factors were determined by ELISA and RT-qPCR, respectively. Apoptosis was investigated by TUNEL assays and the protein levels of apoptosis-related factors were analyzed by western blotting. RT-qPCR and western blotting were used to examine the expression of extracellular matrix (ECM) degradation-associated proteins and ECM components. Dimethylmethylene blue analysis was used to analyze the production of soluble glycosamine sulfate additive. A co-immunoprecipitation assay was used to confirm the protein interaction between CKLF1 and CCR5. The results revealed that CKLF1 expression was increased in IL-1β-exposed murine chondrogenic ATDC5 cells. Furthermore, CKLF1 silencing enhanced the viability of IL-1β-induced ATDC5 cells, while inflammation, apoptosis and degradation of the ECM were reduced. Additionally, CKLF1 knockdown led to decreased CCR5 expression in IL-1β-challenged ATDC5 cells, and CKLF1 bound with CCR5. The enhanced viability, as well as the suppressed inflammation, apoptosis and degradation of the ECM, following CKLF1 knockdown in the IL-1β-induced ATDC5 cells were all restored after CCR5 was overexpressed. In conclusion, CKLF1 might serve a detrimental role in the development of OA by targeting its receptor CCR5.

show abstract

Chemokine‐like factor 1 (CKLF1) aggravates neointimal hyperplasia through activating the NF‐κB /VCAM‐1 pathway

Cited by 5 publications

References 32 publications

Bletilla striata Polysaccharide Prevents Restenosis of Vein Graft Through Inhibiting Cell Proliferation in Rat Model

Bletilla striata Polysaccharide Prevents Restenosis of Vein Graft Through Inhibiting Cell Proliferation in Rat Model

Role of chemokine-like factor 1 as an inflammatory marker in diseases

CKLF1 interference alleviates IL‑1β‑induced inflammation, apoptosis and degradation of the extracellular matrix in chondrocytes via CCR5

Contact Info

Product

Resources

About