Apoptosis in Keratocytes Caused by Mitomycin C

Kim, Tae Im; Tchah, Hungwon; Lee, Seung Ah; Sung, Kyung Jeh; Cho, Beom Jin; Kook, Michael S.

doi:10.1167/iovs.02-0977

Cited by 80 publications

(63 citation statements)

References 24 publications

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“…As expected, the above-mentioned substances effectively induced the early and late stages of apoptosis, identified as the Annexin V positive (ϩ)/7AAD negative (Ϫ) population and the Annexin V positive (ϩ)/7AAD positive (ϩ) population, respectively, in the U937 cells; the mechanism(s) responsible for this process were suspected to closely depend on the activation of some kind of caspase cascade, as previously described (19,34,36,37,42,48).…”

Section: Discussionsupporting

confidence: 78%

“…Since CD93 (C1qRp) on myeloid cells is involved in C1q-mediated phagocytosis, an analysis of the modulation of CD93 expression on myeloid cells with apoptotic properties should provide important information on the roles of CD93 during phagocytic activities in innate and adaptive human immune responses. Thus, we investigated the modulation of CD93 expression on a human monocyte-like cell line (U937), a model cell line for myeloid cells, after (34,41,48), and MMC (19,22,38).…”

Section: Discussionmentioning

confidence: 99%

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Decrease in CD93 (C1qRp) Expression in a Human Monocyte‐Like Cell Line (U937) Treated with Various Apoptosis‐Inducing Chemical Substances

Ikewaki

Tamauchi

Inoko

2007

Microbiology and Immunology

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Human CD93, a receptor for complement component 1, subcomponent q phagocytosis (C1qRp), has been shown to be selectively expressed by cells of a myeloid lineage and was originally reported to be involved in the C1q-mediated enhancement of phagocytosis in innate and adaptive immune responses. The modulation of CD93 expression has been investigated in various cells, particularly in granulocytes and monocytes. We previously reported that a protein kinase C activator (PKC), phorbol myristate acetate (PMA), effectively up-regulated CD93 expression on several cultured cell lines and that its regulation was mainly controlled by a PKC delta-isoenzyme. However, the expression pattern of CD93 in myeloid cells with apoptotic properties remains poorly understood. In this study, we examined the modulation of CD93 expression on a human monocyte-like cell line (

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Decrease in CD93 (C1qRp) Expression in a Human Monocyte‐Like Cell Line (U937) Treated with Various Apoptosis‐Inducing Chemical Substances

Ikewaki

Tamauchi

Inoko

2007

Microbiology and Immunology

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“…This was in agreement with recent invitro studies that illustrated that 5-FU induced apoptosis in cultured corneal epithelial and endothelial cells through upregulation of apoptosis-related proteins mainly p53, p21 and Bax [59,60] . Other invitro study revealed that mitomycin C (an alkylating agent) induced apoptosis in cultured corneal keratocytes, and they attributed this to be due to the caspase cascade related to the mitochondrial pathway of apoptosis [61] .…”

Section: Discussionmentioning

confidence: 99%

The Potential Protective Role of Hesperidin Against Capecitabine-Induced Corneal Toxicity in Adult Male Albino Rat. Light and Electron Microscopic Study

Elwan

Kassab

2017

Egyptian Journal of Histology

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Background: Capecitabine is a chemotherapeutic agent widely used for the treatment of malignancies. Ocular disorders have been reported with capecitabine therapy. Hesperidin is a naturally occurring compound derived mainly from citrus fruits and has a wide range of pharmacological activities and a proposed role in combating many ocular diseases. Aim: To evaluate the potential protective role of hesperidin against the corneal toxicity caused by capecitabine in adult male albino rats. Material and Methods: Thirty-six adult male albino rats were divided into four equal groups; control group, hesperidintreated group (50 mg/kg), capecitabine-treated group (40 mg/kg), and combination-treated "capecitabine and hesperidintreated" group. Animals were orally administered once daily for one month. Specimens from the cornea were processed for light and electron microscopy. Immunohistochemical study was performed using antibodies against p53. Results: Specimens from capecitabine-treated animals showed significant decrease of epithelial thickness. The corneal epithelial cells showed nuclear alteration and vacuolated cytoplasm. The stromal collagen fibers were irregularlyarranged and widely separated with neovascularization and mononuclear cellular infiltration. Ultrastructurally, focal widening of the intercellular spaces, partial loss of desmosomal junctions and swollen mitochondria were observed. The immunohistochemical study showed a significant increase in p53 immunoreaction. In contrast, minimal changes were observed in rats treated concomitantly with both capecitabine and hesperidin, with a non significant increase in the immunoreactions. Conclusion: Capecitabine induced structural changes in cornea of adult albino rat that could be ameliorated by concomitant treatment with hesperidin.

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“…However, the results at 6 and 12 weeks indicated significantly less apoptosis in the MMC, rapamycin, and bevacizumab groups compared to the control group. Kim et al investigated that MMC induced apoptosis in cultured corneal keratocytes through the caspase pathway, 34 and when applied immediately after PRK, MMC increased keratocyte apoptosis; however, at later times, it suppressed keratocyte apoptosis, keratocyte proliferation, and postoperative opacity after UV-B irradiation.…”

Section: Discussionmentioning

confidence: 99%

Bevacizumab and Rapamycin Can Decrease Corneal Opacity and Apoptotic Keratocyte Number following Photorefractive Keratectomy

Lee

Ko²,

Kim³

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. We investigated the effects of bevacizumab and rapamycin on central corneal opacity and apoptotic keratocyte number after photorefractive keratectomy (PRK) followed by ultraviolet B (UV-B) irradiation. METHODS.A total of 60 right eyes of Sprague-Dawley rats in four groups (n ¼ 15 each) underwent PRK ablation to 80 lm with a 3-mm zone. Sponges soaked with 0.02% mitomycin C (MMC), 2.5% bevacizumab, 0.01% rapamycin, and balanced saline solution were applied for 2 minutes to these eyes in the MMC, bevacizumab, rapamycin, and control groups, respectively. At 3 weeks after PRK, all right eyes were exposed to 100 mJ/cm 2 UV-B irradiation. Biomicroscopy was used to determine the amount of haze, and TUNEL staining for apoptosis and histology were performed at 3, 6, and 12 weeks.RESULTS. Contrary to the results at 3 weeks, central corneal haze, and apoptotic keratocyte and keratocyte number decreased significantly in the MMC, bevacizumab, and rapamycin groups compared to the control group, and the keratocyte number was lower in the MMC group than the bevacizumab and rapamycin groups at 6 weeks (all P < 0.05). At 12 weeks, the apoptotic keratocyte number was lower in the MMC, bevacizumab, and rapamycin groups than the control group, and the keratocyte number was significantly lower in the MMC than the rapamycin and control groups (all P < 0.05).CONCLUSIONS. Intraoperative bevacizumab and rapamycin administration decreases central corneal haze and apoptotic keratocyte number after PRK. Bevacizumab and rapamycin may be safe alternatives to MMC during refractive surgery to prevent postoperative corneal opacity less affecting the keratocyte number. (Invest Ophthalmol Vis Sci. 2012; 53:7645-7653)

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Apoptosis in Keratocytes Caused by Mitomycin C

Abstract: Mitomycin C induced apoptosis, not necrosis, in cultured corneal keratocytes through the caspase pathway-specifically, caspase-8 and -9-related to the mitochondrial pathway.

Cited by 80 publications

References 24 publications

Decrease in CD93 (C1qRp) Expression in a Human Monocyte‐Like Cell Line (U937) Treated with Various Apoptosis‐Inducing Chemical Substances

Decrease in CD93 (C1qRp) Expression in a Human Monocyte‐Like Cell Line (U937) Treated with Various Apoptosis‐Inducing Chemical Substances

The Potential Protective Role of Hesperidin Against Capecitabine-Induced Corneal Toxicity in Adult Male Albino Rat. Light and Electron Microscopic Study

Bevacizumab and Rapamycin Can Decrease Corneal Opacity and Apoptotic Keratocyte Number following Photorefractive Keratectomy

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