scholarly journals Deletion of the epidermis derived laminin γ1 chain leads to defects in the regulation of late hair morphogenesis

2016 ◽  
Vol 56 ◽  
pp. 42-56 ◽  
Author(s):  
Anja Fleger-Weckmann ◽  
Yasemin Üstün ◽  
Jennifer Kloepper ◽  
Ralf Paus ◽  
Wilhelm Bloch ◽  
...  
Keyword(s):  
2007 ◽  
Vol 143 (3) ◽  
pp. 1220-1230 ◽  
Author(s):  
Chul Min Kim ◽  
Sung Han Park ◽  
Byoung Il Je ◽  
Su Hyun Park ◽  
Soon Ju Park ◽  
...  

2013 ◽  
Vol 7 (4) ◽  
pp. 1111-1116 ◽  
Author(s):  
JING HE ◽  
HUICHUAN DUAN ◽  
YAO XIONG ◽  
WENJIE ZHANG ◽  
GUANGDONG ZHOU ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 969 ◽  
Author(s):  
Shanhe Wang ◽  
Fang Li ◽  
Jinwang Liu ◽  
Yuelang Zhang ◽  
Yujie Zheng ◽  
...  

Studies in humans and mice have revealed that hair follicle morphogenesis relies on tightly coordinated ectodermal–mesodermal interactions, involving multiple signals and regulatory factors. DNA methylation and long non-coding RNA (lncRNA) play a critical role in early embryonic skin development by controlling gene expression. Acting as an indirect regulator, lncRNA could recruit DNA methyltransferases to specific genomic sites to methylate DNA. However, the molecular regulation mechanisms underlying hair follicle morphogenesis is unclear in cashmere goat. In this study, RNA-seq and whole-genome bisulfite sequencing (WGBS) in embryonic day 65 (E 65) and E 120 skin tissues of cashmere goat were used to reveal this complex regulatory process. The RNA-seq, qRT-PCR, and immunohistochemistry results showed that Wnt signaling played an important role in both hair follicle induction and differentiation stage; transcriptional factors (TFs), including HOXC13, SOX9, SOX21, JUNB, LHX2, VDR, and GATA3, participated in hair follicle differentiation via specific expression at E 120. Subsequently, the combination of WGBS and RNA-seq analysis showed that the expression of some hair follicle differentiation genes and TF genes were negatively correlated with the DNA methylation level generally. A portion of hair follicle differentiation genes were methylated and repressed in the hair follicle induction stage but were subsequently demethylated and expressed during the hair follicle differentiation stage, suggesting that DNA methylation plays an important role in hair morphogenesis by regulating associated gene expression. Furthermore, 45 upregulated and 147 downregulated lncRNAs in E 120 compared with E 65 were identified by lncRNA mapping, and then the potential differentially expressed lncRNAs associated with DNA methylation on the target gene were revealed. In conclusion, critical signals and genes were revealed during hair follicle morphogenesis in the cashmere goat. In this process, DNA methylation was lower in the hair follicle differentiation compared with the hair follicle induction stage and may play an important role in hair morphogenesis by regulating associated gene expression. Furthermore, potential lncRNAs associated with DNA methylation on target genes were delineated. This study enriches the regulatory network and molecular mechanisms on hair morphogenesis.


1994 ◽  
Vol 46 (2) ◽  
pp. 101-107 ◽  
Author(s):  
Paul N. Adler ◽  
Jeannette Charlton ◽  
Katherine H. Jones ◽  
Jingchun Liu

2014 ◽  
Vol 2014 ◽  
pp. 1-6
Author(s):  
Alexandra Rippa ◽  
Olga Leonova ◽  
Vladimir Popenko ◽  
Andrey Vasiliev ◽  
Vasily Terskikh ◽  
...  

In adult skin, hair follicles cyclically self-renew in a manner that recapitulates embryonic hair follicle morphogenesis. The most common pathology of hair in adults is alopecia, which is hair loss to different extent. There are a number of murine models of alopecia including spontaneous mutations. In the present study, we worked with double homozygouswe/we wal/walmice which demonstrate symptoms closely resembling human alopecia. Using whole-mount preparations of epidermis of E18.5 embryos we show that hair follicle defects can be revealed as early as during embryonic morphogenesis in these mutants. The number of hair follicles was reduced almost 1.5-fold in mutant skin. The shape of the early stage small follicles was altered in mutant animals as compared to control ones. Additionally, follicles of mutant embryos were wider at the point of conjunction with interfollicular epidermis. We believe that the mutant mice studied represent a fascinating model to address the problem of hair loss. We demonstrated alterations in the morphogenesis of embryonic hair follicle inwe/we wal/waldouble homozygous mice developing alopecia postnatally. We suppose that incorrect morphogenesis of hair follicles during embryogenesis is closely related to alopecia in the adult life. Unveiling the mechanisms involved in altered embryogenesis may elucidate the pathogenesis of alopecia.


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