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Lens Epithelium (lens + epithelium)
Selected AbstractsSequential Effects of Ultraviolet Radiation on the Histomorphology, Cell Density and Antioxidative Status of the Lens Epithelium,An In Vivo Study ,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2003S. R. Kaid Johar ABSTRACT In vivo progressive effects of UV irradiation on the lens epithelium were studied using various histomorphological and biochemical parameters. Fifteen day old rat pups were exposed to 600 mW/m2 of radiation, including UV-A and UV-B, 12 h daily for 90, 120, 150 and 180 days. Biochemical parameters such as protein-bound and non,protein-bound sulfhydryl groups in both soluble and insoluble fractions and enzymes, which play an important role in combating the oxidative stress, were studied. Decreased cell density of lens epithelial cells (LEC) was observed in all three zones along with the decrease in the levels of soluble sulfhydryls (S-SH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). On the other hand, an increase in insoluble sulfhydryls was observed. Because of the decrease in S-SH and GR activities, the LEC became vulnerable to oxidative stress. Decreased activities of SOD, GPx and CAT suggest elevated oxidative stress. This effect of UV radiation may lead to cell death that may be responsible for the observed decrease in the cell density in all three zones of the lens epithelium. [source] The role of mitochondria, cytochrome c and caspase-9 in embryonic lens fibre cell denucleationJOURNAL OF ANATOMY, Issue 2 2002E. J. Sanders Abstract During the differentiation of secondary lens fibre cells from the lens epithelium, the fibre cells lose all of their cytoplasmic organelles as well as their nuclei. The fibre cells, containing crystallins, which confer optical clarity, then persist in the adult lens. The process of denucleation of these cells has been likened to an apoptotic event which is not followed by the plasma membrane changes that are characteristic of apoptosis. We have examined the expression and subcellular translocation of molecules of the apoptotic cascade in differentiating lens epithelial cells in culture. In this culture system, the epithelial cells differentiate into lentoids composed of lens fibre cells. We find that caspase-9, which is expressed and activated before embryonic day 12 in intact lenses, is localized in the cytosol outside mitochondria in non-differentiating cultured cells. In lentoid cells, caspase-9 migrates into mitochondria after the latter undergo a membrane permeability transition that is characteristic of apoptotic cells. At the same time, caspase-9 co-localizes with cytochrome c in the cytosol. The cytochrome c is apparently released from the mitochondria in lentoid cells after the mitochondrial membrane permeability transition and during the period of nuclear shrinkage. Also during this time, the mitochondria aggregate around the degenerating nuclei. Cytochrome c disappears rapidly, while mitochondrial breakdown occurs approximately coincident with the disappearance of the nuclei, but mitochondrial remnants persist together with cytochrome c oxidase, which is a mitochondrial marker protein. Apaf-1, another cytosolic protein of the apoptotic cascade, also migrates to the permeabilized mitochondria and also co-localizes with caspase-9 and cytochrome c in the cytosol or mitochondria of denucleating cells, thus providing evidence for the formation of an ,apoptosome' in these cells, as in apoptotic cells. At no time did we observe the translocation of molecules between cytoplasmic compartments and the nucleus in differentiating lentoid cells. We suggest that the uncoupling of nuclear and membrane apoptotic events in these cells may be due to the early permeability changes in the mitochondria, resulting in the loss of mitochondrial signalling molecules, or to the failure of molecules to migrate to the nucleus in these cells, thus failing to activate nuclear-plasma membrane signalling pathways. [source] Sequential Effects of Ultraviolet Radiation on the Histomorphology, Cell Density and Antioxidative Status of the Lens Epithelium,An In Vivo Study ,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2003S. R. Kaid Johar ABSTRACT In vivo progressive effects of UV irradiation on the lens epithelium were studied using various histomorphological and biochemical parameters. Fifteen day old rat pups were exposed to 600 mW/m2 of radiation, including UV-A and UV-B, 12 h daily for 90, 120, 150 and 180 days. Biochemical parameters such as protein-bound and non,protein-bound sulfhydryl groups in both soluble and insoluble fractions and enzymes, which play an important role in combating the oxidative stress, were studied. Decreased cell density of lens epithelial cells (LEC) was observed in all three zones along with the decrease in the levels of soluble sulfhydryls (S-SH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT). On the other hand, an increase in insoluble sulfhydryls was observed. Because of the decrease in S-SH and GR activities, the LEC became vulnerable to oxidative stress. Decreased activities of SOD, GPx and CAT suggest elevated oxidative stress. This effect of UV radiation may lead to cell death that may be responsible for the observed decrease in the cell density in all three zones of the lens epithelium. [source] 2124: Src family tyrosine kinase activation is required for endothelin-1 to inhibit Na,K-ATPase in porcine lens epitheliumACTA OPHTHALMOLOGICA, Issue 2010NA DELAMERE Purpose Earlier studies point to the involvement of Src family tyrosine kinases (SFKs) in the stimulation of of Na,K-ATPase activity by purinergic receptor agonists ATP and UTP. Src itself was activated (Tamiya, et al. 2007, Am. J. Physiol. 293: C790-6). Here, we examined the role of SFKs in the response to endothelin-1 (ET-1), an ET receptor agonist that causes Na,K-ATPase inhibition. Methods Porcine lenses were incubated 30 min in Krebs' solution with ET-1 or other test agents. The epithelium was removed, homogenized and analyzed by western blot or Na,K-ATPase activity assay. Results Exposure of the intact lens to ET-1 caused a reduction in Na,K-ATPase activity. The Na,K-ATPase response was not observed when lenses were pretreated with 10 uM PP2, a selective inhibitor of SFKs. ET-1 caused SFK activation evident from an increase in Y416 phosphorylation and decrease in Y527 phosphorylation of a ~61kDa SFK. The SFK inhibitor PP2 abolished the SFK phosphorylation response. Since SFKs Fyn, Src, Hck and Yes may contribute to the observed 61kDa band, these SFKs were isolated by immunoprecipitation and analyzed separately. Based on Y416 phosphorylation, ET-1 appeared to activate Fyn, while Src and Hck were inhibited. Yes activity was unaltered. Conclusion ET-1, which causes Na,K-ATPase inhibition, elicits a different pattern of SFK activation from that reported earlier for purinergic agonists which stimulate Na,K-ATPase activity. Previously, Na,K-ATPase stimulation was observed when Src was activated. The ET-1 response points to Na,K-ATPase inhibition when Fyn kinase is activated. [source] The distribution of neuroglobin in mouse eyeACTA OPHTHALMOLOGICA, Issue 2009Y YOU Purpose To determine the distribution of neuroglobin (Ngb) in mouse eye. Ngb is predominantly expressed in the nervous system,and at particularly high levels in the retina. Ngb may serve as a reactive oxygen scavenger and may protect the tissue of eye from ischemia/hypoxia injuries. However,the distribution of Ngb in the eye is still controversial. Methods Two polyclonal antibodies against Ngb were used in this immunohistochemical study, both of which were raised in rabbits. One of these two antibodies was generated against the whole recombinant protein of mouse Ngb and the other was generated against amino acid positions 55-70 of mouse and human Ngb. The expression of Ngb was analyzed with light microscopy on tissue sections. Results These two antibodies showed comparable results. Ngb was expressed in the layers of the retina, including the ganglion cell layer, inner and outer nuclear layers, inner and outer plexiform layers, the inner segments of the photoreceptors and the retinal pigment epithelium. Ngb was also detected in other structures of the eye, including the epithelium and endothelium of cornea,the stroma of iris,the ciliary body, the lens epithelium, and the sclera. However, Ngb was not expressed in the corneal stroma, the lens capsule, the lamellar fibers of lens, the pigment epithelium of ciliary body or the pigment layer of iris. Conclusion Ngb was found widely distributed in mouse eye. This finding can be explained by the fact that most of the structures of the eye originated from neural crest/neural ectoderm. Future experiments will focus on the distribution of Ngb at the mRNA level (in situ hybridization),and the quantitative expression levels at baseline and after hypoxic/ischemic challenge. [source] | ||||||||||