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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Cell+Infect+Microbiol
2017 ; 7
(ä): 253
Nephropedia Template TP
gab.com Text
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English Wikipedia
Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter
Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of
Fibronectin and ?-SMA-Implications for Epithelial-Mesenchymal Transition
#MMPMID28660176
Raji? J
; Inic-Kanada A
; Stein E
; Dini? S
; Schuerer N
; Uskokovi? A
; Ghasemian E
; Mihailovi? M
; Vidakovi? M
; Grdovi? N
; Barisani-Asenbauer T
Front Cell Infect Microbiol
2017[]; 7
(ä): 253
PMID28660176
show ga
Chlamydia trachomatis (Ct) can induce scarring disease of the ocular mucosa,
known as trachoma, the most common infectious cause of blindness worldwide. We
hypothesized that epithelial-mesenchymal transition (EMT) contributes to the
fibrotic process in trachomatous scarring. Infection of human conjunctival
epithelial cells (HCjE) with Ct activated signaling pathways involved in EMT
induction, which was correlated with decreased expression of E-cadherin, guardian
of the epithelial phenotype. In addition, Ct infection was associated with
increased expression of two mesenchymal cell markers: fibronectin and ?-SMA. The
DNA methylation statuses of selected regions of E-cadherin, fibronectin, and
?-SMA genes revealed that Ct infection was accompanied with changes in DNA
methylation of the E-cadherin promoter, while the expression of the two
mesenchymal markers was not related with this epigenetic event. Our data suggest
that Ct infection of conjunctival epithelial cells induces EMT-like changes that
go along with modification of the methylation profile of the E-cadherin promoter
and could, as one of the earliest events, contribute to processes triggering
conjunctival scarring.