The Function and Regulation of Sip1 in the Lens
Date
2013-05
Authors
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Journal ISSN
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Publisher
University of Delaware
Abstract
Cataract ensues when there is a deviation from normal lens development
and/or maintenance (Chiu 2008). After extracapsular lens extraction surgery is
performed to remove and replace the damaged tissue, a phenomenon known as
posterior capsule opacification (PCO) occurs when any remaining cells proliferate and migrate to the posterior portion of the lens and undergo either epithelial-tomesenchymal transition (EMT), or aberrant fiber cell differentiation (Wormstone et
al., 2009). This wound healing process can result in poor visual acuity, and what is
known as a “second cataract” (Spalton 2011). Two proteins known to upregulate
during PCO were specifically studied to help determine their regulatory mechanisms during this phenomenon: Sip1 and αV integrin. Smad Interacting Protein 1 (SIP1) is a transcription factor shown to have a vital role in embryonic development of several tissues of the eye and lens fiber cell maturation (Yoshimoto et al., 2005). Because SIP1 is able to repress epithelial gene expression and activate mesenchymal gene expression in other tissues (Andersen et al., 2005), it may also have a role in PCO. This study found that miRNAs of the miR200 family, which can regulate EMT, control cellular phenotype, and lead to the development of tumors (Bracken et al., 2012), are not present in appreciable levels in the lens, confirming that it is highly unlikely that PCO is under miR200 family control.