Proteomic Analysis in Esophageal Eosinophilia Reveals Differential Galectin-3 Expression and S-Nitrosylation

Davis, Carla M.; Hiremath, Girish; Wiktorowicz, John E.; Soman, Kizhake V.; Straub, C.; Nance, Christina; Quintanilla, Norma; Pazdrak, Konrad; Thakkar, Kalpesh; Olivé, Anthony; Kurosky, Alexander

doi:10.1159/000444675

Cited by 11 publications

(7 citation statements)

References 43 publications

(60 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This cytokine array did, however, identify 6 cytokines/soluble factors whose expression was significantly upregulated in epithelium-enriched esophageal tissue of aged mice: bFGF, OPN, CRP, Lipocalin-2, NOV and Galectin-3. Among these, bFGF, OPN, and Galectin-3 have been shown to be upregulated in biospecimens from EoE patients with bFGF detected in plasma, OPN in urine, and Galectin-3 in esophageal biopsies (38)(39)(40). Although these factors have not been linked to EoE fibrosis, they have been associated with fibrosis in other tissue sites.…”

Section: Discussionmentioning

confidence: 99%

A role for age-associated alterations in esophageal epithelium in eosinophilic esophagitis-associated fibrosis

Klochkova

Fuller²,

Miller³

et al. 2022

Front. Allergy

View full text Add to dashboard Cite

Subepithelial fibrosis occurs in a subset of eosinophilic esophagitis (EoE) patients and is associated with esophageal stricture. While mechanisms driving EoE fibrosis remain incompletely understood, findings from experimental systems support roles for epithelial-fibroblast crosstalk in this type of tissue remodeling. The current paradigm presents EoE as a progressive fibrostenotic disease in which aged patients develop fibrosis as a function of disease chronicity. In the current study we provide evidence that altered epithelial biology in the aging esophagus may also contribute to EoE-associated fibrosis. We find that induction of EoE inflammation in young and aged mice using the MC903/Ovalbumin protocol for the same time period results in increased lamina propria thickness uniquely in aged animals. Additionally, epithelial cells from aged mice less efficiently limit fibroblast contractility in collagen plug contraction assays compared to those from their young counterparts. Finally, to identify potential mechanisms through which aged esophageal epithelial cells may stimulate fibrotic remodeling, we perform cytokine array experiments in young and aged mice. These studies are significant as identification of age-associated factors that contribute to fibrotic remodeling may aid in the design of strategies toward early detection, prevention, and therapy of fibrostenotic EoE.

show abstract

Section: Discussionmentioning

confidence: 99%

A role for age-associated alterations in esophageal epithelium in eosinophilic esophagitis-associated fibrosis

Klochkova

Fuller²,

Miller³

et al. 2022

Front. Allergy

View full text Add to dashboard Cite

show abstract

“…All these observations further add to the functional repertoire of galectins since such interactions have been shown to contribute to, e.g., intracellular signaling and splicing [ 28 , 33 , 34 ]. Finally, it is noteworthy to point out that galectins can form heterodimers with family members as well as with cytokines [ 35 , 36 ] and that they can be subjected to both post-transcriptional and post-translational modifications [ 37 , 38 , 39 ], aspects of which we are only beginning to understand the functional consequences. Nevertheless, it is nowadays well established that galectins constitute a protein family with versatile functions that contributes to a plethora of molecular, cellular and biological processes.…”

Section: The Galectin Protein Familymentioning

confidence: 99%

Galectins in Esophageal Cancer: Current Knowledge and Future Perspectives

Godefa

Derks

Thijssen

2022

Cancers

View full text Add to dashboard Cite

Esophageal cancer is a disease with poor overall survival. Despite advancements in therapeutic options, the treatment outcome of esophageal cancer patients remains dismal with an overall 5-year survival rate of approximately 20 percent. To improve treatment efficacy and patient survival, efforts are being made to identify the factors that underlie disease progression and that contribute to poor therapeutic responses. It has become clear that some of these factors reside in the tumor micro-environment. In particular, the tumor vasculature and the tumor immune micro-environment have been implicated in esophageal cancer progression and treatment response. Interestingly, galectins represent a family of glycan-binding proteins that has been linked to both tumor angiogenesis and tumor immunosuppression. Indeed, in several cancer types, galectins have been identified as diagnostic and/or prognostic markers. However, the role of galectins in esophageal cancer is still poorly understood. Here, we summarize the current literature with regard to the expression and potential functions of galectins in esophageal cancer. In addition, we highlight the gaps in the current knowledge and we propose directions for future research in order to reveal whether galectins contribute to esophageal cancer progression and provide opportunities to improve the treatment and survival of esophageal cancer patients.

show abstract

“…The need for more research also applies to the role of post-translational modifications of galectins in endothelial cells. Different protein modifications with different functional effects on galectins have been reported, including proteolytic cleavage, phosphorylation, and S-nitrosylation [ 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 ]. With regard to angiogenesis, it was shown that proteolytic processing of galectin-3 influences the angioregulatory activity of the protein (see also next section) [ 52 ].…”

Section: Endothelial Galectin Expressionmentioning

confidence: 99%

Galectins in Endothelial Cell Biology and Angiogenesis: The Basics

Thijssen

2021

Biomolecules

View full text Add to dashboard Cite

Angiogenesis, the growth of new blood vessels out of existing vessels, is a complex and tightly regulated process. It is executed by the cells that cover the inner surface of the vasculature, i.e., the endothelial cells. During angiogenesis, these cells adopt different phenotypes, which allows them to proliferate and migrate, and to form tube-like structures that eventually result in the generation of a functional neovasculature. Multiple internal and external cues control these processes and the galectin protein family was found to be indispensable for proper execution of angiogenesis. Over the last three decades, several members of this glycan-binding protein family have been linked to endothelial cell functioning and to different steps of the angiogenesis cascade. This review provides a basic overview of our current knowledge regarding galectins in angiogenesis. It covers the main findings with regard to the endothelial expression of galectins and highlights their role in endothelial cell function and biology.

show abstract

Proteomic Analysis in Esophageal Eosinophilia Reveals Differential Galectin-3 Expression and S-Nitrosylation

Cited by 11 publications

References 43 publications

A role for age-associated alterations in esophageal epithelium in eosinophilic esophagitis-associated fibrosis

A role for age-associated alterations in esophageal epithelium in eosinophilic esophagitis-associated fibrosis

Galectins in Esophageal Cancer: Current Knowledge and Future Perspectives

Galectins in Endothelial Cell Biology and Angiogenesis: The Basics

Contact Info

Product

Resources

About