TY - JOUR
T1 - Roles of TGF β and FGF signals in the lens
T2 - Tropomyosin regulation for posterior capsule opacity
AU - Kubo, Eri
AU - Shibata, Teppei
AU - Singh, Dhirendra P.
AU - Sasaki, Hiroshi
N1 - Funding Information:
Conflicts of Interest: This study was partly funded by Ono Pharmaceutical Co. Ltd. (Osaka, Japan).
Funding Information:
Acknowledgments: This work was supported by a KAKENHI grant from the Japan Society for the Promotion of Science (JSPS) (no. JP23592588 to EK), a grant from the National Eye Institute of the National Institute of Health (NIH) (no. EY024589 to DPS) and a grant for Research for Preventing Blindness (to DPS). Their support is gratefully acknowledged.
Publisher Copyright:
© 2018 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2018/10/9
Y1 - 2018/10/9
N2 - Transforming growth factor (TGF) β and fibroblast growth factor (FGF) 2 are related to the development of posterior capsule opacification (PCO) after lens extraction surgery and other processes of epithelial–mesenchymal transition (EMT). Oxidative stress seems to activate TGF β1 largely through reactive oxygen species (ROS) production, which in turn alters the transcription of several survival genes, including lens epithelium-cell derived growth factor (LEDGF). Higher ROS levels attenuate LEDGF function, leading to down-regulation of peroxiredoxin 6 (Prdx6). TGF β is regulated by ROS in Prdx6 knock-out lens epithelial cells (LECs) and induces the up-regulation of tropomyosins (Tpms) 1/2, and EMT of LECs. Mouse and rat PCO are accompanied by elevated expression of Tpm2. Further, the expression of Tpm1/2 is induced by TGF β2 in LECs. Importantly, we previously showed that TGF β2 and FGF2 play regulatory roles in LECs in a contrasting manner. An injury-induced EMT of a mouse lens as a PCO model was attenuated in the absence of Tpm2. In this review, we present findings regarding the roles of TGF β and FGF2 in the differential regulation of EMT in the lens. Tpms may be associated with TGF β2-and FGF2-related EMT and PCO development.
AB - Transforming growth factor (TGF) β and fibroblast growth factor (FGF) 2 are related to the development of posterior capsule opacification (PCO) after lens extraction surgery and other processes of epithelial–mesenchymal transition (EMT). Oxidative stress seems to activate TGF β1 largely through reactive oxygen species (ROS) production, which in turn alters the transcription of several survival genes, including lens epithelium-cell derived growth factor (LEDGF). Higher ROS levels attenuate LEDGF function, leading to down-regulation of peroxiredoxin 6 (Prdx6). TGF β is regulated by ROS in Prdx6 knock-out lens epithelial cells (LECs) and induces the up-regulation of tropomyosins (Tpms) 1/2, and EMT of LECs. Mouse and rat PCO are accompanied by elevated expression of Tpm2. Further, the expression of Tpm1/2 is induced by TGF β2 in LECs. Importantly, we previously showed that TGF β2 and FGF2 play regulatory roles in LECs in a contrasting manner. An injury-induced EMT of a mouse lens as a PCO model was attenuated in the absence of Tpm2. In this review, we present findings regarding the roles of TGF β and FGF2 in the differential regulation of EMT in the lens. Tpms may be associated with TGF β2-and FGF2-related EMT and PCO development.
KW - Epithelial-mesenchymal transition
KW - FGF
KW - Lens epithelium-cell derived growth factor
KW - Peroxiredoxin 6
KW - Reactive oxygen species
KW - TGF β
KW - Tropomyosin
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U2 - 10.3390/ijms19103093
DO - 10.3390/ijms19103093
M3 - Review article
C2 - 30304871
AN - SCOPUS:85055535846
SN - 1661-6596
VL - 19
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 10
M1 - 3093
ER -