Overexpression of Laminin-8 in Human Dermal Microvascular Endothelial Cells Promotes Angiogenesis-Related Functions

Li, Jie; Zhou, Lisa; Tran, Hoang Thi; Chen, Yi; Nguyen, Ngon E.; Karasek, Marvin A.; Marinkovich, M. Peter

doi:10.1038/sj.jid.5700089

Cited by 32 publications

(22 citation statements)

References 50 publications

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“…As discussed above, HEV angiogenesis occurs concurrently with LN hypertrophy (54). Treating tolerant mice with anti-laminin α4 may inhibit this restructuring, as endothelial cell interactions with the G domain of laminin α4 are necessary for angiogenesis (79,80). Blockade of laminin α4 and overexpression of laminin α5 also likely affected the ability of T cells to exit the HEVs and traffic through the CR, as we observed less association of alloreactive T cells and tolerance-inducing pDCs and Tregs encircling the HEVs and within the CR.…”

Section: Days) Data Presented As Mean ± Sem (A-d) or Percent Survivamentioning

confidence: 99%

Laminins affect T cell trafficking and allograft fate

Warren¹,

Iwami²,

Harris³

et al. 2014

J. Clin. Invest.

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Lymph nodes (LNs) are integral sites for the generation of immune tolerance, migration of CD4 + T cells, and induction of Tregs. Despite the importance of LNs in regulation of inflammatory responses, the LN-specific factors that regulate T cell migration and the precise LN structural domains in which differentiation occurs remain undefined. Using intravital and fluorescent microscopy, we found that alloreactive T cells traffic distinctly into the tolerant LN and colocalize in exclusive regions with alloantigen-presenting cells, a process required for Treg induction. Extracellular matrix proteins, including those of the laminin family, formed regions within the LN that were permissive for colocalization of alloantigen-presenting cells, alloreactive T cells, and Tregs. We identified unique expression patterns of laminin proteins in high endothelial venule basement membranes and the cortical ridge that correlated with alloantigen-specific immunity or immune tolerance. The ratio of laminin α4 to laminin α5 was greater in domains within tolerant LNs, compared with immune LNs, and blocking laminin α4 function or inducing laminin α5 overexpression disrupted T cell and DC localization and transmigration through tolerant LNs. Furthermore, reducing α4 laminin circumvented tolerance induction and induced cardiac allograft inflammation and rejection in murine models. This work identifies laminins as potential targets for immune modulation.

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Section: Days) Data Presented As Mean ± Sem (A-d) or Percent Survivamentioning

confidence: 99%

Laminins affect T cell trafficking and allograft fate

Warren¹,

Iwami²,

Harris³

et al. 2014

J. Clin. Invest.

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“…Each experiment was done in triplicate. Short-term (30 min) cell attachment assays to dishes coated with purified laminin-332 (2 Ag/well) in the presence of 15 Ag/mL of integrin-inhibiting antibodies was done as previously described (25). Binding of normal keratinocytes to uncoated dishes was found to be <1% of the binding observed on normal laminin-332-coated dishes after the 30 min assay (data not shown).…”

Section: Cancer Researchmentioning

confidence: 99%

A Laminin-Collagen Complex Drives Human Epidermal Carcinogenesis through Phosphoinositol-3-Kinase Activation

et al. 2007

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Laminin-332 ( formerly laminin-5) and collagen VII are basement membrane proteins expressed at the invasive front of human squamous cell carcinoma (SCC) tumors. These proteins have protumorigenic properties, but whether laminin-332 and collagen VII promote SCC tumors by providing adhesion or other nonadhesive extracellular cues, or whether laminin-332 and collagen VII interact together in this process remains unknown. In this study, we examined the role of these molecules by a structural approach using an in vivo model of human SCC tumorigenesis. Here, we show that individual domains (VI and V-III) on the laminin-332 B3 chain provide distinct and highly divergent cell adhesion and tumorpromoting functions. We found that laminin B3 domain VI provided a critical role in the assembly of stable adhesion complexes, but this domain was not required in SCC tumors. Instead, we found that laminin B3 domain V-III played an essential role in SCC carcinogenesis/invasion through binding to collagen VII, which in turn, led to phosphoinositol-3-kinase activation and protection from apoptosis. Overexpression of constitutively active p110 phosphoinositol-3-kinase subunit was sufficient to restore invasion and tumorigenesis in transformed cells lacking laminin-332/collagen VII interaction in a manner independent of cellular adhesion. These studies show distinctive adhesive and signaling functions in individual domains of laminin-332, one which is required for normal epithelial adhesion and one which is required for SCC tumorigenesis. This uncoupling of stable adhesion from tumor progression in our studies suggests that laminin-332/collagen VII interaction promotes epidermal carcinogenesis through signaling rather than adhesion. [Cancer Res 2007;67(9):4264-70]

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“…Oxidized keratin was tested in human skin primary keratinocytes in a scratch migration assay (16). The cell extracts were analysed by Western blot for protein expression of collagen types IV and VII and keratin 17 (see Data S1).…”

Section: Experimental Designmentioning

confidence: 99%

Wool‐derived keratin stimulates human keratinocyte migration and types IV and VII collagen expression

Tang

Ollague

Kelly

et al. 2012

Experimental Dermatology

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Keratinocyte migration is essential for wound repair. Keratin-based products have recently shown stimulatory effects on wound repair. This study was to test the cellular response to wool-derived oxidized keratin in wound healing to further understand the biological mechanisms underlying observed clinical benefits of keratin-based products as wound treatments. In vitro scratch migration assays examined the effects of oxidized keratin on the migration of human skin keratinocytes. Western blotting analysis determined the effects on the marker protein expression of type IV and type VII collagens and keratin 17. We found wool-derived oxidized keratin promoted keratinocyte migration and induced protein expression of type IV and type VII collagens, but not keratin 17. The data suggest that the beneficial effects of keratin-based treatment in wounds may be related to its positive effects on re-epithelialization via stimulating keratinocyte migration and production of basement membrane proteins of types IV and VII collagens.

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Overexpression of Laminin-8 in Human Dermal Microvascular Endothelial Cells Promotes Angiogenesis-Related Functions

Cited by 32 publications

References 50 publications

Laminins affect T cell trafficking and allograft fate

Laminins affect T cell trafficking and allograft fate

A Laminin-Collagen Complex Drives Human Epidermal Carcinogenesis through Phosphoinositol-3-Kinase Activation

Wool‐derived keratin stimulates human keratinocyte migration and types IV and VII collagen expression

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