Lutheran Blood Group Antigen as a Receptor for α5 Laminins in Gingival Epithelia

Willberg, Jaana; Hormia, M; Takkunen, Minna; Kikkawa, Yamato; Sekiguchi, Kiyotoshi; Virtanen, Ismo

doi:10.1902/jop.2007.060482

Cited by 3 publications

(3 citation statements)

References 57 publications

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“…Lutheran is a speciWc receptor of 5 chain laminins (Moulson et al 2001;Parsons et al 2001), of which only laminin-511 was found in our cell model. We have shown before that Lutheran is expressed coaligned with laminin 5 chain in normal oral BM (Willberg et al 2007). Here, a strong cell surface-conWned immunoreactivity was evident for Lutheran in 43A cells, whereas in 43B cells, only a diVuse and faint expression was found.…”

Section: Discussionmentioning

confidence: 94%

Epithelial-mesenchymal transition downregulates laminin α5 chain and upregulates laminin α4 chain in oral squamous carcinoma cells

Takkunen

Ainola

Vainionpää

et al. 2008

Histochem Cell Biol

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Basement membranes maintain the epithelial phenotype and prevent invasion and metastasis. We hypothesized that expression of basement membrane laminins might be regulated by epithelial-mesenchymal transition (EMT), hallmark of cancer progression. As EMT is mediated by transcription factor Snail, we used oral squamous carcinoma cells obtained from a primary tumor (43A), from its EMT-experienced recurrence (43B) and Snail-transfected 43A cells (43A-SNA) displaying full EMT, as a model to study laminins and their receptors. Northern blotting, immunofluorescence, and immunoprecipitation showed a gradual loss of laminin-511 and its receptor Lutheran from 43A to 43B and 43A-SNA cells. In contrast, neoexpression of laminin alpha4 mRNA was found congruent with synthesis of laminin-411. Chromatin immunoprecipitation disclosed direct binding of Snail to regions upstream of laminin alpha5 and alpha4 genes. Immunofluorescence and immunoprecipitation showed a switch from hemidesmosomal integrin alpha(6)beta(4) to alpha(6)beta(1) and neoexpression of alpha(1)beta(1) in 43A-SNA cells, and upregulation of integrin-linked kinase in both 43B and 43A-SNA cells. The cells adhered potently to laminin-511 and fibronectin, whereas adhesion to laminin-411 was minimal. In contrast, laminin-411 inhibited cell adhesion to other extracellular matrix proteins. In conclusion, EMT induces a switch from laminin-511 to laminin-411 expression, which may be directly controlled by Snail. Concomitant changes take place in laminin- and collagen-binding receptors. Laminin-411 reduces adhesion to laminin-511 and fibronectin, suggesting that tumor cells could utilize laminin-411 in their invasive behavior.

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Section: Discussionmentioning

confidence: 94%

Epithelial-mesenchymal transition downregulates laminin α5 chain and upregulates laminin α4 chain in oral squamous carcinoma cells

Takkunen

Ainola

Vainionpää

et al. 2008

Histochem Cell Biol

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“…However, in sickle cell disease (SCD), the vascular endothelium can be substantially damaged, causing exposure of the ECM to the circulation, 8,9 potentially allowing an interaction between erythrocytes and laminin-a5 to occur. 7,10 Such Lu/BCAM-mediated adhesion of sickle erythrocytes to the vascular wall is believed to contribute to vaso-occlusive crises. 11 Activation is required for Lu/BCAM to interact with laminin-a5.…”

Section: Introductionmentioning

confidence: 99%

Glycophorin-C sialylation regulates Lu/BCAM adhesive capacity during erythrocyte aging

et al. 2018

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Key Points• The Lu/BCAM adhesion molecule is gradually activated during erythrocyte aging due to loss of sialic acid on glycophorin-C.• Upon activation, Lu/ BCAM engages a sialic acid-dependent interaction with the extracellular matrix protein laminin-a5.Lutheran/basal cell adhesion molecule (Lu/BCAM) is a transmembrane adhesion molecule expressed by erythrocytes and endothelial cells that can interact with the extracellular matrix protein laminin-a5. In sickle cell disease, Lu/BCAM is thought to contribute to adhesion of sickle erythrocytes to the vascular wall, especially during vaso-occlusive crises.On healthy erythrocytes however, its function is unclear. Here we report that Lu/BCAM is activated during erythrocyte aging. We show that Lu/BCAM-mediated binding to laminin-a5 is restricted by interacting, in cis, with glycophorin-C-derived sialic acid residues. Following loss of sialic acid during erythrocyte aging, Lu/BCAM is released from glycophorin-C and allowed to interact with sialic acid residues on laminin-a5.

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“…Spontaneously immortalized human gingival keratinocytes (HMK cell line) (Willberg et al, 2007) of passage 24 and human normal gingival fibroblasts (Ruutu, Rautava, Turunen, Tirri, & Syrjanen, 2017) of passage 8 were cultured in standard 96‐well plates in a humidified incubator with 5% CO 2 and 95% air at 37°C until the confluence of 60% per well. Cells were passaged at regular intervals using 25% trypsin.…”

Section: Methodsmentioning

confidence: 99%

Gingival cell growth with antiresorptive treatment combined with corticosteroids or antiestrogen

Ekholm

Löyttyniemi

Soukka

et al. 2021

Clinical & Exp Dental Res

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Objectives: Antiresorptive treatment has been shown to impair mucosal cell proliferation, migration, and viability. However, in the clinic, antiresorptives are often used in combination with other drugs. We studied the effect of antiresorptives combined with a corticosteroid or antiestrogen on oral mucosal keratinocytes and fibroblasts.Material and methods: Human gingival keratinocyte and fibroblast cell lines were exposed to bisphosphonates (BPs) and denosumab in different concentrations and durations together with an antiestrogen or corticosteroid. Changes in cell viability, proliferation and migration after exposures were measured. Data were evaluated with hierarchical linear mixed model for repeated measurements.Results: Bisphosphonate exposure suppressed keratinocyte and fibroblast cell viability, proliferation, and migration in a time-dependent manner. Combining a corticosteroid or antiestrogen with BPs further increased this negative effect. Denosumab alone had a mild positive effect on keratinocyte and fibroblast growth. When denosumab was combined with a corticosteroid or antiestrogen, cell growth was suppressed.Conclusions: Our results show that coexisting medications may increase the negative impact of BPs or denosumab on oral mucosal cells.

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Lutheran Blood Group Antigen as a Receptor for α5 Laminins in Gingival Epithelia

Abstract: Lu was in coalignment with Lm alpha5 chain in gingival epithelia. Lu also seemed to have a role in gingival epithelial cell adhesion together with integrin alpha(3)beta(1).

Cited by 3 publications

References 57 publications

Epithelial-mesenchymal transition downregulates laminin α5 chain and upregulates laminin α4 chain in oral squamous carcinoma cells

Epithelial-mesenchymal transition downregulates laminin α5 chain and upregulates laminin α4 chain in oral squamous carcinoma cells

Glycophorin-C sialylation regulates Lu/BCAM adhesive capacity during erythrocyte aging

Gingival cell growth with antiresorptive treatment combined with corticosteroids or antiestrogen

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