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Title: Inactivation of Smad4 leads to impaired ocular development and cataract formation

Abstract

Research highlights: {yields} Inactivation of Smad4 caused disruption in the development of the anterior segment. {yields} Inactivation of Smad4 failed to disrupt early lens development. {yields} Smad4 controlled lens cell cycle and cell death processes. {yields} Smad4 may regulate actin stress fiber assembly and eyelid epithelial movement. -- Abstract: Purpose: Signaling by members of the TGF{beta} superfamily of molecules is essential for embryonic development and homeostasis. Smad4, a key intracellular mediator in TGF{beta} signaling, forms transcriptional activator complexes with Activin-, BMP-, and TGF{beta}-restricted Smad proteins. However, the functional role of Smad4 in controlling different visual system compartments has not been fully investigated. Methods: Using the Pax6 promoter-driven Cre transgenic, smad4 was conditionally inactivated in the lens, cornea and ectoderm of the eyelids. Standard histological and molecular analytical approaches were employed to reveal morphological and cellular changes. Results: Inactivation of Smad4 in the lens led to microphthalmia and cataract formation in addition to the persistent adhesion of the retina to the lens and the iris to the cornea. Inactivation of Smad4 from the ectoderm of the eyelid and cornea caused disruption to eyelid fusion and proper development of the corneal epithelium and corneal stroma. Conclusions: Smad4 is required for the developmentmore » and maintenance of the lens in addition to the proper development of the cornea, eyelids, and retina.« less

Authors:
 [1]; ;  [1];  [2]; ;  [1]
  1. Department of Ophthalmology and Doheny Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033 (United States)
  2. Laboratory of Biochemistry and Metabolism, NIDDK, National Institutes of Health, Bethesda, MD 20892 (United States)
Publication Date:
OSTI Identifier:
22202785
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 400; Journal Issue: 4; Other Information: Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ACTIN; CATARACTS; CORNEA; CUMULATIVE RADIATION EFFECTS; EPITHELIUM; FIBERS; HOMEOSTASIS; INACTIVATION; LENSES; RETINA

Citation Formats

Liu, Ying, Sun Yet-sen University, Zhongshan Ophthalmic Center, State Key Ophthalmic Laboratory, Guangzhou 510060, Kawai, Kirio, Khashabi, Shabnam, Deng, Chuxia, Liu, Yi-Hsin, and Yiu, Samuel. Inactivation of Smad4 leads to impaired ocular development and cataract formation. United States: N. p., 2010. Web. doi:10.1016/J.BBRC.2010.08.065.
Liu, Ying, Sun Yet-sen University, Zhongshan Ophthalmic Center, State Key Ophthalmic Laboratory, Guangzhou 510060, Kawai, Kirio, Khashabi, Shabnam, Deng, Chuxia, Liu, Yi-Hsin, & Yiu, Samuel. Inactivation of Smad4 leads to impaired ocular development and cataract formation. United States. https://doi.org/10.1016/J.BBRC.2010.08.065
Liu, Ying, Sun Yet-sen University, Zhongshan Ophthalmic Center, State Key Ophthalmic Laboratory, Guangzhou 510060, Kawai, Kirio, Khashabi, Shabnam, Deng, Chuxia, Liu, Yi-Hsin, and Yiu, Samuel. 2010. "Inactivation of Smad4 leads to impaired ocular development and cataract formation". United States. https://doi.org/10.1016/J.BBRC.2010.08.065.
@article{osti_22202785,
title = {Inactivation of Smad4 leads to impaired ocular development and cataract formation},
author = {Liu, Ying and Sun Yet-sen University, Zhongshan Ophthalmic Center, State Key Ophthalmic Laboratory, Guangzhou 510060 and Kawai, Kirio and Khashabi, Shabnam and Deng, Chuxia and Liu, Yi-Hsin and Yiu, Samuel},
abstractNote = {Research highlights: {yields} Inactivation of Smad4 caused disruption in the development of the anterior segment. {yields} Inactivation of Smad4 failed to disrupt early lens development. {yields} Smad4 controlled lens cell cycle and cell death processes. {yields} Smad4 may regulate actin stress fiber assembly and eyelid epithelial movement. -- Abstract: Purpose: Signaling by members of the TGF{beta} superfamily of molecules is essential for embryonic development and homeostasis. Smad4, a key intracellular mediator in TGF{beta} signaling, forms transcriptional activator complexes with Activin-, BMP-, and TGF{beta}-restricted Smad proteins. However, the functional role of Smad4 in controlling different visual system compartments has not been fully investigated. Methods: Using the Pax6 promoter-driven Cre transgenic, smad4 was conditionally inactivated in the lens, cornea and ectoderm of the eyelids. Standard histological and molecular analytical approaches were employed to reveal morphological and cellular changes. Results: Inactivation of Smad4 in the lens led to microphthalmia and cataract formation in addition to the persistent adhesion of the retina to the lens and the iris to the cornea. Inactivation of Smad4 from the ectoderm of the eyelid and cornea caused disruption to eyelid fusion and proper development of the corneal epithelium and corneal stroma. Conclusions: Smad4 is required for the development and maintenance of the lens in addition to the proper development of the cornea, eyelids, and retina.},
doi = {10.1016/J.BBRC.2010.08.065},
url = {https://www.osti.gov/biblio/22202785}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 4,
volume = 400,
place = {United States},
year = {Fri Oct 01 00:00:00 EDT 2010},
month = {Fri Oct 01 00:00:00 EDT 2010}
}