From: Hepcidin, an emerging and important player in brain iron homeostasis
Methods | Study conditions | Main results | References |
---|---|---|---|
Expression measured with RT-PCR from human tissues | Physiological conditions | mRNA of hepcidin present in brain tissue | Krause et al. [31] |
Expression measured with RT-PCR from human tissues | Physiological conditions | mRNA of hepcidin present in spinal cord | Pigeon et al. [1] |
Expression measured with RT-PCR, in situ hybridization, immunohistochemistry in murine brain | Physiological conditions | Hepcidin expression detected with RT-PCR and in situ hybridization Immunohistochemistry showed a wide distribution of the protein across the brain tissue compared to narrow distribution of mRNA of hepcidin measured by in situ hybridization | Zechel et al. [32] |
Expression measured with RT-PCR and in situ hybridization, while protein levels were measured with western blotting and immunohistochemistry (rat brain samples) | Physiological conditions | Hepcidin expression was low with highest signal detected in choroidal plexus and to a lesser extent in blood vessels Protein levels were abundant, especially in blood vessels, choroidal plexus and cortical astrocytes in close proximity to blood vessels | Raha-Chowdhury et al. [33] |
Protein levels measured with western blotting and immunohistochemistry (mouse brain samples) | Physiological conditions | Abundant protein levels of hepcidin across the brain tissue | Raha et al. [35] |
Expression measured with RT-PCR, while protein levels were measured with western blotting (mouse brain and cell cultures) | Physiological and stimulated conditions | Hepcidin expression was abundant but still in low levels Hepcidin induced FPN downregulation in mouse brain Hepcidin decreases iron-release in cultured neurons due to FPN downregulation | Wang et al. [34] |
Expression measured with RT-PCR (human brain samples) | Physiological conditions | HJV mRNA was not observed Hepcidin, neogenin, TFR2, HFE mRNA was present | Hänninen et al. [69] |
Expression measured with RT-PCR, while protein levels were measured with western blotting (mouse brain) | Different stimulated conditions | TFR2 loss does not affect brain hepcidin protein levels | Pellegrino et al. [73] |
Expression measured with RT-PCR, while protein levels were measured with western blotting and immunohistochemistry (rat cultured cells) | Inflammation | Microglia react to LPS by producing IL-6 Astrocytes produce hepcidin in response to IL-6 secreted by microglia Hepcidin increases iron-load in neurons Inflammation has hepcidin-independent actions in reducing iron-export and enhancing iron-import in neurons | You et al. [54] |
Expression measured with RT-PCR, while protein levels were measured by western blotting and immunohistochemistry (rat cultured cells) | Inflammation and iron-stimulation | TNF-α, IL-6 and LPS increase cellular iron content in neurons TNF-α, IL-6 and LPS do not affect cellular iron content in astrocytes TNF-α, IL-6 and LPS increase cellular iron content in microglia TNF-α, IL-6 and LPS cause DMT1↑ and FPN↓ (protein levels) in neurons TNF-α, IL-6 and LPS cause DMT1↑ (protein levels) in astrocytes TNF-α, IL-6 and LPS cause DMT1↑ (protein levels) in microglia TNF-α, IL-6 and LPS cause DMT1↑ (mRNA) in neurons TNF-α, IL-6 and LPS cause DMT1↑ (mRNA), while LPS causes FPN↓ in astrocytes TNF-α, IL-6 and LPS cause DMT1↑ (mRNA), while TNF-α and LPS cause FPN↓ (mRNA) in microglia TNF-α, IL-6, LPS and FeNTA cause hepcidin↑(mRNA) in astrocytes and microglia but not in neurons | Urrutia et al. [56] |
Protein levels measured with western blotting and ELISA in rat cultured cells | Inflammation | LPS increases hepcidin expression in rat brain LPS increases IL-6 production from microglia IL-6 from microglia induces hepcidin production in neurons (via STAT3 pathway) No observed hepcidin↑ in neurons without co-cultured microglia due to LPS stimulation | Qian et al. [55] |
Expression measured with RT-PCR, while protein levels were measured with western blotting and immunohistochemistry (rat brain and cultured cells) | Iron-overload | Hepcidin↑ in rat brain and cultured cells Hepcidin mRNA↑ in cultured neurons in response to iron-overload | Sun et al. [64] |
Expression measured with RT-PCR, while protein levels were measured with western blotting and ELISA in rat brain and cultured cells | Iron-overload | Hepcidin reduces iron-load in rat brains Hepcidin induces TFR1↓, DMT1↓ and FPN↓ in BMEC Hepcidin induces TFR1↓, DMT1↓ and FPN↓ in neurons | Du et al. [59] |
Expression measured with RT-PCR, while protein levels were measured with western blotting and ELISA in rat brain and cultured cells | Physiological conditions | Hepcidin induces TFR1↓, DMT1↓ and FPN↓ in astrocytes TFR1↓ is realized through AMPK pathway | Du et al. [58] |
Expression measured by RT-PCR, while levels of chemicals were measured with ELISA | Inflammation induced by Aβ aggregates | Hepcidin pre-treatment reduces expression and secretion of IL-6 and TNF-α in astrocytes and microglia | Urrutia et al. [65] |