Comparative Analysis of Human Conjunctival and Corneal Epithelial Gene Expression with Oligonucleotide Microarrays

Turner, Helen; Budak, Murat T.; Akıncı, Mehmet-Ali; Wolosin, J. Mario

doi:10.1167/iovs.06-0998

Cited by 57 publications

(51 citation statements)

References 48 publications

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“…Cartilage acidic protein 1 (CRTAC1) is a matrix component with high affinity for integrins. It is profusely expressed in cartilage, a mostly avascular tissue [27]. The corneal expression of CRTAC1 indicated that its function may be related to the avascular environs.…”

Section: +mentioning

confidence: 99%

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Xiao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Ultraviolet B (UVB) irradiation can easily induce apoptosis in human lens epithelial cells (HLECs) and further lead to various eye diseases including cataract. Here for the first time, we investigated the role of cartilage acidic protein 1 (CRTAC1) gene in UVB irradiation induced-apoptosis in HLECs. Methods: Three groups of HLECs were employed including model group, empty vector group, and CRTAC1 interference group. Results: After UVB irradiation, the percentage of primary apoptotic cells was obviously fewer in CRTAC1 interference group. Meanwhile, inhibition of CRTAC1 also reduced both reactive oxygen species (ROS) production and intracellular Ca²⁺ concentration, but the level of mitochondrial membrane potential (Δψm) was increased in HLECs. Further studies indicated that superoxide dismutase (SOD) activity and total antioxidative (T-AOC) level were significantly increased in CRTAC1-inhibited cells, while the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) were significantly decreased. ELISA analysis of CRTAC1-inhibited cells showed that the concentrations of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were significantly decreased, but the concentration of interleukin-10 (IL-10) was significantly increased. Western blot analyses of eight apoptosis-associated proteins including Bax, Bcl-2, p38, phospho-p38 (p-p38), Jun amino-terminal kinases (JNK1/2), phospho-JNK1/2 (p-JNK1/2), calcium-sensing receptor (CasR), and Ca²⁺/calmodulin-dependent protein kinase II (CaMKII) indicated that the inhibition of CRTAC1 alleviated oxidative stress and inflammation response, inactivated calcium-signaling pathway, p38 and JNK1/2 signal pathways, and eventually reduced UVB irradiation induced-apoptosis in HLECs. Conclusion: These results provided new insights into the mechanism of cataract development, and demonstrated that CRTAC1 could be a potentially novel target for cataract treatment.

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Section: +mentioning

confidence: 99%

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Xiao

et al. 2016

Cell Physiol Biochem

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“…Actually, a small cluster of cytochrome P450 genes at 7q22.1 (CYP3A4, CYP3A5 , CYP3A7 , and CYP3A43) was deleted in our patient; in fact, most of the deletions in 7q associated with glaucoma or other ocular abnormalities such as cloudy corneas, macrocornea or abnormal pupils involved q22 and likely, CYP s genes [Young et al, 1984;Montgomery et al, 2000]. Remarkably, CY-P3A43 was found differentially expressed in human cornea epithelium tissue [Turner et al, 2007]. In general, members of the subfamily 3A were found expressed in human iris, ciliary body and cornea [Zhang et al, 2008;Volotinen et al, 2011].…”

Section: Discussionmentioning

confidence: 62%

Delineation of a de novo 7q21.3q31.1 Deletion by CGH-SNP Arrays in a Girl with Multiple Congenital Anomalies Including Severe Glaucoma

et al. 2013

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In this study, we present a female patient with a constitutional de novo deletion in 7q21.3q31.1 as determined by G-banding and CGH-SNP arrays. She exhibited, among other features, psychomotor retardation, congenital severe bilateral glaucoma, a cleft palate, and heart defect. Microarray assay disclosed a deleted 12.5-Mb region roughly 88 kb downstream the ectrodactyly critical region; thus, the patient's final karyotype was 46,XX.arr 7q21.3q31.1(96,742,140- 109,246,085)×1 dn. This girl represents the fourth patient described so far with congenital glaucoma and a deletion encompassing or overlapping the 7q21.3q31.1 region, and confirms the presence of a locus or loci related to such a clinical feature. According to our results, the proneness to ocular defects secondary to 7q intermediate deletions could be caused by co-deletion of TAC1, HBP1, and a small cluster of cytochrome P450 genes (subfamily 3A). This conclusion is supported by their functional roles and expression locations as well as because TAC1 is related to the functional pathway of the MYOC gene whose mutations are linked to glaucoma. Moreover, given that this girl is clinically reminiscent of several phenotypes related to diverse deletions within 7q21q32, our results and observations offer a general overview of the gene content of deletions/phenotypes overlapping 7q21.3q31.1 and confirm that loci distal to DLX genes including the CUX1 gene and potential regulatory elements downstream from DLX5 are unrelated to ectrodactyly.

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“…5B) produced a transitory increase in negative current to Ϫ8.7 Ϯ 1.2 A⅐cm Ϫ2 (n ϭ 4 conjunctivae; P Ͻ 0.05), a 7% rise that was followed by a gradual current decline. 36 Cl Ϫ fluxes across conjunctivae in the direction of the Cl Ϫ gradient. To corroborate the electrical results with the transepithelial Cl Ϫ gradient, 36 Cl Ϫ was added to the high-Cl Ϫ apical side bath and unidirectional fluxes were measured in the apical-to-basolateral direction for 1 h under baseline conditions, followed by three sequential, 1-h periods in which nystatin, EBIO, and glibenclamide were introduced to the bathing solutions (Table 2).…”

Section: Resultsmentioning

confidence: 99%

Cl⁻ secretory effects of EBIO in the rabbit conjunctival epithelium

Alvarez¹,

Zamudio²,

Candia³

2005

American Journal of Physiology-Cell Physiology

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Experiments were conducted to determine whether the Cl- secretagogue, 1-ethyl-2-benzimidazolinone (EBIO), stimulates Cl- transport in the rabbit conjunctival epithelium. For this study, epithelia were isolated in an Ussing-type chamber under short-circuit conditions. The effects of EBIO on the short-circuit current (I(sc)) and transepithelial resistance (R(t)) were measured under physiological conditions, as well as in experiments with altered electrolyte concentrations. Addition of 0.5 mM EBIO to the apical bath stimulated the control I(sc) by 64% and reduced R(t) by 21% (P < 0.05; paired data). Under Cl(-)-free conditions, I(sc) stimulation using EBIO was markedly attenuated. In the presence of an apical-to-basolateral K+ gradient and permeabilization of the apical membrane, the majority of the I(sc) reflected the transcellular movement of K+ via basolateral K+ channels. Under these conditions, EBIO in combination with A23187 elicited nearly instantaneous 60-90% increases in I(sc) that were sensitive to the calmodulin antagonist calmidazolium and the K+ channel blocker tetraethyl ammonium. In the presence of an apical-to-basolateral Cl- gradient and nystatin permeabilization of the basolateral aspect, EBIO increased the Cl(-)-dependent I(sc), an effect prevented by the channel blocker glibenclamide (0.3 mM). The latter compound also was used to determine the proportion of EBIO-evoked unidirectional 36Cl- fluxes in the presence of the Cl- gradient that traversed the epithelium transcellularly. Overall, EBIO activated apical Cl- channels and basolateral K+ channels (presumably those that are Ca2+ dependent), thereby suggesting that this compound, or related derivatives, may be suitable as topical agents to stimulate fluid transport across the tissue in individuals with lacrimal gland deficiencies.

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Comparative Analysis of Human Conjunctival and Corneal Epithelial Gene Expression with Oligonucleotide Microarrays

Abstract: Comparative gene expression profiling leads to the identification of many biological processes and previously unknown genes that are potentially active in the function of corneal and conjunctival epithelia.

Cited by 57 publications

References 48 publications

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Delineation of a de novo 7q21.3q31.1 Deletion by CGH-SNP Arrays in a Girl with Multiple Congenital Anomalies Including Severe Glaucoma

Cl⁻ secretory effects of EBIO in the rabbit conjunctival epithelium

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Comparative Analysis of Human Conjunctival and Corneal Epithelial Gene Expression with Oligonucleotide Microarrays

Abstract: Comparative gene expression profiling leads to the identification of many biological processes and previously unknown genes that are potentially active in the function of corneal and conjunctival epithelia.

Cited by 57 publications

References 48 publications

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Inhibition of Cartilage Acidic Protein 1 Reduces Ultraviolet B Irradiation Induced-Apoptosis through P38 Mitogen-Activated Protein Kinase and Jun Amino-Terminal Kinase Pathways

Delineation of a de novo 7q21.3q31.1 Deletion by CGH-SNP Arrays in a Girl with Multiple Congenital Anomalies Including Severe Glaucoma

Cl− secretory effects of EBIO in the rabbit conjunctival epithelium

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Cl⁻ secretory effects of EBIO in the rabbit conjunctival epithelium