"Laura Bassi Centers of Expertise" program of the Austrian Federal Ministry of Economy through the Austrian Research Promotion Agency (822768)

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"Laura Bassi Centers of Expertise" program of the Austrian Federal Ministry of Economy through the Austrian Research Promotion Agency (822768)

Authors

Publications

Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of Fibronectin and α-SMA—Implications for Epithelial-Mesenchymal Transition

Rajić, Jovana; Inic-Kanada, Aleksandra; Stein, Elisabeth; Dinić, Svetlana; Schuerer, Nadine; Uskoković, Aleksandra; Ghasemian, Ehsan; Mihailović, Mirjana; Vidaković, Melita; Grdović, Nevena; Barisani-Asenbauer, Talin

(2017)

TY  - JOUR
AU  - Rajić, Jovana
AU  - Inic-Kanada, Aleksandra
AU  - Stein, Elisabeth
AU  - Dinić, Svetlana
AU  - Schuerer, Nadine
AU  - Uskoković, Aleksandra
AU  - Ghasemian, Ehsan
AU  - Mihailović, Mirjana
AU  - Vidaković, Melita
AU  - Grdović, Nevena
AU  - Barisani-Asenbauer, Talin
PY  - 2017
UR  - http://journal.frontiersin.org/article/10.3389/fcimb.2017.00253/full
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2836
AB  - 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 α-SMA. The DNA methylation statuses of selected regions of E-cadherin, fibronectin, and α-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.
T2  - Frontiers in Cellular and Infection Microbiology
T1  - Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of Fibronectin and α-SMA—Implications for Epithelial-Mesenchymal Transition
IS  - JUN
VL  - 7
DO  - 10.3389/fcimb.2017.00253
SP  - 253
EP  - 253
ER  - 
@article{
author = "Rajić, Jovana and Inic-Kanada, Aleksandra and Stein, Elisabeth and Dinić, Svetlana and Schuerer, Nadine and Uskoković, Aleksandra and Ghasemian, Ehsan and Mihailović, Mirjana and Vidaković, Melita and Grdović, Nevena and Barisani-Asenbauer, Talin",
year = "2017",
abstract = "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 α-SMA. The DNA methylation statuses of selected regions of E-cadherin, fibronectin, and α-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.",
journal = "Frontiers in Cellular and Infection Microbiology",
title = "Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of Fibronectin and α-SMA—Implications for Epithelial-Mesenchymal Transition",
number = "JUN",
volume = "7",
doi = "10.3389/fcimb.2017.00253",
pages = "253-253"
}
Rajić, J., Inic-Kanada, A., Stein, E., Dinić, S., Schuerer, N., Uskoković, A., Ghasemian, E., Mihailović, M., Vidaković, M., Grdović, N.,& Barisani-Asenbauer, T.. (2017). Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of Fibronectin and α-SMA—Implications for Epithelial-Mesenchymal Transition. in Frontiers in Cellular and Infection Microbiology, 7(JUN), 253-253.
https://doi.org/10.3389/fcimb.2017.00253
Rajić J, Inic-Kanada A, Stein E, Dinić S, Schuerer N, Uskoković A, Ghasemian E, Mihailović M, Vidaković M, Grdović N, Barisani-Asenbauer T. Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of Fibronectin and α-SMA—Implications for Epithelial-Mesenchymal Transition. in Frontiers in Cellular and Infection Microbiology. 2017;7(JUN):253-253.
doi:10.3389/fcimb.2017.00253 .
Rajić, Jovana, Inic-Kanada, Aleksandra, Stein, Elisabeth, Dinić, Svetlana, Schuerer, Nadine, Uskoković, Aleksandra, Ghasemian, Ehsan, Mihailović, Mirjana, Vidaković, Melita, Grdović, Nevena, Barisani-Asenbauer, Talin, "Chlamydia trachomatis Infection Is Associated with E-Cadherin Promoter Methylation, Downregulation of E-Cadherin Expression, and Increased Expression of Fibronectin and α-SMA—Implications for Epithelial-Mesenchymal Transition" in Frontiers in Cellular and Infection Microbiology, 7, no. JUN (2017):253-253,
https://doi.org/10.3389/fcimb.2017.00253 . .
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