Kaempferol regulates OPN–CD44 pathway to inhibit the atherogenesis of apolipoprotein E deficient mice

Xiao, Hong-Bo; Lu, Xiangyang; Sun, Zhi-Liang; Zhang, Hengbo

doi:10.1016/j.taap.2011.09.024

Cited by 36 publications

(26 citation statements)

References 39 publications

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“…There is increasing evidence to suggest that OPN may be a key factor contributing to inflammation. In vivo, plasma levels of OPN are elevated in ApoE À/À mice [7]. 2,4,6-Trinitrobenzenesulfonic acid-treated wild type mice develop Values are mean AE SD, n = 10; LPS: lipopolysaccharide; TNFa: tumor necrosis factor alpha; IL-1b: interleukin-1b; IL-6: interleukin-6.…”

Section: Discussionmentioning

confidence: 99%

“…As a pleiotropic T-helper 1 cytokine, OPN contributes to cell adhesion, chemotaxis, apoptosis, migration, invasion, and anchorage-independent growth of tumor cells. Studies in vitro, animal testing and clinical trials show that OPN plays an important role in acute and chronic inflammatory diseases [7,8]. Some data suggests that mastitis is an inflammation disease [9].…”

Section: Introductionmentioning

confidence: 99%

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LPS induces pro-inflammatory response in mastitis mice and mammary epithelial cells: Possible involvement of NF-κB signaling and OPN

Xiao

Wang

Liu

et al. 2015

Pathologie Biologie

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

LPS induces pro-inflammatory response in mastitis mice and mammary epithelial cells: Possible involvement of NF-κB signaling and OPN

Xiao

Wang

Liu

et al. 2015

Pathologie Biologie

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“…With specific respect to CD44, several lines of evidence suggest that increased CD44 expression plays a role in atherogenesis. For example, the expression of CD44 has been shown to be upregulated in macrophage-laden atherosclerotic lesions relative to simple fibrous lesions [13], and several CD44 ligands have been shown to be upregulated in the extracellular matrix of atherosclerotic lesions [14]. Moreover, CD44 expression has been shown to be upregulated in the vessel walls of apoE-deficient mice during early AS [6,15], while CD44-null mice display reduced activated monocyte/macrophage recruitment to atherosclerotic lesions as well as reductions in atherosclerotic lesion size [16].…”

Section: Discussionmentioning

confidence: 99%

Injection of hTERT-Transduced Endothelial Progenitor Cells Promotes Beneficial Aortic Changes in a High-Fat Dietary Model of Early Atherosclerosis

Deng²,

Zhao³

et al. 2016

Cardiology

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Objectives: Cultured endothelial progenitor cells (EPCs) display troubling issues that adversely affect their applicability to endothelial regeneration. We hypothesized that transduction of the human telomerase catalytic subunit (hTERT) gene would enhance EPC function in treating dietary-induced early atherosclerosis (AS). Methods: A dietary-induced early AS model was successfully constructed in 90 healthy male rats, while 30 healthy control (HC) rats were normally fed. Four experimental groups were constructed: an untreated HC group; an untreated AS group injected with PBS; a null EPC AS group injected with null vector-transduced EPCs, and an hTERT EPC AS group injected with hTERT-transduced EPCs. Two months postinjection, abdominal aortas were extracted to validate EPC integration and comparatively assess mRNA and protein expression of the early atherosclerotic markers VCAM-1, ICAM-1, LFA-1, Mac-1, CD44, MCP-1, endothelial nitric oxide synthase (eNOS), and apolipoprotein E. Results: In vitro, hTERT transduction of EPCs resulted in a significantly superior proliferative capacity as well as significantly higher NO, iNOS, and LDH secretory capacity. In vivo injection of hTERT-transduced EPCs produced significant reductions in CD44 and MCP-1 expression as well as a significant increase in eNOS expression relative to injection with null vector-transduced EPCs (all p < 0.05). Conclusion: hTERT-transduced human EPCs may be useful in treating dietary-induced early AS.

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“…However, little is known about the mechanisms responsible for these anti-inflammatory effects. Our recent work also found that kaempferol could regulate the OPN-CD44 pathway to inhibit the atherogenesis of apolipoprotein E deficient mice (Xiao et al 2011); however, the regulatory effect of kaempferol on the OPN-CD44 pathway in vitro has not yet been defined. In addition, aldosterone can produce reactive oxygen species (ROS) (Miyata et al 2005).…”

Section: Introductionmentioning

confidence: 93%

“…As a flavonoid compound, kaempferol has potent anti-inflammatory properties (Xiao et al 2011). Dietary kaempferol ameliorates inflammatory diseases by interfering with NF-B signaling (Gong et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory properties of kaempferol via its inhibition of aldosterone signaling and aldosterone-induced gene expression

Liu

Xiao

Fang

2014

Can. J. Physiol. Pharmacol.

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Osteopontin (OPN), also called cytokine Eta-1, is a pro-inflammatory cytokine. Recent studies have shown that aldosterone increases OPN gene expression in endothelial cells. As a flavonoid compound, kaempferol has potent anti-inflammatory properties, but whether kaempferol regulates aldosterone signaling and aldosterone-induced gene expression is still unknown. Human umbilical vein endothelial cells (HUVECs) were pretreated with kaempferol (0, 1, 3, or 10 μmol/L) for 1 h prior to exposure to aldosterone (10(-6) mol/L) for 24 h. Aldosterone induced generation of reactive oxygen species; OPN and cluster of differentiation 44 gene expression; phospho-p38 MAPK and NF-κB binding activity. The effect of aldosterone was abrogated by kaempferol and spironolactone (10(-6) mol/L). The present results suggest that kaempferol exerts its anti-inflammatory properties via its inhibition of aldosterone signaling and aldosterone-induced gene expression in HUVECs.

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Kaempferol regulates OPN–CD44 pathway to inhibit the atherogenesis of apolipoprotein E deficient mice

Cited by 36 publications

References 39 publications

LPS induces pro-inflammatory response in mastitis mice and mammary epithelial cells: Possible involvement of NF-κB signaling and OPN

LPS induces pro-inflammatory response in mastitis mice and mammary epithelial cells: Possible involvement of NF-κB signaling and OPN

Injection of hTERT-Transduced Endothelial Progenitor Cells Promotes Beneficial Aortic Changes in a High-Fat Dietary Model of Early Atherosclerosis

Anti-inflammatory properties of kaempferol via its inhibition of aldosterone signaling and aldosterone-induced gene expression

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