NDLI: The effects of tenascin C knockdown on trabecular meshwork outflow resistance.

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The effects of tenascin C knockdown on trabecular meshwork outflow resistance.

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The effects of tenascin C knockdown on trabecular meshwork outflow resistance.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Rhee, Douglas J. Oh, Dong-Jin Kang, Min-Hyung Acott, Ted S. Keller, Kate E. Haddadin, Ramez I. Kelley, Mary J. Yang, Yong-Feng Vranka, Janice A. Sun, Ying Ying
Description	Country affiliation: United States Author Affiliation: Keller KE ( Casey Eye Institute, Oregon Health & Science University, Portland, Oregon 97239, USA. gregorka@ohsu.edu)
Abstract	PURPOSE: Tenascin C (TNC) is a matricellular glycoprotein whose expression in adult tissue is indicative of tissue remodeling. The purpose of the current study was to determine the localization of TNC in trabecular meshwork (TM) tissue and to analyze the effects of TNC on intraocular pressure (IOP). METHODS: Human TM frontal sections were immunostained with anti-TNC and imaged by confocal microscopy. TNC mRNA and protein levels were quantitated in anterior segments perfused at physiological and elevated pressure. Short, hairpin RNA (shRNA) silencing lentivirus targeting full-length TNC (shTNC) was applied to anterior segment perfusion organ cultures. The IOPs and central corneal thickness (CCT) of wild-type, TNC(-/-), and tenascin X (TNX(-/-)) knockout mice were measured. RESULTS: TNC was distributed in the juxtacanalicular (JCT) region of adult human TM, predominantly in the basement membrane underlying the inner wall of Schlemm's canal. Application of shTNC lentivirus to human and porcine anterior segments in perfusion culture did not significantly affect outflow rate. Although TNC was upregulated in response to pressure, there was no difference in outflow rate when shTNC-silenced anterior segments were subjected to elevated pressure. Furthermore, IOPs and CCTs were not significantly different between TNC(-/-) or TNX(-/-) and wild-type mice. CONCLUSIONS: TNC does not appear to contribute directly to outflow resistance. However, TNC immunolocalization in the JCT of adult human eyes suggests that certain areas of the TM are being continuously remodeled with or without an IOP increase.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.13-11620
Journal	Investigative Opthalmology & Visual Science
Issue Number	8
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-08-19
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Intraocular Pressure Physiology Tenascin Genetics Metabolism Trabecular Meshwork Animals Anterior Eye Segment Cadaver Ciliary Body Extracellular Matrix Gene Silencing Homeostasis Lentivirus Mice Mice, Knockout Organ Culture Techniques Osteonectin Rna, Messenger Sclera Swine Uvea Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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