LncRNA GAS5 regulates migration and epithelial-to-mesenchymal transition in lens epithelial cells via the miR-204-3p/TGFBR1 axis

2021 ◽  
Author(s):  
Xiao Li ◽  
Miaomiao Sun ◽  
Anran Cheng ◽  
Guangying Zheng
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Lens Epithelial Cells ◽  
Mesenchymal Transition ◽  
Lncrna Gas5

Adenoviral gene transfer of BMP-7, Id2, or Id3 suppresses injury-induced epithelial-to-mesenchymal transition of lens epithelium in mice

2006 ◽  
Vol 290 (1) ◽  
pp. C282-C289 ◽  
Author(s):  
Shizuya Saika ◽  
Kazuo Ikeda ◽  
Osamu Yamanaka ◽  
Kathleen C. Flanders ◽  
Yoshitaka Ohnishi ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Expression Patterns ◽  
Lens Epithelium ◽  
Lens Epithelial Cells ◽  
Hypodermic Needle ◽  
Rt Pcr ◽  
Mesenchymal Transition ◽  
Adenoviral Gene Transfer

We have examined the effect of adenovirus-mediated expression of bone morphogenic protein-7 (BMP-7) and inhibitors of differentiation 2 and 3 (Id2 and Id3) on injury-induced epithelial-to-mesenchymal transition (EMT) of lens epithelium in mice. Id2 and Id3 are known to be upregulated by BMP-7 and to antagonize Smad2/3 signaling. The Cre-LoxP system adenoviral gene transfer was used. Three microliters of adenoviral solution (2 × 107 PFU/μl) were injected into the right lens of adult male C57BL/6 mice ( n = 144) at the time of capsular injury induced using a hypodermic needle under both general and topical anesthesia. A mixture of Cre-adenovirus (Cre-Ad) and vector encoding mBMP-7, mId2, or mId3 was administered in a test group. Control lenses were treated with Cre-Ad alone. After healing intervals of 5 or 10 days, the animals were killed and then we performed histological processes or RNA extraction from the lens. RT-PCR, real-time RT-PCR, and immunohistochemistry showed expression of each introduced gene in the lens. Exogenous BMP-7 upregulated expression of Id2 and Id3 in injured lenses, and gene introduction of Id2 or Id3 also upregulated BMP-7 expression. Gene transfer of BMP-7, Id2, or Id3 delayed injury-induced EMT of the lens epithelial cells as evaluated by histology and expression patterns of α-smooth muscle actin and collagens in association with reduction of Smad2 COOH-terminal phosphorylation. Gene transfer of BMP-7, Id2, or Id3 delayed injury-induced EMT of lens epithelial cells and subsequent sealing of the capsular break with fibrous tissue in mice.

scholarly journals Aspirin inhibits TGFβ2-induced epithelial to mesenchymal transition of lens epithelial cells: selective acetylation of K56 and K122 in histone H3

2020 ◽  
Vol 477 (1) ◽  
pp. 75-97 ◽  
Author(s):  
Mi-Hyun Nam ◽  
Andrew J.O. Smith ◽  
Mina B. Pantcheva ◽  
Ko Uoon Park ◽  
Joseph A. Brzezinski ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Smooth Muscle Actin ◽  
Histone H3 ◽  
Posterior Capsule ◽  
Human Lens ◽  
Lens Epithelial Cells ◽  
Promoter Regions ◽  
Mesenchymal Transition

Posterior capsule opacification (PCO) is a complication after cataract surgery that can disrupt vision. The epithelial to mesenchymal transition (EMT) of lens epithelial cells (LECs) in response to transforming growth factor β2 (TGFβ2) has been considered an obligatory mechanism for PCO. In this study, we tested the efficacy of aspirin in inhibiting the TGFβ2-mediated EMT of human LECs, LECs in human lens capsular bags, and lensectomized mice. In human LECs, the levels of the EMT markers α-smooth muscle actin (α-SMA) and fibronectin were drastically reduced by treatment with 2 mM aspirin. Aspirin also halted the EMT response of TGFβ2 when introduced after EMT initiation. In human capsular bags, treatment with 2 mM aspirin significantly suppressed posterior capsule wrinkling and the expression α-SMA in capsule-adherent LECs. The inhibition of TGFβ2-mediated EMT in human LECs was not dependent on Smad phosphorylation or MAPK and AKT-mediated signaling. We found that aspirin significantly increased the acetylation of K56 and K122 in histone H3 of human LECs. Chromatin immunoprecipitation assays using acetyl-H3K56 or acetyl-H3K122 antibody revealed that aspirin blocked the TGFβ2-induced acetylation of H3K56 and H3K122 at the promoter regions of ACTA2 and COL1A1. After lensectomy in mice, we observed an increase in the proliferation and α-SMA expression of the capsule-adherent LECs, which was ameliorated by aspirin administration through drinking water. Taken together, our results showed that aspirin inhibits TGFβ2-mediated EMT of LECs, possibly from epigenetic down-regulation of EMT-related genes.

scholarly journals αB-crystallin is essential for the TGF-β2-mediated epithelial to mesenchymal transition of lens epithelial cells

2016 ◽  
Vol 473 (10) ◽  
pp. 1455-1469 ◽  
Author(s):  
Rooban B. Nahomi ◽  
Mina B. Pantcheva ◽  
Ram H. Nagaraj
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Therapeutic Target ◽  
Epithelial To Mesenchymal Transition ◽  
Transforming Growth Factor ◽  
Lens Epithelial Cell ◽  
Lens Epithelial Cells ◽  
Mesenchymal Transition ◽  
Αb Crystallin

We found that αB-crystallin promoted transforming growth factor (TGF)-β2-induced epithelial to mesenchymal transition (EMT) in lens epithelial cell (LEC) and its depletion resulted in reduced EMT in cultured LEC and in lensectomized mice. αB-Crystallin could be a therapeutic target to block secondary cataract.

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