The expression and function of galectins in skin physiology and pathology

Wu, Nan; Liu, Fu‐Tong

doi:10.1111/exd.13512

Cited by 19 publications

(8 citation statements)

References 91 publications

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“…Non-malignant skin pathologies with high inflammatory background, such as atopic dermatitis, psoriasis, contact dermatitis and wound healing are associated with an increased galectin expression. But recently, skin cancers have been demonstrated to express these known inflammatory proteins involved in regulatory mechanisms (44). Patterns of galectin-3 expression in BCC and SCC were evaluated in relation to cellular differentiation.…”

Section: Non-melanoma Tumors: Squamous Cell and Basal Cell Skin Carcimentioning

confidence: 99%

Inflammation: A key process in skin tumorigenesis (Review)

et al. 2018

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The extremely delicate shift from an inflammatory process to tumorigenesis is a field of major scientific interest. While the inflammation induced by environmental agents has well known underlying mechanisms, less is known concerning the oncogenic changes that follow an inflammatory chronic status in the tissue microenvironment that can lead to pro-tumorigenic processes. Regardless of the origin of the environmental factors, the maintenance of an inflammatory microenvironment is a clear condition that favors tumorigenesis. Inflammation sustains the proliferation and survival of malignant transformed cells, can promote angiogenesis and metastatic processes, can negatively regulate the antitumoral adaptive and innate immune responses and may alter the efficacy of therapeutic agents. There is an abundance of studies focusing on molecular pathways that trigger inflammation-mediated tumorigenesis, and these data have revealed a series of biomarkers that can improve the diagnosis and prognosis in oncology. In skin there is a clear connection between tissue destruction, inflammation and tumor onset. Inflammation is a self-limiting process in normal physiological conditions, while tumor is a constitutive process activating new pro-tumor mechanisms. Among skin cancers, the most commonly diagnosed skin cancers, squamous cell carcinoma and basal cell carcinoma (BCC) have important inflammatory components. The most aggressive skin cancer, melanoma, is extensively research in regards to the new context of novel developed immune-therapies. In skin cancers, inflammatory markers can find their place in the biomarker set for improvement of diagnosis and prognosis.

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Section: Non-melanoma Tumors: Squamous Cell and Basal Cell Skin Carcimentioning

confidence: 99%

Inflammation: A key process in skin tumorigenesis (Review)

et al. 2018

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“…Given that in human skin some galectins play a crucial role in diverse cutaneous disorders, 38,43,[52][53][54] we sought to determine whether Gal-1, -3 and -8 were present in PG. We also examined whether these galectins could generate gal-glycan lattices able to regulate the behaviour of the plump ECs through the interactions with platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31), VEGFR-2, VEGFR-3, CD44, integrin β 1 and fibronectin (FN).…”

Section: Lay Summarymentioning

confidence: 99%

Plump endothelial cells integrated into pre-existing venules contribute to the formation of ‘mother’ and ‘daughter’ vessels in pyogenic granuloma: possible role of galectin-1, -3 and -8

Arciniegas

Carrillo

Rojas

et al. 2021

Scars, Burns & Healing

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Introduction: Pyogenic granuloma (PG) is a reactive inflammatory vascular lesion of the skin and mucous membranes, characterised by the presence of enlarged venules and seamed and seamless capillaries with plump endothelial cells (EC), and numerous macrophages. EC activation upregulates the synthesis of galectins and induces their translocation to the EC surface promoting angiogenesis and lymphangiogenesis, particularly galectin-1 (Gal-1), Gal-3 and Gal-8. However, the presence and distribution of Gal-1, -3 and -8, as well as their implications in the pathogenesis of PG, has not been considered. Materials and methods: Eight biopsies from patients diagnosed with PG were selected. The presence of PECAM-1/CD31, IL-1β, VEGF-C, VEGFR-2, VEGFR-3, integrin β1, CD44, fibronectin and Gal-1, -3 and -8 was assessed by immunofluorescence staining using confocal laser scanning microscopy. Results and Discussion: Immunostaining revealed that these molecules were present in the enlarged venules with plump ECs, in some macrophages and other immune cells. We propose that macrophages release VEGF-A and VEGF-C inducing VEGFR-2/VEGFR-3 expression and activation, leading macrophages to transdifferentiate into plump ECs that might integrate into pre-existing venules, contributing to the formation of enlarged venules with transluminal bridges and capillaries. EC activation, induced by certain cytokines, has been shown to stimulate galectin expression and changes in the cellular localisation through association and activation of specific EC surface glycoproteins. Therefore, it is plausible that Gal-1, -3 and -8, acting in a concerted manner, could be mediating the transdifferentiation of macrophages into plump ECs and facilitating their migration and incorporation into the new vessels. Lay Summary In this study, immunostaining of pyogenic granuloma (PG) tissue sections showed immunoreactivity for PECAM-1/CD31, IL-1β, VEGF-C, VEGFR-2 and VEGFR-3, and galectin-1, -3 and -8 in enlarged venules with plump endothelial cells (EC), as well as in some macrophages and other immune cells. Interestingly, enlarged and thin-walled transient vessels lined by PECAM-1/CD31 and VEGFR-2 immunopositive ECs that form from pre-existing normal venules in response to VEGF-A (called ‘mother’ vessels [MV]) and that undergo intraluminal bridging evolving into various types of capillaries (called ‘daughter’ vessels [DV]) have been observed in benign and malignant tumours, in physiological and pathological angiogenesis as well as in vascular malformations, suggesting an important role for VEGF-A and VEGFR-2 in such a process. However, it is not only the mechanisms by which the MVs evolve in different types of DVs that remains to be elucidated, but also whether the cells that form intraluminal bridges proceed from locally activated ECs or whether they are derived from bone marrow precursors or from resident macrophages. Given that the formation of homodimers by Gal-1 and Gal-8 and pentamers by Gal-3 to generate gal–glycan lattices at the cell surface and in the extracellular space has been shown, it is possible that in PG tissue Gal-1, -3 and -8, through their binding partners, form a supramolecular structure at the surface of ECs and plump ECs, macrophages and in the extracellular space that might be mediating the transdifferentiation of macrophages into plump ECs and facilitating the migration and incorporation of these cells into the pre-existing venules, thus contributing to the formation of MVs and DVs.

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“…Interestingly, the expression profile of galectins is altered during several pathological conditions (expert opinions for each disease have been reviewed in [ 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 ]). In particular, the production of galectins-1, -3, -7, -8, and -9 is deregulated during tumorigenesis [ 15 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Unraveling How Tumor-Derived Galectins Contribute to Anti-Cancer Immunity Failure

Laderach

Compagno

2021

Cancers

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Current data indicates that anti-tumor T cell-mediated immunity correlates with a better prognosis in cancer patients. However, it has widely been demonstrated that tumor cells negatively manage immune attack by activating several immune-suppressive mechanisms. It is, therefore, essential to fully understand how lymphocytes are activated in a tumor microenvironment and, above all, how to prevent these cells from becoming dysfunctional. Tumors produce galectins-1, -3, -7, -8, and -9 as one of the major molecular mechanisms to evade immune control of tumor development. These galectins impact different steps in the establishment of the anti-tumor immune responses. Here, we carry out a critical dissection on the mechanisms through which tumor-derived galectins can influence the production and the functionality of anti-tumor T lymphocytes. This knowledge may help us design more effective immunotherapies to treat human cancers.

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The expression and function of galectins in skin physiology and pathology

Cited by 19 publications

References 91 publications

Inflammation: A key process in skin tumorigenesis (Review)

Inflammation: A key process in skin tumorigenesis (Review)

Plump endothelial cells integrated into pre-existing venules contribute to the formation of ‘mother’ and ‘daughter’ vessels in pyogenic granuloma: possible role of galectin-1, -3 and -8

Unraveling How Tumor-Derived Galectins Contribute to Anti-Cancer Immunity Failure

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