scholarly journals Activated Kras Alters Epidermal Homeostasis of Mouse Skin, Resulting in Redundant Skin and Defective Hair Cycling

2011 ◽  
Vol 131 (2) ◽  
pp. 311-319 ◽  
Author(s):  
Anandaroop Mukhopadhyay ◽  
Suguna R. Krishnaswami ◽  
Benjamin D.-Y. Yu
2004 ◽  
Vol 24 (13) ◽  
pp. 5733-5745 ◽  
Author(s):  
Raffi Gugasyan ◽  
Anne Voss ◽  
George Varigos ◽  
Tim Thomas ◽  
Raelene J. Grumont ◽  
...  

ABSTRACT Determining the roles of Rel/NF-κB transcription factors in mouse skin development with loss-of-function mutants has been limited by redundancy among these proteins and by embryonic lethality associated with the absence of RelA. Using mice lacking RelA and c-rel, which survive throughout embryogenesis on a tumor necrosis factor alpha (TNF-α)-deficient background (rela −/− c-rel −/− tnfα−/−), we show that c-rel and RelA are required for normal epidermal development. Although mutant fetuses fail to form tylotrich hair and have a thinner epidermis, mutant keratinocyte progenitors undergo terminal differentiation to form an outer cornified layer. Mutant basal keratinocytes are abnormally small, exhibit a delay in G1 progression, and fail to form keratinocyte colonies in culture. In contrast to the reduced proliferation of mutant keratinocytes during embryogenesis, skin grafting experiments revealed that the mutant epidermis develops a TNF-α-dependent hyperproliferative condition. Collectively, our findings indicate that RelA and c-rel control the development of the epidermis and associated appendages during embryogenesis and regulate epidermal homeostasis in a postnatal environment through the suppression of innate immune-mediated inflammation.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Kazuyuki Kitazawa ◽  
Satomi Nadanaka ◽  
Kenji Kadomatsu ◽  
Hiroshi Kitagawa

AbstractChondroitin sulfates are implicated in epidermal biology, but functional significance of chondroitin sulfates remains unclear. Here, we report that chondroitin 6-sulfate is important for the maintenance of epidermal homeostasis. Mice deficient in chondroitin 6-O-sulfotransferase-1 (C6st-1), which is involved in biosynthesis of chondroitin 6-sulfate, exhibited keratinocyte hyperproliferation and impaired skin permeability barrier function. Chondroitin 6-sulfate directly interacted with the EGF receptor and negatively controlled ligand-induced EGF receptor signaling. Normal function of hyperproliferative C6st-1-knockout mouse-derived keratinocytes was rescued by treatment with exogenous chondroitin 6-sulfate. Epidermal hyperplasia, induced using imiquimod, was more severe in C6st-1-knockout mice than in C6st-1 wild-type mice. Taken together, these findings indicate that chondroitin 6-sulfate represses keratinocyte proliferation in normal skin, and that the expression level of C6st-1 may be associated with susceptibility to psoriasis.


1998 ◽  
Vol 67 (2) ◽  
pp. 227 ◽  
Author(s):  
Honnavara N. Ananthaswamy ◽  
Anny Fourtanier ◽  
Randall L. Evans ◽  
Sylvie Tison ◽  
Chantal Medaisko ◽  
...  

Author(s):  
Moammir Hasan Aziz ◽  
Amaninderpal S. Ghotra ◽  
Yogeshwer Shukla ◽  
Nihal Ahmad

Sign in / Sign up

Export Citation Format

Share Document