YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

Li, Te‐Mao; Liu, Shan‐Chi; Huang, Ya-Hsin; Huang, Chien-Chung; Hsu, Chin‐Jung; Tsai, Chun‐Hao; Wang, Shih‐Wei; Tang, Chih‐Hsin

doi:10.3390/ijms18050920

Cited by 40 publications

(32 citation statements)

References 42 publications

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“…We made several potentially novel observations comparing aGVHD onset with normal biopsies in this analysis. For example, we observed a significant elevation of CHI3L1, also known as YKL-40, a proinflammatory factor with known pathogenic roles in neovascularization, macrophage recruitment, and bacterial adhesion, in aGVHD (16)(17)(18)(19). The potential role of CHI3L1 in clinical allogeneic HCT has otherwise not been described aside from a report identifying elevated plasma CHI3L1 in transplant recipients with a very high HCT comorbidity index of 5+ (20).…”

Section: Discussionmentioning

confidence: 78%

Stress responses, M2 macrophages, and a distinct microbial signature in fatal intestinal acute graft-versus-host disease

Holtan¹,

Shabaneh²,

Betts³

et al. 2019

JCI Insight

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Section: Discussionmentioning

confidence: 78%

Stress responses, M2 macrophages, and a distinct microbial signature in fatal intestinal acute graft-versus-host disease

Holtan¹,

Shabaneh²,

Betts³

et al. 2019

JCI Insight

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“…The protein encoding by Chi3l1 gene is an inflammatory marker associated with insulin resistance and having a role in endothelial dysfunction and atherosclerosis [40]. It contributes to stimulation of angiogenesis of endothelial progenitor cells [41]. The increased expression of this gene in the brain stem (in nucleus tractus solitarii) of spontaneously hypertensive rats (SHR) was considered as a sign of NTS inflammatory state in SHR rats [42].…”

Section: Discussionmentioning

confidence: 99%

The differences in brain stem transcriptional profiling in hypertensive ISIAH and normotensive WAG rats

et al. 2019

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Background: The development of essential hypertension is associated with a wide range of mechanisms. The brain stem neurons are essential for the homeostatic regulation of arterial pressure as they control baroreflex and sympathetic nerve activity. The ISIAH (Inherited Stress Induced Arterial Hypertension) rats reproduce the human stress-sensitive hypertensive disease with predominant activation of the neuroendocrine hypothalamic-pituitaryadrenal and sympathetic adrenal axes. RNA-Seq analysis of the brain stems from the hypertensive ISIAH and normotensive control WAG (Wistar Albino Glaxo) rats was performed to identify the differentially expressed genes (DEGs) and the main central mechanisms (biological processes and metabolic pathways) contributing to the hypertensive state in the ISIAH rats. Results: The study revealed 224 DEGs. Their annotation in databases showed that 22 of them were associated with hypertension and blood pressure (BP) regulation, and 61 DEGs were associated with central nervous system diseases. In accordance with the functional annotation of DEGs, the key role of hormonal metabolic processes and, in particular, the enhanced biosynthesis of aldosterone in the brain stem of ISIAH rats was proposed. Multiple DEGs associated with several Gene Ontology (GO) terms essentially related to modulation of BP were identified. Abundant groups of DEGs were related to GO terms associated with responses to different stimuli including response to organic (hormonal) substance, to external stimulus, and to stress. Several DEGs making the most contribution to the inter-strain differences were detected including the Ephx2, which was earlier defined as a major candidate gene in the studies of transcriptional profiles in different tissues/organs (hypothalamus, adrenal gland and kidney) of ISIAH rats. Conclusions:The results of the study showed that inter-strain differences in ISIAH and WAG brain stem functioning might be a result of the imbalance in processes leading to the pathology development and those, exerting the compensatory effects. The data obtained in this study are useful for a better understanding of the genetic mechanisms underlying the complexity of the brain stem processes in ISIAH rats, which are a model of stresssensitive form of hypertension.

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“…In myocarditis, miR‐590‐3p was also identified as a novel miRNA that could target nuclear factor κ‐B in vivo (Zhao et al, ). On a related note, in endothelial progenitor cells, miR‐590‐3p likely inhibited interleukin‐18 expression to promote angiogenesis in vivo (Li et al, ). In our current in vitro cell culture model of using trophoblast cell line HTR‐8/SVneo, miR‐590‐3p was demonstrated to directly target LRP6 to downregulate its expression.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐590‐3p inhibits trophoblast‐dependent maternal spiral artery remodeling by repressing low‐density lipoprotein receptor‐related protein 6

Zhang

Pan

et al. 2018

Molec Gen & Gen Med

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BackgroundThe remodeling of maternal spiral artery following embryo implantation, which relies on well‐regulated trophoblast functions, is a pivotal process to ensure a successful pregnancy. Low‐density lipoprotein receptor‐related protein 6 (LRP6) and microRNAs (miRNAs, miRs) are suggested to be involved in angiogenesis and several vascular diseases; however, their functions in the control of trophoblast remain elusive. We therefore aimed to examine the roles of LRP6 and miR‐590‐3p in the regulation of trophoblast during the remodeling of maternal spiral artery.MethodsHTR‐8/SVneo cell, a trophoblast cell line, was utilized to study the effects of LRP6 and miR‐590‐3p on apoptosis, cell proliferation, migration, invasion, as well as tube formation. Expression of angiogenic factors placental growth factor (PlGF), matrix metalloproteinases (MMPs), vascular endothelial growth factor (VEGF), and activities of canonical Wnt/β‐catenin signaling pathway, which were implicated in the process of artery remodeling, were also examined.ResultsMiR‐590‐3p directly targeted 3′ untranslated region (3′‐UTR) of LRP6 mRNA and repressed LRP6 expression, which in turn inhibited proliferation, migration, invasion, as well as tube formation, and resulted in apoptosis in HTR‐8/SVneo cells. Further, inhibition of LRP6 through miR‐590‐3p significantly suppressed the expression of PlGF, MMPs, and VEGF and reduced the activation of Wnt/β‐catenin signaling pathway.ConclusionMicroRNAs‐590‐3p may inhibit trophoblast‐dependent maternal spiral artery remodeling, via both trophoblast invasion and endovascular formation, by repressing LRP6.

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YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells

Cited by 40 publications

References 42 publications

Stress responses, M2 macrophages, and a distinct microbial signature in fatal intestinal acute graft-versus-host disease

Stress responses, M2 macrophages, and a distinct microbial signature in fatal intestinal acute graft-versus-host disease

The differences in brain stem transcriptional profiling in hypertensive ISIAH and normotensive WAG rats

MicroRNA‐590‐3p inhibits trophoblast‐dependent maternal spiral artery remodeling by repressing low‐density lipoprotein receptor‐related protein 6

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