Kinetics of manganese transport and gene expressions of manganese transport carriers in Caco-2 cell monolayers

Li, Xiao-Li; Xie, Jingjing; Lü, Lin; Zhang, Jintao; Zhang, Lingyan; Zou, Yaxue; Wang, Qiuyue; Luo, Xugang; Li, Sufen

doi:10.1007/s10534-013-9670-y

Cited by 23 publications

(21 citation statements)

References 53 publications

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“…For example, inducible expression of Fpn in HEK293T cells reduces Mn accumulation and toxicity (26). Kinetic studies in Caco-2 cell monolayers, an in vitro model for intestinal absorption, also support a role for Fpn in basolateral export of Mn (41). However, more recent studies in Xenopus oocytes injected to express Fpn demonstrated efflux of 55 Fe, 65 Zn, and 57 Co but not 64 Cu, 109 Cd, or 54 Mn (25).…”

Section: Discussionmentioning

confidence: 99%

Ferroportin deficiency impairs manganese metabolism in flatiron mice

Seo

Wessling‐Resnick

2015

FASEB j.

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We examined the physiologic role of ferroportin (Fpn) in manganese (Mn) export using flatiron (ffe/+) mice, a genetic model of Fpn deficiency. Blood (0.0123 vs. 0.0107 mg/kg; P = 0.0003), hepatic (1.06 vs. 0.96 mg/kg; P = 0.0125), and bile Mn levels (79 vs. 38 mg/kg; P = 0.0204) were reduced in ffe/+ mice compared to +/+ controls. Erythrocyte Mn-superoxide dismutase was also reduced at 6 (0.154 vs. 0.096, P = 0.0101), 9 (0.131 vs. 0.089, P = 0.0162), and 16 weeks of age (0.170 vs. 0.090 units/mg protein/min; P < 0.0001). 54 Mn uptake after intragastric gavage was markedly reduced in ffe/+ mice (0.0187 vs. 0.0066% dose; P = 0.0243), while clearance of injected isotope was similar in ffe/+ and +/+ mice. These values were compared to intestinal absorption of 59 Fe, which was significantly reduced in ffe/+ mice (8.751 vs. 3.978% dose; P = 0.0458). The influence of the ffe mutation was examined in dopaminergic SH-SY5Y cells and human embryonic HEK293T cells. While expression of wild-type Fpn reversed Mn-induced cytotoxicity, ffe mutant H32R failed to confer protection. These combined results demonstrate that Fpn plays a central role in Mn transport and that flatiron mice provide an excellent genetic model to explore the role of this exporter in Mn homeostasis.-Seo, Y. A., Wessling-Resnick, M. Ferroportin deficiency impairs manganese metabolism in flatiron mice. FASEB J. 29, 2726-2733 (2015). www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

Ferroportin deficiency impairs manganese metabolism in flatiron mice

Seo

Wessling‐Resnick

2015

FASEB j.

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“…37 Studies of manganese transfer across Caco-2 cell monolayers, an in vitro model for intestinal absorption, are consistent with DMT1 and Fpn mediating apical uptake and basolateral export of manganese. 38 In other studies, inducible expression of Fpn in HEK293T cells reduced manganese accumulation and toxicity. 39 Treatment with manganese 40,41 and other metals 42 has been shown to regulate Fpn expression.…”

Section: Ferroportin (Slc40a1)mentioning

confidence: 87%

“…39 Treatment with manganese 40,41 and other metals 42 has been shown to regulate Fpn expression. In macrophages, Fpn expression is altered by exposure to manganese, 43 Hepcidin is also present in alveolar macrophages, 38,44 but the possible role for Fpn in manganese transport, its speculative function in the respiratory uptake of the metal and/or its detoxification, and the potential role for hepcidin in the regulation of these processes remain to be fully explored.…”

Section: Ferroportin (Slc40a1)mentioning

confidence: 99%

Manganese Transport Across the Pulmonary Epithelium

Thompson¹,

Kim²,

Wessling‐Resnick³

2014

Manganese in Health and Disease

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Our lungs represent a significant exposure site to airborne metals. Manganese and other metals enter the bloodstream from a variety of airborne sources across the pulmonary epithelium. Once absorbed, manganese can be taken up by other organ systems like the brain, where it is known to exert neurotoxic effects. Models of pulmonary manganese absorption have been developed based on known pathways of uptake across the intestinal epithelium, which are regulated by iron status. The sum of evidence suggests that additional and perhaps unique transport pathways are available to manganese in order to transit the pulmonary epithelium. Both in vitro and in vivo models have been established to characterize not only the transport but also toxicity of manganese on pulmonary epithelial cells. Handling of manganese by the lungs plays an important role in the inflammatory response, and has a strong influence on lung infection. These issues and emerging new questions are discussed in this chapter.

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“…Several organic forms of dietary Mn including metal‐amino acid complexes had been developed as dietary Mn supplements in poultry and livestock. Several studies demonstrated that Mn‐amino acid complex was more bioavailable than inorganic Mn sulphate, using ligated chicken intestinal loop (Bai et al., , ) and Caco‐2 cell models (Li et al., ). Others reported no differences in Mn bioavailability between organic and inorganic Mn sources (Baker and Halpin, ; Scheideler, ).…”

Section: Introductionmentioning

confidence: 99%

Uptake of manganese from manganese–lysine complex in the primary rat intestinal epithelial cells

Zhang

Gilbert

Zhang

et al. 2015

Animal Physiology Nutrition

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This study was conducted to compare the differences of the uptake of Mn from Mn-lysine complex (MnLys) and MnSO and to determine the potential mechanisms of the uptake of Mn from MnLys. We first established the primary rat intestinal epithelial cell culture model and used it to determine the uptake of Mn from different Mn sources. The MnLys increased (p < 0.001) Mn uptake when compared to MnSO . The uptake of Mn decreased (p < 0.05) with added Fe concentration increasing in the medium regardless of Mn source. The MnLys decreased (p < 0.01) Mn efflux transporter ferroportin 1 (FPN1) mRNA level, but did not influence (p > 0.06) Mn influx transporter DMT1 mRNA expression when compared to MnSO . The results above indicated that the increase of Mn accumulation for MnLys at least partly was due to the decrease of Mn efflux by reduced FPN1 expression. The N-ethylmaleimide, as an l-lysine transport system y inhibitor, decreased (p < 0.001) the uptake of Mn from MnLys, but did not affect (p > 0.10) the uptake of Mn from MnSO . The cycloheximide, as an l-lysine transport system b activator, increased (p < 0.001) the uptake of Mn from MnLys, whereas also did not influence the uptake of Mn from MnSO . The MnLys increased (p < 0.01) the system y member cationic amino acid transporter (CAT) 1, and system b components rBAT and b AT mRNA expression when compared to MnSO . These results suggested that the uptake of Mn from MnLys complex might be transported by CAT1 and system b , which was different from ionized Mn uptake pathway. In conclusion, the uptake of MnLys complex not only might be absorbed as Mn , but also appeared to be transported through CAT1 and system b in the primary rat intestinal epithelial cells.

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Kinetics of manganese transport and gene expressions of manganese transport carriers in Caco-2 cell monolayers

Cited by 23 publications

References 53 publications

Ferroportin deficiency impairs manganese metabolism in flatiron mice

Ferroportin deficiency impairs manganese metabolism in flatiron mice

Manganese Transport Across the Pulmonary Epithelium

Uptake of manganese from manganese–lysine complex in the primary rat intestinal epithelial cells

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