scholarly journals Changes in phosphatidylinositol metabolism during differentiation of lens epithelial cells into lens fiber cells in the embryonic chick.

1980 ◽  
Vol 255 (4) ◽  
pp. 1296-1300 ◽  
Author(s):  
P.S. Zelenka
2007 ◽  
Vol 27 (20) ◽  
pp. 7236-7247 ◽  
Author(s):  
Junling Jia ◽  
Min Lin ◽  
Lingna Zhang ◽  
J. Philippe York ◽  
Pumin Zhang

ABSTRACT The size of an organ must be tightly controlled so that it fits within an organism. The mammalian lens is a relatively simple organ composed of terminally differentiated, amitotic lens fiber cells capped on the anterior surface by a layer of immature, mitotic epithelial cells. The proliferation of lens epithelial cells fuels the growth of the lens, thus controling the size of the lens. We report that the Notch signaling pathway defines the boundary between proliferation and differentiation in the developing lens. The loss of Notch signaling results in the loss of epithelial cells to differentiation and a much smaller lens. We found that the Notch effector Herp2 is expressed in lens epithelium and directly suppresses p57 Kip2 expression, providing a molecular link between Notch signaling and the cell cycle control machinery during lens development.


Development ◽  
1991 ◽  
Vol 113 (4) ◽  
pp. 1293-1304 ◽  
Author(s):  
A. Yoshiki ◽  
M. Hanazono ◽  
S. Oda ◽  
N. Wakasugi ◽  
T. Sakakura ◽  
...  

This study investigates the primary effect of the eye lens obsolescence (Elo) gene of the mouse. Morphological features of the Elo lens were defined as follows: (1) deficient elongation of lens fiber cells, (2) morphological abnormality of nuclei of lens fiber cells, (3) lack of eosinophilic granules in the central fiber cells and (4) rupture of lens capsule in the posterior region. We have immunohistologically examined, by means of an in vivo BrdU incorporation system, whether or not the Elo gene regulates cell proliferation during lens development. The lens fiber cells were morphologically abnormal in day 13 embryonic Elo lens. However, there were no significant differences in morphology or cell proliferation between normal and Elo lens epithelium until day 14 of gestation. After day 15, the total cell number in the Elo lens epithelium was significantly less than that in the normal, but the total numbers of S-phase cells in the two genotypes were not significantly different. The ratio of the total S-phase cell number to the total number of lens epithelial cells may be affected by the developmental stage, but not directly by the genotype. The genotype, however, may be having a direct influence at later ages because malformation of Elo lens fiber cells must cause reduction of the total number of lens epithelial cells in older embryos. Although, at 30 days old, Elo lens cells were externally extruded through the ruptured capsule into the vitreous cavity, BrdU-labelled lens epithelial cells were detectable. To investigate whether the Elo lens phenotype is determined by its own genotype or by its cellular environment, we produced aggregation chimeras between C3H-Elo/+(C/C) and BALB/c(c/c). Most lenses of BALB/c dominant chimeras were oval in shape without the ruptured lens capsule. However, they were opaque in the center and slightly smaller in size than normal. The lenses of C3H-Elo/+ dominant chimeras were morphologically similar to the Elo lens. Although normal nuclei were regularly arranged in the anterior region, Elo-type nuclei were located in the posterior region. Immunohistological staining by using anti-C3H strain-specific antibody demonstrated that the lens fiber cells with abnormal nuclei were derived only from C3H-Elo/+, not from BALB/c. These observations suggest that the primary effect of the Elo gene in the developing lens may be specific to the fiber cell differentiation rather than to the cell proliferation.(ABSTRACT TRUNCATED AT 400 WORDS)


2016 ◽  
Vol 94 ◽  
Author(s):  
K. Galichanin ◽  
Z. Yu ◽  
N. Talebizadeh ◽  
M. Burmakin ◽  
P. Söderberg

1990 ◽  
Vol 143 (3) ◽  
pp. 455-459 ◽  
Author(s):  
David C. Beebe ◽  
Judith T. Parmelee ◽  
Karla S. Belcher

2000 ◽  
Vol 23 (6) ◽  
pp. 704-707 ◽  
Author(s):  
Masanori NARAHARA ◽  
Keiichirou TACHIBANA ◽  
Narumi KURISU ◽  
Michiko KANAZAWA ◽  
Masaharu MIYAKE

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Hidetoshi Ishida ◽  
Teppei Shibata ◽  
Yuka Nakamura ◽  
Yasuhito Ishigaki ◽  
Dhirendra P. Singh ◽  
...  

The Shumiya cataract rat (SCR) is a model for hereditary cataract. Two-thirds of these rats develop lens opacity within 10-11 weeks. Onset of cataract is attributed to the synergetic effect of lanosterol synthase (Lss) and farnesyl-diphosphate farnesyltransferase 1 (Fdft1) mutant alleles that lead to cholesterol deficiency in the lenses, which in turn adversely affects lens biology including the growth and differentiation of lens epithelial cells (LECs). Nevertheless, the molecular events and changes in gene expression associated with the onset of lens opacity in SCR are poorly understood. In the present study, a microarray-based approach was employed to analyze comparative gene expression changes in LECs isolated from the precataractous and cataractous stages of lenses of 5-week-old SCRs. The changes in gene expression observed in microarray results in the LECs were further validated using real-time reverse transcribed quantitative PCR (RT-qPCR) in 5-, 8-, and 10-week-old SCRs. A mild posterior and cortical opacity was observed in 5-week-old rats. Expressions of approximately 100 genes, including the major intrinsic protein of the lens fiber (Mip and Aquaporin 0), deoxyribonuclease II beta (Dnase2B), heat shock protein B1 (HspB1), and crystallin γ (γCry) B, C, and F, were found to be significantly downregulated (0.07-0.5-fold) in rat LECs derived from cataract lenses compared to that in noncataractous lenses (control). Thus, our study was aimed at identifying the gene expression patterns during cataract formation in SCRs, which may be responsible for cataractogenesis in SCR. We proposed that cataracts in SCR are associated with reduced expression of these lens genes that have been reported to be related with lens fiber differentiation. Our findings may have wider implications in understanding the effect of cholesterol deficiency and the role of cholesterol-lowering therapeutics on cataractogenesis.


1998 ◽  
Vol 45 (2) ◽  
pp. 501-507 ◽  
Author(s):  
M Ogiso

Mammalian lens contains Lewis(x), sialyl-Lewis(x) and alpha-galactosyl epitopes in neolactoseries glycosphingolipids. The expression of these three epitopes is not observed in lens epithelial cells, but is immunohistochemically detected in the inner cortical fibers and the lens nucleus. In embryonic chick lens, sialyl-Lewis(x)-containing gangliosides were also detected in the transitional zone and elongating lens fibers. Thus, the Lewis(x), sialyl-Lewis(x) and alpha- galactosyl epitopes may be associated with the differentiation and maturation of lens epithelial cells to lens fibers.


1995 ◽  
Vol 269 (3) ◽  
pp. C590-C600 ◽  
Author(s):  
P. J. Donaldson ◽  
Y. Dong ◽  
M. Roos ◽  
C. Green ◽  
D. A. Goodenough ◽  
...  

The differentiation of mouse lens epithelial cells into fiber cells is a useful model for studying the changes of the electrical properties of gap junction (cell-to-cell) channels that are induced by an alteration in connexin expression patterns. In this model, cuboidal lens epithelial cells differentiate into elongated fiber cells, and the expression of connexin43 (Cx43) in the epithelial cells is replaced with the production of high levels of Cx50 and Cx46 in the fiber cells. We now report a new procedure to isolate mouse lens fiber cell pairs suitable for double whole cell patch-clamp analysis. Analysis was also performed for fiberlike cell pairs differentiated from epithelial cells in culture. Voltage dependence and unitary conductance of fiber cell gap junction channels were determined and compared with the corresponding values previously measured for the channels joining lens epithelial cells and for lens connexin channels formed in Xenopus oocyte pairs. Our results support a differentiation-induced shift toward stronger gap junctional voltage dependence and larger unitary conductances in the fiber cells. Our data further reflect a balanced functional contribution of Cx50 and Cx46 in the fiber cell-to-cell channels rather than a predominance of a single connexin.


1998 ◽  
Vol 140 (1) ◽  
pp. 153-158 ◽  
Author(s):  
Yasuki Ishizaki ◽  
Michael D. Jacobson ◽  
Martin C. Raff

There is increasing evidence that programmed cell death (PCD) depends on a novel family of intracellular cysteine proteases, called caspases, that includes the Ced-3 protease in the nematode Caenorhabditis elegans and the interleukin-1β–converting enzyme (ICE)-like proteases in mammals. Some developing cells, including lens epithelial cells, erythroblasts, and keratinocytes, lose their nucleus and other organelles when they terminally differentiate, but it is not known whether the enzymatic machinery of PCD is involved in any of these normal differentiation events. We show here that at least one CPP32 (caspase-3)-like member of the caspase family becomes activated when rodent lens epithelial cells terminally differentiate into anucleate lens fibers in vivo, and that a peptide inhibitor of these proteases blocks the denucleation process in an in vitro model of lens fiber differentiation. These findings suggest that at least part of the machinery of PCD is involved in lens fiber differentiation.


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