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Differential accumulation of non-transferrin-bound iron by cardiac myocytes and fibroblasts
Ying Liu1, Joel G Parkes, Douglas M Templeton
1Department of Laboratory Medicine and Pathobiology, University of Toronto, Medical Sciences Building Rm 6302, 1 King's College Circle, M5S 1A8, Toronto, Canada.
Insights
Cardiac myocytes accumulate more iron than fibroblasts due to a higher capacity for non-transferrin-bound iron (NTBI) uptake. This inherent difference in NTBI transport explains preferential iron accumulation in heart cells.
Area of Science:
- Cardiovascular Biology
- Cellular Iron Metabolism
- Biochemistry
Background:
- Cardiac myocytes show preferential iron accumulation over fibroblasts in clinical iron overload and co-culture settings.
- The underlying cellular mechanisms for this preferential iron uptake remain unclear.
Purpose of the Study:
- To investigate whether preferential iron accumulation in cardiac myocytes is an inherent cellular property or dependent on tissue context.
- To compare iron transport kinetics and efflux in isolated rat cardiac myocytes and fibroblasts.
Main Methods:
- Homogeneous cultures of rat cardiac myocytes and fibroblasts were used.
- Iron uptake from transferrin and non-transferrin-bound iron (NTBI) was measured using 59Fe.
- Expression of iron transporters (transferrin receptor, DMT1) was assessed.
- Iron efflux and Michaelis-Menten kinetics (Km, Vmax) for NTBI uptake were determined.
Main Results:
- Iron uptake from transferrin was negligible in both cell types.
- Uptake of NTBI, particularly Fe2+, was significantly higher in myocytes compared to fibroblasts.
- While Michaelis constants (Km) were similar, Vmax values for NTBI uptake were approximately 10-fold higher in myocytes.
- Iron efflux rates were similar between myocytes and fibroblasts.
Conclusions:
- Preferential iron accumulation in cardiac myocytes is an inherent cellular characteristic.
- This preference is attributed to a higher transport capacity for non-transferrin-bound iron (NTBI) in myocytes.
- Differences in the Vmax of NTBI transporter systems drive differential iron accumulation between cardiac myocytes and fibroblasts.
Abstract:
Cardiac myocytes accumulate iron preferentially over fibroblast-like non-myocytes, both in clinical iron overload and when the cells are grown together in culture. In order to determine whether this reflects the tissue context or is an inherent property of the cells, we studied iron transporters, transport kinetics, and iron efflux in homogeneous cultures of rat cardiac myocytes and fibroblasts. In both cells, the rate of uptake of 59Fe from transferrin was insignificant, compared to the rate of uptake from non-transferrin-bound iron (NTBI). Expression of transferrin receptor mRNA and protein, and divalent metal transporter 1 (DMT1) mRNA, could not account for any difference in iron accumulation, and proportional efflux after iron loading was similar in both cells. Nevertheless, iron accumulation from NTBI over 72 h was greater in myocytes as determined by histological staining and quantitative iron measurement. NTBI uptake was greater for Fe2+ than Fe3+ in both cells, was increased by iron loading in both cells to a similar extent, and was characterized bysimilar Michaelis constants (K(m)) in all cases (redox state and presence or absence of iron loading). However, V(max) values were about 10-fold higher in myocytes. We conclude that preferential iron accumulation in cardiac myocytes, compared to fibroblasts, is due to a higher capacity of the NTBI-transporter system, and reflects an inherent difference in NTBI acquisition by the individual cell types.
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