ArticleFertility and sterility2011
Retrovirus-mediated multidrug resistance gene (MDR1) overexpression inhibits chemotherapy-induced toxicity of granulosa cells.
Article in Fertility and sterility, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Ovarian Reserve Disorders, Can We Prevent Them? A Review.International journal of molecular sciences · 2022Review
- Ovarian damage from chemotherapy and current approaches to its protection.Human reproduction update · 2019Review
- Ovarian Follicle Depletion Induced by Chemotherapy and the Investigational Stages of Potential Fertility-Protective Treatments-A Review.International journal of molecular sciences · 2019Review
- Multidrug Resistance Protein 1 Deficiency Promotes Doxorubicin-Induced Ovarian Toxicity in Female Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Docetaxel induces moderate ovarian toxicity in mice, primarily affecting granulosa cells of early growing follicles.Molecular human reproduction · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
objectiveTo protect granulosa cells from chemotherapy-induced toxicity by retrovirus-mediated multidrug resistance (MDR1) gene transfection.
designLaboratory study.
settingAcademic research laboratory in a university hospital. PATIENT(S): None. INTERVENTION(S): KK15 immortalized murine granulosa cell line transiently transduced with sf91m3 retrovirus vector carrying MDR1 complementary DNA that encodes P-glycoprtoein (P-gp); transduced cells selected with colchicine and treated with doxorubicin or paclitaxel for 24-72 hours; expression and function of MDR1 and the messenger RNA (mRNA) expression of selected steroidogenesis enzymes evaluated by flow cytometry, cell viability assays, Western blot, and reverse-transcriptase polymerase chain reaction (RT-PCR). MAIN OUTCOME MEASURE(S): Viability of sf91m3-transduced KK15 cells after treatment with doxorubicin and paclitaxel. RESULT(S): The sf91m3-transduced KK15 demonstrated high expression of biologically active MDR1, as shown by flow cytometry analysis and immunoblotting using P-gp monoclonal antibody and Rhodamine 123 efflux assays. The sf91m3-transduced KK15 exhibited statistically significant resistance to toxicity of 10 μM paclitaxel. The MDR1-transduced KK15 cells were also protected from doxorubicin toxicity (10 nM to 2.5 μM), as shown by cell viability assay. Both flow cytometry and cell viability assays showed that the protection of KK15 from doxorubicin toxicity was lost at 5 μM of doxorubicin; equivalent to 500 times LD50. The sf91m3-transduced KK15 showed normal mRNA expression of a panel of selected steroidogenesis enzymes. CONCLUSION(S): Retroviral gene delivery of human MDR1 inhibited chemotherapy-induced granulosa cell toxicity and offered chemoprotection in an in vitro model.
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Registered trials
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