Expression of visfatin in the diabetic rat retina

Qu, Shen; Mo, Lijuan; Niu, Yunli; Sun, Xiaoting; Li, Houshuo; Wang, Zhen; Xu, Wei; Rong, Ao

doi:10.1111/ceo.12692

Cited by 3 publications

(2 citation statements)

References 27 publications

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“…Although the exact nature of the newly discovered Pros, Grn and visfatin signaling pathways in cornea remains unclear, it has been observed that these three signaling pathways were associated with retina, including that Pros1 mutation correlates with inherited retinal degenerations, 58 Grn deficiency results in photoreceptor degeneration in mouse retina 59 and visfatin expression in diabetic rat retina. 60 Although chemerin has been shown to promote vessel growth in the mouse corneal angiogenesis model, 61 its specific role in the cornea remains unexplored.…”

Section: Discussionmentioning

confidence: 99%

Single-Cell Transcriptomics Reveals Cellular Heterogeneity and Complex Cell–Cell Communication Networks in the Mouse Cornea

Wu,

Chang,

Chu

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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Purpose To generate a single-cell RNA-sequencing (scRNA-seq) map and construct cell–cell communication networks of mouse corneas. Methods C57BL/6 mouse corneas were dissociated to single cells and subjected to scRNA-seq. Cell populations were clustered and annotated for bioinformatic analysis using the R package “Seurat.” Differential expression patterns were validated and spatially mapped with whole-mount immunofluorescence staining. Global intercellular signaling networks were constructed using CellChat. Results Unbiased clustering of scRNA-seq transcriptomes of 14,732 cells from 40 corneas revealed 17 cell clusters of six major cell types: nine epithelial cell, three keratocyte, two corneal endothelial cell, and one each of immune cell, vascular endothelial cell, and fibroblast clusters. The nine epithelial cell subtypes included quiescent limbal stem cells, transit-amplifying cells, and differentiated cells from corneas and two minor conjunctival epithelial clusters. CellChat analysis provided an atlas of the complex intercellular signaling communications among all cell types. Conclusions We constructed a complete single-cell transcriptomic map and the complex signaling cross-talk among all cell types of the cornea, which can be used as a foundation atlas for further research on the cornea. This study also deepens the understanding of the cellular heterogeneity and heterotypic cell–cell interaction within corneas.

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Section: Discussionmentioning

confidence: 99%

Single-Cell Transcriptomics Reveals Cellular Heterogeneity and Complex Cell–Cell Communication Networks in the Mouse Cornea

Wu,

Chang,

Chu

et al. 2023

Invest. Ophthalmol. Vis. Sci.

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“…Therefore, visfatin binds to the insulin receptor-1 and exerts an insulin-like effect ( 230 ). Being adipocytokines with various pleiotropic effects visfatin exerts IR, inhibits WAT oxidative stress and inflammation, promotes vascular reparation, and suppresses ischemia-induced apoptosis of cardiac myocytes mainly through up-regulation of proinflammatory cytokines, such as TNF-α and MCP-1 ( 231 ). On the other hand, visfatin also up-regulates NF-κB in endothelial progenitor cells inducing apoptosis of these precursors leading to a decrease in the number of circulating endothelial progenitor cells with angiopoietic activity ( 232 , 233 ).…”

Section: Adipose Tissue Dysfunction and Heart Failurementioning

confidence: 99%

Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus

Berezin

Lichtenauer

2020

Front. Cardiovasc. Med.

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Adipose tissue dysfunction is a predictor for cardiovascular (CV) events and heart failure (HF) in patient population with obesity, metabolic syndrome, and known type 2 diabetes mellitus. Previous preclinical and clinical studies have yielded controversial findings regarding the role of accumulation of adipose tissue various types in CV risk and HF-related clinical outcomes in obese patients. There is evidence for direct impact of infiltration of epicardial adipocytes into the underlying myocardium to induce adverse cardiac remodeling and mediate HF development and atrial fibrillation. Additionally, perivascular adipocytes accumulation is responsible for release of proinflammatory adipocytokines (adiponectin, leptin, resistin), stimulation of oxidative stress, macrophage phenotype switching, and worsening vascular reparation, which all lead to microvascular inflammation, endothelial dysfunction, atherosclerosis acceleration, and finally to increase in CV mortality. However, systemic effects of white and brown adipose tissue can be different, and adipogenesis including browning of adipose tissue and deficiency of anti-inflammatory adipocytokines (visfatin, omentin, zinc-α2-glycoprotein, glypican-4) was frequently associated with adipose triglyceride lipase augmentation, altered glucose homeostasis, resistance to insulin of skeletal muscles, increased cardiomyocyte apoptosis, lowered survival, and weak function of progenitor endothelial cells, which could significantly influence on HF development, as well as end-organ fibrosis and multiple comorbidities. The exact underlying mechanisms for these effects are not fully understood, while they are essential to help develop improved treatment strategies. The aim of the review is to summarize the evidence showing that adipocyte dysfunction may induce the onset of HF and support advance of HF through different biological mechanisms involving inflammation, pericardial, and perivascular adipose tissue accumulation, adverse and electrical cardiac remodeling, and skeletal muscle dysfunction. The unbalancing effects of natriuretic peptides, neprilysin, and components of renin-angiotensin system, as exacerbating cause of altered adipocytokine signaling Berezin et al. Adipocyte Dysfunction in Heart Failure on myocardium and vasculature, in obesity patients at high risk of HF are disputed. The profile of proinflammatory and anti-inflammatory adipocytokines as promising biomarker for HF risk stratification is discussed in the review.

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Visfatin promotes angiogenesis of RF/6A cells through upregulation of VEGF/VEGFR‑2 under high‑glucose conditions

et al. 2021

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Expression of visfatin in the diabetic rat retina

Cited by 3 publications

References 27 publications

Single-Cell Transcriptomics Reveals Cellular Heterogeneity and Complex Cell–Cell Communication Networks in the Mouse Cornea

Single-Cell Transcriptomics Reveals Cellular Heterogeneity and Complex Cell–Cell Communication Networks in the Mouse Cornea

Emerging Role of Adipocyte Dysfunction in Inducing Heart Failure Among Obese Patients With Prediabetes and Known Diabetes Mellitus

Visfatin promotes angiogenesis of RF/6A cells through upregulation of VEGF/VEGFR‑2 under high‑glucose conditions

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