Laminin 332 Is Indispensable for Homeostatic Epidermal Differentiation Programs

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dc.contributor.author Tayem, Raneem
dc.contributor.author Niemann, Catherin
dc.contributor.author Pesch, Monika
dc.contributor.author Morgner, Jessica
dc.contributor.author Niessen, Carien M.
dc.contributor.author Wickström, Sara A.
dc.contributor.author Aumailley, Monique
dc.date.accessioned 2021-12-01T07:31:02Z
dc.date.available 2021-12-01T07:31:02Z
dc.date.issued 2021-11
dc.identifier.citation Tayem , R , Niemann , C , Pesch , M , Morgner , J , Niessen , C M , Wickström , S A & Aumailley , M 2021 , ' Laminin 332 Is Indispensable for Homeostatic Epidermal Differentiation Programs ' , Journal of Investigative Dermatology , vol. 141 , no. 11 , pp. 2602-+ . https://doi.org/10.1016/j.jid.2021.04.008
dc.identifier.other PURE: 170787377
dc.identifier.other PURE UUID: 634dfe3d-a76b-4545-a519-f3edca9eb231
dc.identifier.other WOS: 000710159100012
dc.identifier.uri http://hdl.handle.net/10138/336965
dc.description.abstract The skin epidermis is attached to the underlying dermis by a laminin 332 (Lm332)-rich basement membrane. Consequently, loss of Lm332 leads to the severe blistering disorder epidermolysis bullosa junctionalis in humans and animals. Owing to the indispensable role of Lm332 in keratinocyte adhesion in vivo, the severity of the disease has limited research into other functions of the protein. We have conditionally disrupted Lm332 expression in basal keratinocytes of adult mice. Although blisters develop along the interfollicular epidermis, hair follicle basal cells provide sufficient anchorage of the epidermis to the dermis, making inducible deletion of the Lama3 gene compatible with life. Loss of Lm332 promoted the thickening of the epidermis and exaggerated desquamation. Global RNA expression analysis revealed major changes in the expression of keratins, cornified envelope proteins, and cellular stress markers. These modifications of the keratinocyte genetic program are accompanied by changes in cell shape and disorganization of the actin cytoskeleton. These data indicate that loss of Lm332-mediated progenitor cell adhesion alters cell fate and disturbs epidermal homeostasis. en
dc.format.extent 12
dc.language.iso eng
dc.relation.ispartof Journal of Investigative Dermatology
dc.rights cc_by_nc_nd
dc.rights.uri info:eu-repo/semantics/openAccess
dc.subject ALPHA-6-BETA-4 INTEGRIN
dc.subject EPIDERMOLYSIS-BULLOSA
dc.subject TARGETED DISRUPTION
dc.subject MOLECULAR-BASIS
dc.subject HAIR FOLLICLE
dc.subject LAMA3 GENE
dc.subject KERATINOCYTES
dc.subject ADHESION
dc.subject BETA
dc.subject ALPHA-3-BETA-1
dc.subject 3121 General medicine, internal medicine and other clinical medicine
dc.title Laminin 332 Is Indispensable for Homeostatic Epidermal Differentiation Programs en
dc.type Article
dc.contributor.organization Department of Biochemistry and Developmental Biology
dc.contributor.organization Helsinki Institute of Life Science HiLIFE
dc.description.reviewstatus Peer reviewed
dc.relation.doi https://doi.org/10.1016/j.jid.2021.04.008
dc.relation.issn 0022-202X
dc.rights.accesslevel openAccess
dc.type.version publishedVersion

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