Comparison of Laser Epithelial Keratomileusis With and Without Mitomycin C for Wavefront Customized Surface Ablations

Nakano, Eliane Mayumi; Bains, Harkaran S; Hirai, Flávio E.; Portellinha, Waldir; Oliveira, Marivaldo; Nakano, Kozo

doi:10.3928/1081-597x-20071102-08

Cited by 14 publications

(5 citation statements)

References 26 publications

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“…MMC is a chemotherapy and anti-fibrotic drug characterized by clastogenic activity [37][38][39][40][41][42][43][44]. The ability of MMC to induce genotoxic stress is due to the peculiarities of its metabolism.…”

Section: Discussionmentioning

confidence: 99%

Proteomic Profiling of Endothelial Cells Exposed to Mitomycin C: Key Proteins and Pathways Underlying Genotoxic Stress-Induced Endothelial Dysfunction

Sinitsky,

Repkin,

Sinitskaya

et al. 2024

IJMS

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Mitomycin C (MMC)-induced genotoxic stress can be considered to be a novel trigger of endothelial dysfunction and atherosclerosis—a leading cause of cardiovascular morbidity and mortality worldwide. Given the increasing genotoxic load on the human organism, the decryption of the molecular pathways underlying genotoxic stress-induced endothelial dysfunction could improve our understanding of the role of genotoxic stress in atherogenesis. Here, we performed a proteomic profiling of human coronary artery endothelial cells (HCAECs) and human internal thoracic endothelial cells (HITAECs) in vitro that were exposed to MMC to identify the biochemical pathways and proteins underlying genotoxic stress-induced endothelial dysfunction. We denoted 198 and 71 unique, differentially expressed proteins (DEPs) in the MMC-treated HCAECs and HITAECs, respectively; only 4 DEPs were identified in both the HCAECs and HITAECs. In the MMC-treated HCAECs, 44.5% of the DEPs were upregulated and 55.5% of the DEPs were downregulated, while in HITAECs, these percentages were 72% and 28%, respectively. The denoted DEPs are involved in the processes of nucleotides and RNA metabolism, vesicle-mediated transport, post-translation protein modification, cell cycle control, the transport of small molecules, transcription and signal transduction. The obtained results could improve our understanding of the fundamental basis of atherogenesis and help in the justification of genotoxic stress as a risk factor for atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Proteomic Profiling of Endothelial Cells Exposed to Mitomycin C: Key Proteins and Pathways Underlying Genotoxic Stress-Induced Endothelial Dysfunction

Sinitsky,

Repkin,

Sinitskaya

et al. 2024

IJMS

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“…Mitomycin C (MMC) is a chemotherapy and anti-fibrotic drug used in cancer therapy and various eye surgeries [ 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 ]. In mammalian cells, MMC undergoes reductive activation to form mitosene [ 9 , 10 ], which reacts via N-alkylation with 7-N-guanine nucleotide residues in the minor groove of DNA followed by DNA crosslinking [ 11 ], replication and transcription arrest, and finally, apoptosis [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Atorvastatin Can Modulate DNA Damage Repair in Endothelial Cells Exposed to Mitomycin C

Sinitsky

Asanov

Цепокина

et al. 2023

IJMS

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HMG-CoA reductase inhibitors (statins) are widely used in the therapy of atherosclerosis and have a number of pleiotropic effects, including DNA repair regulation. We studied the cytogenetic damage and the expression of DNA repair genes (DDB1, ERCC4, and ERCC5) in human coronary artery (HCAEC) and internal thoracic artery endothelial cells (HITAEC) in vitro exposed to mitomycin C (MMC) (positive control), MMC and atorvastatin (MMC+Atv), MMC followed by atorvastatin treatment (MMC/Atv) and 0.9% NaCl (negative control). MMC/Atv treated HCAEC were characterized by significantly decreased micronuclei (MN) frequency compared to the MMC+Atv group and increased nucleoplasmic bridges (NPBs) frequency compared to both MMC+Atv treated cells and positive control; DDB1, ERCC4, and ERCC5 genes were upregulated in MMC+Atv and MMC/Atv treated HCAEC in comparison with the positive control. MMC+Atv treated HITAEC were characterized by reduced MN frequency compared to positive control and decreased NPBs frequency in comparison with both the positive control and MMC/Atv group. Nuclear buds (NBUDs) frequency was significantly lower in MMC/Atv treated cells than in the positive control. The DDB1 gene was downregulated in the MMC+Atv group compared to the positive control, and the ERCC5 gene was upregulated in MMC/Atv group compared to both the positive control and MMC+Atv group. We propose that atorvastatin can modulate the DNA damage repair response in primary human endothelial cells exposed to MMC in a cell line- and incubation scheme-dependent manner that can be extremely important for understanding the fundamental aspects of pleoitropic action of atorvastatin and can also be used to correct the therapy of patients with atherosclerosis characterized by a high genotoxic load.

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“…Prophylactic use of 0.02% MMC reduces corneal opacity, improves uncorrected visual acuity, and yields better visual results after keratorefractive surgery [8][9][10]. The application of 0.02% MMC solution for 12 to 120 s is variably recommended for corrections of ≥ 4.00 diopters (D) or an estimated ablation depth of > 60 µm [11,12].…”

Section: Introductionmentioning

confidence: 99%

Effects of mitomycin-C on tear film function following photorefractive keratectomy for mild-to-moderate myopia

Shahraki¹,

Saeidi²,

Boroumand³

et al. 2022

Med Hypothesis Discov Innov Optom

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Background: Mitomycin C (MMC) is used to prevent corneal opacity after photorefractive keratectomy (PRK). This study sought to determine the effect of MMC on tear film function after PRK in eyes with mild-to-moderate myopia.Methods: This prospective, contralateral eye comparison was conducted on 30 eyes of 15 patients with low-to-moderate myopia referred to Alzahra Eye Hospital, Zahedan, Iran. The eyes of the control group underwent PRK with a balanced salt solution, while the fellow eyes in the intervention group underwent PRK with 0.02% MMC for 25 s. The tear breakup time test (TBUT) and basic Schirmer test results of eyes in the control and intervention groups were compared at baseline and 1, 3, and 6 months postoperatively. Tear osmolarity was recorded and compared at baseline and 3 months postoperatively. Results: The mean ± standard deviation (SD) age of participants was 27.53 ± 7.04 years. No statistically significant differences were observed in the means ± SDs for tear osmolarity, TBUT, and basic Schirmer test values (all P > 0.05) between MMC-treated eyes and untreated fellow eyes at baseline and during postoperative follow-up. The means ± SDs for tear osmolarity, TBUT, and basic Schirmer test results were comparable in both groups between the baseline and postoperative follow-ups (all P > 0.05). Conclusions: Single application of a standard dose of MMC (0.02%) for 25 s in PRK did not change tear stability, tear production, or variation in tear dynamics up to 6 months postoperatively in eyes with low-to-moderate myopia. Future longitudinal studies with a longer follow-up and a larger sample size are warranted to confirm our findings.

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Comparison of Laser Epithelial Keratomileusis With and Without Mitomycin C for Wavefront Customized Surface Ablations

Cited by 14 publications

References 26 publications

Proteomic Profiling of Endothelial Cells Exposed to Mitomycin C: Key Proteins and Pathways Underlying Genotoxic Stress-Induced Endothelial Dysfunction

Proteomic Profiling of Endothelial Cells Exposed to Mitomycin C: Key Proteins and Pathways Underlying Genotoxic Stress-Induced Endothelial Dysfunction

Atorvastatin Can Modulate DNA Damage Repair in Endothelial Cells Exposed to Mitomycin C

Effects of mitomycin-C on tear film function following photorefractive keratectomy for mild-to-moderate myopia

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