βig-h3 supports keratinocyte adhesion, migration, and proliferation through α3β1 integrin

Bae, Jong Sup; Lee, Suk Hee; Kim, Jung Eun; Choi, Je Yong; Park, Rang Woon; Park, Jae Yong; Park, Hyun Sook; Sohn, Young Sook; Lee, Dong Sin; Lee, Eunhee Bae; Kim, In San

doi:10.1016/s0006-291x(02)00576-4

Cited by 131 publications

(117 citation statements)

References 29 publications

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“…βig-h3 plays a role in cell adhesion, migration, and wound healing (LeBaron et al, 1995;Bae et al, 2002;Park et al, 2004). In addition, βig-h3 is involved in certain human diseases.…”

Section: Introductionmentioning

confidence: 99%

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

Lee

Bae²,

Park³

et al. 2006

Exp Mol Med

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Adhesion and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of atherosclerosis. These processes involve the interaction of VSMCs with extracellular matrix proteins. Here, we investigated integrin isoforms and signaling pathways mediating the adhesion and migration of VSMCs on βig-h3, a transforming growth factor (TGF)-β-inducible extracellular matrix protein that is elevated in atherosclerotic plaques. Adhesion assays showed that the αvβ5 integrin is a functional receptor for the adhesion of aortic VSMCs to βig-h3. An YH18 motif containing amino acids between 563 and 580 of βig-h3 was an essential motif for the adhesion and growth of VSMCs. Interaction between the YH18 motif and the αvβ5 integrin was responsible for the migration of VSMCs on βig-h3. Inhibitors of phosphatidylinositide 3-kinase, extracellular signalregulated kinase (ERK), and Src kinase reduced the adhesion and migration of VSMCs on βig-h3. βig-h3 triggered phosphorylation and activation of AKT, ERK, focal adhesion kinase, and paxillin mediating the adhesion and migration of VSMCs. Taken together, these results suggest that βig-h3 and αvβ5 integrin play a role in the adhesion and migration of VSMCs during the pathogenesis of atherosclerosis.

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“…βig-h3 plays a role in cell adhesion, migration, and wound healing (LeBaron et al, 1995;Bae et al, 2002;Park et al, 2004). In addition, βig-h3 is involved in certain human diseases.…”

Section: Introductionmentioning

confidence: 99%

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

Lee

Bae²,

Park³

et al. 2006

Exp Mol Med

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“…However, growth promoting activities for T-CAM, FN, FN115, βigh3-WT and D-IV were more or less similar. Previous studies have also demonstrated growth promoting activities of pFN, βig-h3 and its FAS1 domain (Bae et al, 2002).…”

Section: T-cam Support Proliferation Of Fibroblast and Hacat Cellsmentioning

confidence: 87%

“…The PHSRN and RGD motifs in FN are known to act synergistically in mediating cell adhesion (Grant et al, 1997). The EPDIM in 4 th FAS1 domain is known to mediate α3β1 integrinmediated adhesion of human corneal epithelial cells and keratinocytes to βig-h3 (Kim et al, 2000;Bae et al, 2002). The YH motif which is present in all four FAS1 domains of βig-h3 is active in mediating adhesion of fibroblasts .…”

Section: Discussionmentioning

confidence: 99%

“…At present, NKDIL in second, Glu-Pro-Asp-Ile-Met (EPDIM) in fourth FAS1 domain and Try-His (YH) in each FAS1 domain are the known-cell adhesion motifs so far identified in βig-h3 and interact with various integrins mediating adhesion of cells to βig-h3 (Kim et al, 2000. The previous two integrinbinding sites are known to interact with α3β1 integrin and mediate the adhesion of keratinocytes to βig-h3 (Bae et al, 2002) whereas YH motif interacts with α vβ3/5 integrins supporting the adhesion of various cell types including fibroblasts, endothelial cells and osteoblasts Thapa et al, 2005). Although, role of βig-h3 in wound healing is obscure, its expression is observed in endothelium and stroma-derived cells in healing corneal wound (Rawe et al, 1997) and reactive astrocytes at stab wound sites in rat cerebral cortex (Yun et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…It is present in papillary dermis (LeBaron et al, 1995) and secreted by keratinocytes (Katz and Taichman, 1999). In vitro study shows βig-h3 supporting adhesion and migration of dermal fibroblasts and keratinocytes (LeBaron et al, 1995;Bae et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Recombinant tetra-cell adhesion motifs supports adhesion, migration and proliferation of keratinocytes/fibroblasts, and promotes wound healing

et al. 2007

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An extracellular matrix protein plays an important role in skin wound healing. In the present study, we engineered a recombinant protein encompassing the 9 th and 10 th type III domains of fibronectin, and 4 th FAS1 domain of βig-h3. This recombinant protein, in total, harbors four known-cell adhesion motifs for integrins: Pro-His-Ser-Arg-Asn (PHSRN) and Arg-Gly-Asp (RGD) in 9 th and 10 th type III domains of fibronectin, respectively, and Glu-Pro-Asp-Ile-Met (EPDIM) and Try-His (YH) in 4 th FAS1 domain of βig-h3, were designated to tetra-cell adhesion motifs (T-CAM). In vitro studies showed T-CAM supporting adhesion, migration and proliferation of different cell types including keratinocytes and fibroblasts. In an animal model of full-thickness skin wound, T-CAM exhibited excellent wound healing effects, superior to both 4 th FAS1 domain of βig-h3 or 9 th and 10 th type III domains of fibronectin. Based on these results, T-CAM can be applied where enhancement of cell adhesion, migration and proliferation are desired, and it could be developed into novel wound healing drug.

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Phenotypical and biochemical characterization of murine psoriasiform and fibrotic skin disease models in Stabilin‐deficient mice

Krzistetzko,

Géraud,

Dormann

et al. 2024

FEBS Open Bio

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Stabilin‐1 (Stab1) and Stabilin‐2 (Stab2) are scavenger receptors expressed by liver sinusoidal endothelial cells (LSECs). The Stabilin‐mediated scavenging function is responsible for regulating the molecular composition of circulating blood in mammals. Stab1 and Stab2 have been shown to influence fibrosis in liver and kidneys and to modulate inflammation in atherosclerosis. In this context, circulating and localized TGFBi and POSTN are differentially controlled by the Stabilins as their receptors. To assess Stab1 and Stab2 functions in inflammatory and fibrotic skin disease, topical Imiquimod (IMQ) was used to induce psoriasis‐like skin lesions in mice and Bleomycin (BLM) was applied subcutaneously to induce scleroderma‐like effects in the skin. The topical treatment with IMQ, as expected, led to psoriasis‐like changes in the skin of mice, including increased epidermal thickness and significant weight loss. Clinical severity was reduced in Stab2‐deficient compared to Stab1‐deficient mice. We did not observe differential effects in the skin of Stabilin‐deficient mice after bleomycin injection. Interestingly, treatment with IMQ led to a significant increase of Stabilin ligand TGFBi plasma levels in Stab2−/− mice, treatment with BLM resulted in a significant decrease in TGFBi levels in Stab1−/− mice. Overall, Stab1 and Stab2 deficiency resulted in minor alterations of the disease phenotypes accompanied by alterations of circulating ligands in the blood in response to the disease models. Stabilin‐mediated clearance of TGFBi was altered in these disease processes. Taken together our results suggest that Stabilin deficiency‐associated plasma alterations may interfere with preclinical disease severity and treatment responses in patients.

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βig-h3 supports keratinocyte adhesion, migration, and proliferation through α3β1 integrin

Cited by 131 publications

References 29 publications

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

βig-h3 triggers signaling pathways mediating adhesion and migration of vascular smooth muscle cells through αvβ5 integrin

Recombinant tetra-cell adhesion motifs supports adhesion, migration and proliferation of keratinocytes/fibroblasts, and promotes wound healing

Phenotypical and biochemical characterization of murine psoriasiform and fibrotic skin disease models in Stabilin‐deficient mice

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