Intermediate steps in cellular iron uptake from transferrin. II. A cytoplasmic pool of iron is released from cultured cells via temperature-dependent mechanical wounding

1996 ◽  
Vol 32 (8) ◽  
pp. 486-495 ◽  
Author(s):  
D. R. Richardson ◽  
L. Dickson ◽  
E. Baker
Keyword(s):  
Iron Uptake ◽  
Cultured Cells ◽  
Temperature Dependent ◽  
Mechanical Wounding ◽  
Cellular Iron ◽  
Cellular Iron Uptake

Marginally excessive iron loading transiently blocks mucosal iron uptake in iron-deficient rats

2014 ◽  
Vol 307 (1) ◽  
pp. G89-G97 ◽  
Author(s):  
Shoko Shinoda ◽  
Shiho Yoshizawa ◽  
Eriko Nozaki ◽  
Kouki Tadai ◽  
Anna Arita
Keyword(s):  
Iron Uptake ◽  
Iron Concentration ◽  
Iron Loading ◽  
Short Acting ◽  
Excess Iron ◽  
Rapid Induction ◽  
Cellular Iron ◽  
Iron Load ◽  
Iron Deficient ◽  
Cellular Iron Uptake

Regular “mucosal block” is characterized by decreased uptake of a normal iron load 3–72 h after the administration of excess iron (generally 10 mg) to iron-deficient animals. We found that short-acting mucosal block could be induced by much lower iron concentration and much shorter induction time than previously reported, without affecting levels of gene expression. A rapid endocytic mechanism was reported to decrease intestinal iron absorption after a high iron load, but the activating iron load and the time to decreased absorption were undetermined. We assessed the effects of 30–2,000 μg iron load on iron uptake in the duodenal loop of iron-deficient and iron-sufficient rats under anesthesia. One hour later, mucosal cellular iron uptake in iron-deficient rats administered 30 μg iron was 76.1%, decreasing 25% to 50.7% in rats administered 2,000 μg iron. In contrast, iron uptake by iron-sufficient rats was 63% (range 60.3–65.5%) regardless of iron load. Duodenal mucosal iron concentration was significantly lower in iron-deficient than in iron-sufficient rats. Iron levels in portal blood were consistently higher in iron-deficient rats regardless of iron load, in contrast to the decreased iron uptake on the luminal side. Iron loading blocked mucosal uptake of marginally excess iron (1,000 μg), with a greater effect at 15 min than at 30 min. The rapid induction of short-acting mucosal block only in iron-deficient rats suggests DMT1 internalization.

scholarly journals The role of transferrin in the mechanism of cellular iron uptake

1990 ◽  
Vol 271 (1) ◽  
pp. 1-9 ◽  
Author(s):  
K Thorstensen ◽  
I Romslo
Keyword(s):  
Iron Uptake ◽  
Cellular Iron ◽  
Cellular Iron Uptake

scholarly journals mRNA-binding protein tristetraprolin is essential for cardiac response to iron deficiency by regulating mitochondrial function

2018 ◽  
Vol 115 (27) ◽  
pp. E6291-E6300 ◽  
Author(s):  
Tatsuya Sato ◽  
Hsiang-Chun Chang ◽  
Marina Bayeva ◽  
Jason S. Shapiro ◽  
Lucia Ramos-Alonso ◽  
...  
Keyword(s):  
Iron Deficiency ◽  
Mitochondrial Function ◽  
Iron Uptake ◽  
Binding Protein ◽  
Complex Iii ◽  
Cardiac Response ◽  
Cellular Iron ◽  
Mrna Binding Protein ◽  
Cellular Iron Uptake ◽  
Mrna Binding

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specificallyNdufs1in complex I andUqcrfs1in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP,Uqcrfs1levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion ofTtpdisplay cardiac dysfunction with iron deficiency, demonstrating that TTP is necessary for maintaining cardiac function in the setting of low cellular iron. Altogether, our results describe a pathway that is activated in iron deficiency to regulate mitochondrial function to match the availability of Fe/S clusters.

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