Laminin 332 Is Indispensable for Homeostatic Epidermal Differentiation Programs

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http://hdl.handle.net/10138/336965

Lähdeviite

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

Julkaisun nimi: Laminin 332 Is Indispensable for Homeostatic Epidermal Differentiation Programs
Tekijä: Tayem, Raneem; Niemann, Catherin; Pesch, Monika; Morgner, Jessica; Niessen, Carien M.; Wickström, Sara A.; Aumailley, Monique
Tekijän organisaatio: Department of Biochemistry and Developmental Biology
Helsinki Institute of Life Science HiLIFE
Päiväys: 2021-11
Kieli: eng
Sivumäärä: 12
Kuuluu julkaisusarjaan: Journal of Investigative Dermatology
ISSN: 0022-202X
DOI-tunniste: https://doi.org/10.1016/j.jid.2021.04.008
URI: http://hdl.handle.net/10138/336965
Tiivistelmä: 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.
Avainsanat: ALPHA-6-BETA-4 INTEGRIN
EPIDERMOLYSIS-BULLOSA
TARGETED DISRUPTION
MOLECULAR-BASIS
HAIR FOLLICLE
LAMA3 GENE
KERATINOCYTES
ADHESION
BETA
ALPHA-3-BETA-1
3121 General medicine, internal medicine and other clinical medicine
Vertaisarvioitu: Kyllä
Tekijänoikeustiedot: cc_by_nc_nd
Pääsyrajoitteet: openAccess
Rinnakkaistallennettu versio: publishedVersion


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