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J.G. Webb, X. Yang, C.E. Crosson; Expression of the Kallikrein/Kinin System in Human Ocular Tissue . Invest. Ophthalmol. Vis. Sci. 2006;47(13):229.
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Tissue kallikrein (KK) acts on the substrate, low molecular weight kininogen (LK), to liberate bradykinin (BK) in a variety of tissues. BK has been shown to stimulate signaling in trabecular meshwork (TM) cells and to also increase conventional outflow facility. The objective of the present study was to determine if the components for kinin generation and response are expressed in ocular tissues.
Expression of mRNA encoding tissue KK, LK, and B1 and B2 kinin receptors was determined by RT–PCR. Component expression was examined in primary cultures of human ciliary muscle (CM) and TM cells, and in transformed non–pigmented epithelial (NPE) cells. Tissue expression of KK protein was also investigated by immunohistochemistry performed on parasagital sections of the anterior segment.
Each of the cell types examined expressed both B1 and B2 kinin receptors. KK expression was observed in NPE, CM, and TM cells, but it was not detectable in all cell isolates. LK, the principal substrate for KK, was expressed by CM cells but was not found in TM or NPE cells. The distribution of KK protein was determined in 10 µm sections of anterior segment and these findings supported the results of the RT–PCR experiments. Intense fluorescence was observed in the cell layer lining the ciliary body consistent with KK expression by cells of the NPE. KK protein expression was also evident in the longitudinal smooth muscle of the ciliary body but little or no expression was found in the circular smooth muscle. KK expression was not clearly discerned within the TM.
These results indicate that the key components required for kinin generation are localized within ocular tissues. In addition, multiple cell types express both B1 and B2 kinin receptors and represent potential targets for kinin action. The composite of the data supports the possibility that kinins produced within the eye may participate in the regulation of aqueous outflow and the control of intraocular pressure. Supported by NIH grants EY014653, EY09741, EY014793 and RPB.
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