Transferrin endocytosis and iron uptake in developing myogenic cells in culture: Effects of microtubular and metabolic inhibitors, sulphydryl reagents and lysosomotrophic agents

Sorokin, Lydia; Morgan, Evan H.; Yeoh, George

doi:10.1002/jcp.1041370313

Cited by 10 publications

(3 citation statements)

References 26 publications

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“…Such an incorporation might lead to stabilization of membrane fluidity thus directly blocking endocytosis phenomenon, and hence interfering e.g. with transferrin turnover [33]. Note that stimulation of iron transport by calcium has been previously shown to depend on membrane fluidity [34].…”

Section: Discussionmentioning

confidence: 98%

Protective effect of monosialoganglioside GM1 against chemically induced apoptosis through targeting of mitochondrial function and iron transport

Gorria¹,

Huc²,

Sergent³

et al. 2006

Biochemical Pharmacology

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Exogenous treatment with monosialoganglioside GM1 has been described to afford protection against different apoptotic insults. However, the underlying mechanisms remain to be determined. In this study, we focused on the effect of GM1 on the apoptotic cascade induced by benzo[a]pyrene (B[a]P) in rat hepatic F258 epithelial cells. We first demonstrated that a co-treatment with GM1 (80 microM) reduced B[a]P (50 nM)-induced apoptosis as evidenced by a decrease of both cell population exhibiting nuclear fragmentation and caspase 3 cleavage and activity. We next showed that the p53 phosphorylation and nuclear translocation as well as the intracellular alkalinization related to Na+/H+ exchanger 1 (NHE1) activation, two early events of the apoptosis induced by B[a]P, were not inhibited by GM1. In contrast, the late mitochondria-dependent acidification elicited by B[a]P was inhibited by GM1 co-treatment, and an inhibition of the oxidative stress was also observed. Because GM1 has been shown to reduce the low-molecular weight iron content related to ethanol-induced oxidative stress, we finally investigated the involvement of iron under our conditions. Using the two iron chelators deferiprone and desferrioxamine, we clearly showed that iron played an important role in B[a]P-induced apoptosis in F258 cells, and that B[a]P-treatment resulted in a significant GM1-sensitive increase in (55)Fe uptake. In conclusion, our results indicate that exogenous GM1 partly prevents B[a]P-induced apoptosis by interfering with mitochondria-related intracellular acidification and iron transport.

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Section: Discussionmentioning

confidence: 98%

Protective effect of monosialoganglioside GM1 against chemically induced apoptosis through targeting of mitochondrial function and iron transport

Gorria¹,

Huc²,

Sergent³

et al. 2006

Biochemical Pharmacology

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“…The decrease in internalization of radiolabeled ferritin seen with these treatments most likely reflects a decrease in external binding because improperly formed intracellular coated vesicles fail to cycle to the cell surface. Diamide also inhibits receptor-mediated uptake, however this inhibition only affects endocytosis and not exocytosis (Sorokin et al, 1988). Thus, unlike the hypertonic medium or potassium depletion conditions, any intracellular ferritin receptors would recycle to the cell surface where they would become immobilized.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, these data show the effect is due to potassium deficiency. Treatment of the cells with the sulfhydryl reagent, diamide that inhibits receptor mediated endocytosis but has no effect on recycling of the clathrin coated vesicles to the cell membrane (Sorokin et al, 1988), results in a significant increase in the amount of externally bound ferritin but a dramatic (60%) decrease in internalized ferritin.…”

Section: Internalization Of Ferritinmentioning

confidence: 99%

Oligodendrocyte progenitor cells internalize ferritin via clathrin-dependent receptor mediated endocytosis

et al. 2000

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Chloroquine accumulation and alterations of proteolysis and pinocytosis in the rat conceptus in vitro

Ambroso

Harris

1994

Biochemical Pharmacology

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The teratogenicity of chloroquine (CQ) has been hypothesized to result from its effects on lysosomal function, specifically the ability of the visceral yolk sac (VYS) to capture and degrade external macromolecules. Using the rat whole embryo culture system, we evaluated the ability of CQ to accumulate in conceptual tissues and its effects on aspects of VYS function known to be important in the uptake and processing of nutrients. When CQ was added directly to the culture medium, it was found to accumulate rapidly in conceptual tissues, particularly the VYS. Tissue concentrations of CQ in the embryo proper reached approximately 10-fold those in the medium, whereas concentrations in the VYS exceeded by 100-fold the medium concentration within a 4-hr exposure on gestational day (GD) 10. Embryotoxic concentrations of CQ (10-30 microM) enhanced the activity of lysosomal cysteine proteinases measured in vitro under optimum pH conditions in both embryonic and VYS homogenates after a 26-hr treatment from GD 10-11. A different pattern of response in enzyme activity was observed between embryos and VYSs that could be attributed to the preferential accumulation of CQ in the VYS. Nonembryotoxic concentrations of CQ (1-7.5 microM) induced a concentration-dependent increase in VYS enzyme activity that peaked in conceptuses exposed to 20 microM CQ (an intermediate embryotoxic concentration). The enhanced cysteine proteinase activity was time dependent and appeared to increase gradually in conceptuses exposed to 10-20 microM CQ during the 26-hr culture period. This was in contrast to the rapid accumulation of CQ in conceptual tissues seen on gestational day 10. Protein content in the VYS was increased significantly after a 9-hr exposure of whole conceptuses to CQ (20 microM), indicating an inhibition of VYS proteolytic activity in situ. After 24 hr of exposure to 20 microM CQ, VYS protein content was not significantly different from control, but embryonic protein was reduced significantly by 20%. These observations are consistent with a model of reversible inhibition of VYS proteolysis by CQ followed by a compensatory increase in lysosomal proteinase activity. VYS fluid-phase pinocytosis was also assessed after CQ exposure and found to be inhibited only in the highest CQ concentration tested (30 microM). Lower concentrations of CQ that were still embryotoxic (10-20 microM) did not affect VYS fluid-phase pinocytosis, suggesting that inhibition of this activity is not primarily responsible for CQ embryotoxicity.

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Transferrin endocytosis and iron uptake in developing myogenic cells in culture: Effects of microtubular and metabolic inhibitors, sulphydryl reagents and lysosomotrophic agents

Cited by 10 publications

References 26 publications

Protective effect of monosialoganglioside GM1 against chemically induced apoptosis through targeting of mitochondrial function and iron transport

Protective effect of monosialoganglioside GM1 against chemically induced apoptosis through targeting of mitochondrial function and iron transport

Oligodendrocyte progenitor cells internalize ferritin via clathrin-dependent receptor mediated endocytosis

Chloroquine accumulation and alterations of proteolysis and pinocytosis in the rat conceptus in vitro

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