Knockdown of <i>YKL‐40</i> inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

Chen, Hongyan; Zhou, Zhao-Yu; Luo, Yan-Lu; Luo, Qian; Fan, Jiangtao

doi:10.1002/cbin.11699

Cited by 6 publications

(5 citation statements)

References 40 publications

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“…HE staining in the AVF reconstruction group showed neovascularization, which further confirmed that VEGF-A might play a role in AVF failure. It is reported that CHI3L1 small interfering RNA could reduce the expression level of VEGF-A in endometrial cancer HEC-1A cells(Chen et al 2021). The expression of CHI3L1 and VEGF-A was positively correlated in all samples in this study, suggesting that VEGF-A may be one of the targets of CHI3L1 in AVF failure.In conclusion, the overexpression of CHI3L1 in local tissues provides further evidence for serum CHI3L1 as a biomarker of AVF failure.…”

supporting

confidence: 51%

The Potential Roles of CHI3L1 in Failed Autologous Arteriovenous Fistula in End-Stage Renal Disease

Zhang

Wang

et al. 2023

Tohoku J. Exp. Med.

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Autologous arteriovenous fistula (AVF) is commonly placed for hemodialysis treatment.Recent studies show that increased baseline serum level of Chitinase-3-like protein 1 (CHI3L1) is independently associated with a higher risk of the early failure of forearm AVFs.However, the changes and mechanisms of CHI3LI in local vascular tissues of failed AVF haven't be revealed. This study aims to conduct the expression and mechanism of CHI3L1 in vascular tissues from patients. Immunoreactivity of CHI3L1, matrix metalloproteinase 2 (MMP-2) and vascular endothelial growth factor-A (VEGF-A) were detected in vascular tissues collected from nine patients of AVF surgery. Due to the significant stenosis clinically, six of the nine patients received arteriovenous fistula reconstruction. The expression differences of CHI3L1 between the initial vascular tissues and failed AVF are significant (P ＜ 0.05). Failed AVF due to stenosis shows intraluminal thrombus, collagen fiber rupture, fibrous connective tissue hyperplasia, tube wall thickening, neovascularization, scattered inflammatory cell infiltration in the tunica media as well as high CHI3L1 expression level, and the expression of MMP-2 (r=0.9022, P=0.0139) and VEGF-A (r=0.8355, P=0.0393) was positively correlated with CHI3L1. CHI3L1 expression in vascular tissues possibly plays an important role in AVF failure. MMP-2 and VEGF-A may participate in venous stenosis with CHI3L1.

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supporting

confidence: 51%

The Potential Roles of CHI3L1 in Failed Autologous Arteriovenous Fistula in End-Stage Renal Disease

Zhang

Wang

et al. 2023

Tohoku J. Exp. Med.

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“…Additionally, in vitro cell culture experiments show an increase in their expression when macrophages or neutrophils are stimulated with IFN-γ, TNF-α, or toll-like receptor ligands ( 30 ). In murine models of parasitic infections, CLPs are secreted in response to IL-4 by alternatively activated macrophages believed to resolve inflammation and lead to wound healing by enhancing fibronectin and TGF-β secretion, extracellular matrix deposition, and angiogenesis ( 15 , 16 , 31 ).…”

Section: Role Of Ykl-40 In the Mechanism Of Asthmamentioning

confidence: 99%

“…The role of CLPs in the pathogenesis of these diseases is not fully understood. It has been suggested that YKL-40 regulates vascular endothelial growth factor (VEGF), which is involved in inflammation and angiogenesis ( 15 , 16 ). In asthma, VEGF enhances the proliferation of bronchial smooth muscles and mucus hypersecretion ( 17 , 18 ).…”

Section: Introductionmentioning

confidence: 99%

YKL-40 as a possible marker of neutrophilic asthma

Specjalski

Romantowski²,

Niedoszytko³

2023

Front. Med.

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Asthma is a heterogeneous chronic disorder of the airways, with inflammation and bronchial hyperresponsiveness as its major underlying phenomena. Asthmatics vary in terms of inflammation pattern, concomitant pathologies, and factors aggravating the course of the disease. As a result, there is a need for sensitive and specific biomarkers that could facilitate diagnosing asthma as well as phenotyping in everyday practice. Chitinases and chitinase-like proteins (CLPs) seem promising in this field. Chitinases are evolutionarily conserved hydrolases that degrade chitin. In contrast, CLPs bind chitin but do not have degrading activity. Mammalian chitinases and CLPs are produced by neutrophils, monocytes, and macrophages in response to parasitic or fungal infections. Recently, several questions have been raised about their role in chronic airway inflammation. Several studies demonstrated that overexpression of CLP YKL-40 was associated with asthma. Moreover, it correlated with exacerbation rate, therapy resistance, poor control of symptoms, and, inversely, with FEV1. YKL-40 facilitated allergen sensitization and IgE production. Its concentration was elevated in bronchoalveolar lavage fluid after an allergen challenge. It was also found to promote the proliferation of bronchial smooth muscle cells and correlate with subepithelial membrane thickness. Thus, it may be involved in bronchial remodeling. Associations between YKL-40 and particular asthma phenotypes remain unclear. Some studies showed that YKL-40 correlates with blood eosinophilia and FeNO, suggesting a role in T2-high inflammation. Quite the opposite, cluster analyses revealed the highest upregulation in severe neutrophilic asthma and obesity-associated asthma. The main limitation in the practical application of YKL-40 as a biomarker is its low specificity. High serum levels of YKL-40 were also found in COPD and several malignancies, in addition to infectious and autoimmune diseases. To conclude, the level of YKL-40 correlates with asthma and some clinical features in the whole asthmatic population. The highest levels are found in neutrophilic and obesity-related phenotypes. However, due to its low specificity, the practical application of YKL-40 remains uncertain but could be useful in phenotyping, especially when combined with other biomarkers.

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“…High CHI3L1 immune reactivity is associated with poor prognosis in endometrial cancer patients, and CHI3L1 also plays a role in angiogenesis and primary and metastatic tumors around tumor blood vessels [151]. As early as 2011, Francescone et al found that CHI3L1 can promote glioblastoma angiogenesis and radioresistance [152], while Chen et al found that silencing CHI3L1 can inhibit the VEGF/VEGFR and ERK1/2 signaling pathways, further reducing tumor angiogenesis and inhibiting tumor metastasis [153].…”

Section: Chi3l1 and Endometrial Cancermentioning

confidence: 99%

Potential Roles and Future Perspectives of Chitinase 3-like 1 in Macrophage Polarization and the Development of Diseases

Zhao,

Huang,

Jiang

2023

IJMS

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Chitinase-3-like protein 1 (CHI3L1), a chitinase-like protein family member, is a secreted glycoprotein that mediates macrophage polarization, inflammation, apoptosis, angiogenesis, and carcinogenesis. Abnormal CHI3L1 expression has been associated with multiple metabolic and neurological disorders, including diabetes, atherosclerosis, and Alzheimer’s disease. Aberrant CHI3L1 expression is also reportedly associated with tumor migration and metastasis, as well as contributions to immune escape, playing important roles in tumor progression. However, the physiological and pathophysiological roles of CHI3L1 in the development of metabolic and neurodegenerative diseases and cancer remain unclear. Understanding the polarization relationship between CHI3L1 and macrophages is crucial for disease progression. Recent research has uncovered the complex mechanisms of CHI3L1 in different diseases, highlighting its close association with macrophage functional polarization. In this article, we review recent findings regarding the various disease types and summarize the relationship between macrophages and CHI3L1. Furthermore, this article also provides a brief overview of the various mechanisms and inhibitors employed to inhibit CHI3L1 and disrupt its interaction with receptors. These endeavors highlight the pivotal roles of CHI3L1 and suggest therapeutic approaches targeting CHI3L1 in the development of metabolic diseases, neurodegenerative diseases, and cancers.

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Knockdown of YKL‐40 inhibits angiogenesis through regulation of VEGF/VEGFR2 and ERK1/2 signaling in endometrial cancer

Cited by 6 publications

References 40 publications

The Potential Roles of CHI3L1 in Failed Autologous Arteriovenous Fistula in End-Stage Renal Disease

The Potential Roles of CHI3L1 in Failed Autologous Arteriovenous Fistula in End-Stage Renal Disease

YKL-40 as a possible marker of neutrophilic asthma

Potential Roles and Future Perspectives of Chitinase 3-like 1 in Macrophage Polarization and the Development of Diseases

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