PMID- 9176390
OWN - NLM
STAT- MEDLINE
DCOM- 19970703
LR  - 20211203
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 150
IP  - 6
DP  - 1997 Jun
TI  - Genetically null mice reveal a central role for epidermal growth factor receptor 
      in the differentiation of the hair follicle and normal hair development.
PG  - 1959-75
AB  - Mice harboring a targeted disruption of the epidermal growth factor receptor 
      (EGFR) allele exhibit a severely disorganized hair follicle phenotype, fuzzy 
      coat, and systemic disease resulting in death before 3 weeks. This skin phenotype 
      was reproduced in whole skin grafts and in grafts of EGFR null hair follicle buds 
      onto nude mice, providing a model to evaluate the natural evolution of skin 
      lacking the EGFR. Hair follicles in grafts of null skin did not progress from 
      anagen to telogen and scanning electron micrografts revealed wavy, flattened hair 
      fibers with cuticular abnormalities. Many of the EGFR null hair follicles in the 
      grafted skin were consumed by an inflammatory reaction resulting in complete hair 
      loss in 67% of the grafts by 10 weeks. Localization of follicular differentiation 
      markers including keratin 6, transglutaminase, and the hair keratins mHa2 and 
      hacl-1 revealed a pattern of premature differentiation within the null hair 
      follicles. In intact EGFR null mice, proliferation in the interfollicular 
      epidermis, but not hair follicles, was greatly decreased in the absence of EGFR. 
      In contrast, grafting of EGFR null skin resulted in a hyperplastic response in 
      the epidermis that did not resolve even after 10 weeks, although the 
      wound-induced hyperplasia in EGFR wild-type grafts had resolved within 3 to 4 
      weeks. Thus, epithelial expression of the EGFR has complex functions in the skin. 
      It is important in delaying follicular differentiation, may serve to protect the 
      hair follicle from immunological reactions, and modifies both normal and 
      wound-induced epidermal proliferation but seems dispensable for follicular 
      proliferation.
FAU - Hansen, L A
AU  - Hansen LA
AD  - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer 
      Institute, National Institute of Health, Bethesda, Maryland 20892-0001, USA.
FAU - Alexander, N
AU  - Alexander N
FAU - Hogan, M E
AU  - Hogan ME
FAU - Sundberg, J P
AU  - Sundberg JP
FAU - Dlugosz, A
AU  - Dlugosz A
FAU - Threadgill, D W
AU  - Threadgill DW
FAU - Magnuson, T
AU  - Magnuson T
FAU - Yuspa, S H
AU  - Yuspa SH
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Antigens, Differentiation)
RN  - 0 (Filaggrin Proteins)
RN  - 0 (Intermediate Filament Proteins)
RN  - 0 (Membrane Proteins)
RN  - 0 (loricrin)
RN  - 68238-35-7 (Keratins)
RN  - EC 2.3.2.13 (Transglutaminases)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Age Factors
MH  - Animals
MH  - Animals, Newborn
MH  - Antigens, Differentiation/metabolism
MH  - Cell Differentiation
MH  - Cell Division
MH  - Epithelium/physiology
MH  - ErbB Receptors/*genetics/*metabolism
MH  - Filaggrin Proteins
MH  - Hair/*physiology/ultrastructure
MH  - Hair Follicle/metabolism/*physiology/ultrastructure
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Intermediate Filament Proteins/analysis
MH  - Keratins/analysis
MH  - Membrane Proteins/analysis
MH  - Mice
MH  - Mice, Knockout
MH  - Mice, Nude
MH  - Microscopy, Electron, Scanning
MH  - *Skin Physiological Phenomena
MH  - Skin Transplantation
MH  - Transglutaminases/metabolism
PMC - PMC1858310
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
PMCR- 1997/12/01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
PHST- 1997/12/01 00:00 [pmc-release]
PST - ppublish
SO  - Am J Pathol. 1997 Jun;150(6):1959-75.