Intracellular Trafficking Characteristics for Magnetic Layered Double Hydroxide/DNA Hybrids to Human Gastric Cancer Cells

Sun, Yue; Gou, Guo Jing; Dong, Li

doi:10.4028/www.scientific.net/amm.320.529

Cited by 1 publication

(2 citation statements)

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“… 44 For Perl’s Prussian Blue staining, a fresh mixture containing an equal proportion of 20% hydrochloric acid and 10% potassium ferrocyanide was used, and nuclear fast red dye was used as a counterstain. 45 Slides containing the stained sections were then washed in water, air-dried, and mounted in DPX. Nonoverlapping microscopic fields were captured using a Nikon Eclipse E600.…”

Section: Methodsmentioning

confidence: 99%

“…The tubulointerstitial fibrosis score was calculated from MT-stained sections varied from 0 to 3; 0 indicating no evidence of fibrosis; 1 indicating <25% fibrosis; 2 indicating 25–50% fibrosis; and 3 indicating >50% fibrosis . For Perl’s Prussian Blue staining, a fresh mixture containing an equal proportion of 20% hydrochloric acid and 10% potassium ferrocyanide was used, and nuclear fast red dye was used as a counterstain . Slides containing the stained sections were then washed in water, air-dried, and mounted in DPX.…”

Section: Methodsmentioning

confidence: 99%

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Effect of Cisplatin on Renal Iron Homeostasis Components: Implication in Nephropathy

2022

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Cisplatin is an important chemotherapeutic drug for the treatment of solid tumors but often causes nephropathy as part of the off-target toxicity. Iron accumulation and related damage were implicated in cisplatin-induced kidney injury. However, the role of cisplatin in the renal iron sensing mechanism and its target genes responsible for iron uptake, storage, and release have not been investigated. Cellular iron homeostasis is controlled by the interaction of iron regulatory proteins (IRP1 and IRP2) and iron-responsive elements (IREs) present in the untranslated regions of iron transport and storage components. Here, we report that cisplatin does not influence the expressions of IRP targets such as transferrin receptor-1 (TfR1), divalent metal transporter-1 (DMT1), and ferroportin in renal cells despite the increased heme oxygenase-1 (HO-1) level. Ferritin subunits (Ft-H and Ft-L) are elevated in different magnitudes due to the increased mRNA expression. Intriguingly, a higher expression of Ft-L mRNA is detected than that of Ft-H mRNA. The inability of cisplatin in altering the IRE–IRP interaction is confirmed by examining IRE-containing luciferase activity, RNA electrophoretic mobility shift assay, and activation of IRPs. The labile iron pool is depleted but reversed by silencing of either Ft-H or Ft-L, suggesting increased iron storage by ferritin. Silencing of Ft-H or Ft-L promotes cell death, suggesting that ferritin acts to protect the renal cells from cisplatin-mediated toxicity. A differential increase of transcripts and equivalent increase of proteins of Ft-H and Ft-L and unaltered TfR1 and DMT1 transcripts are found in the kidneys of cisplatin-treated rats along with iron accumulation. Our results reveal that cisplatin does not influence the IRE–IRP interaction despite alteration of the cellular iron pool in renal cells. This insensitivity of the IRE–IRP system may be implicated in the accumulation of iron to contribute to cisplatin-induced nephropathy.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%