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G Fenna van Breda, Lennart G Bongartz, Wenqing Zhuang, Rachel P L van Swelm, Jeanne Pertijs, Branko Braam, Maarten-Jan Cramer, Dorine W Swinkels, Pieter A Doevendans, Marianne C Verhaar, Roos Masereeuw, Jaap A Joles, Carlo A J M Gaillard
BACKGROUND: Hepcidin regulates systemic iron homeostasis by downregulating the iron exporter ferroportin. Circulating hepcidin is mainly derived from the liver but hepcidin is also produced in the heart. We studied the differential and local regulation of hepcidin gene expression in response to myocardial infarction (MI) and/or chronic kidney disease (CKD). We hypothesized that cardiac hepcidin gene expression is induced by and regulated to severity of cardiac injury, either through direct (MI) or remote (CKD) stimuli, as well as through increased local iron content...
October 22, 2016: American Journal of Nephrology
Xingkang Jiang, Changwen Zhang, Shiyong Qi, Shanqi Guo, Yue Chen, E Du, Hongtuan Zhang, Xiaoming Wang, Ranlu Liu, Baomin Qiao, Kuo Yang, Zhihong Zhang, Yong Xu
Although we and other studies indicated ZNF217 expression was increased in prostate cancer (PCa), the factors mediating its misregulated expression and their oncogenic activity remain largely unexplored. Recent evidence demonstrated that ferroportin (FPN) reduction lead to decreased iron export and increased intercellular iron that consequently aggravates the oncogenic effects of iron. In the present study, ZNF217 was identified as a transcriptional repressor that inhibits FPN expression. Increased of ZNF217 expression led to decreased FPN concentration, coupled with resultant intracellular iron retention, increased iron-related cellular activities and enhanced tumor cell growth...
October 19, 2016: Oncotarget
Tomas Ganz
Macrophages exert multiple important roles in iron metabolism. As scavengers, splenic and hepatic macrophages phagocytize and degrade senescent and damaged erythrocytes to recycle iron, predominantly for the production of hemoglobin in new erythrocytes. Splenic red pulp macrophages are specialized for iron recycling, with increased expression of proteins for the uptake of hemoglobin, breakdown of heme, and export of iron. Iron release from macrophages is closely regulated by the interaction of hepcidin, a peptide hormone produced by hepatocytes, with the macrophage iron exporter ferroportin...
October 2016: Microbiology Spectrum
Ping Chen, Fei-Mi Li, Yu-Fu Zhou, Christopher Qian, Juan Li, Li-Rong Jiang, Zhong-Ming Qian
BACKGROUND: The antioxidant properties of alpha-lipoic acid (ALA) are associated with its ability to reduce iron in cells and tissues, which is partly due to its inhibiting effect on iron uptake from transferrin and its promoting effect on iron deposition into ferritin. However, the relevant mechanisms are unknown. METHODS: We therefore investigated the effects of ALA on the expression of transferrin receptor 1 (TfR1), divalent metal transporter 1 (DMT1), ferroportin 1 (Fpn1) and ferritin in BV-2 microglia cells...
September 11, 2016: Pharmacological Reports: PR
Monika Kasztura, Magdalena Dzięgała, Kamil Kobak, Jacek Bania, Grzegorz Mazur, Waldemar Banasiak, Piotr Ponikowski, Ewa Anita Jankowska
: Background Iron is presumed to play an important role in functioning of cardiomyocytes and skeletal myocytes. There is scarcity of direct data characterizing the cells functioning when exposed to iron depletion or iron overload in cellular environment. There is some clinical evidence demonstrating that iron deficiency has serious negative prognostic consequence in heart failure (HF) patients and its correction brought clinical benefit. BACKGROUND: Iron is presumed to play an important role in functioning of cardiomyocytes and skeletal myocytes...
October 17, 2016: Kardiologia Polska
Mariia Lunova, Peggy Schwarz, Renwar Nuraldeen, Kateryna Levada, Deniz Kuscuoglu, Michael Stützle, Maja Vujic, Johannes Haybaeck, Piotr Ruchala, Milan Jirsa, Jean-Christophe Deschemin, Sophie Vaulont, Christian Trautwein, Pavel Strnad
Iron is both an essential and a potentially toxic element and its systemic homeostasis is controlled by the iron-hormone hepcidin. Hepcidin binds to the cellular iron exporter ferroportin, causes its degradation and thereby diminishes iron uptake from the intestine and the release of iron from macrophages. Given that hepcidin-resistant ferroportin mutant mice display exocrine pancreas dysfunction, we analysed pancreata of aging hepcidin knockout mice (KOs). Hepcidin and Hfe KOs were compared to wild type animals (WTs) kept on standard or iron-rich diets...
October 14, 2016: Journal of Pathology
Sandra Azevedo Antunes, Maria Eugênia Fernandes Canziani
Anemia is a common complication and its impact on morbimortality in patients with chronic kidney disease (CKD) is well known. The discovery of hepcidin and its functions has contributed to a better understanding of iron metabolism disorders in CKD anemia. Hepcidin is a peptide mainly produced by hepatocytes and, through a connection with ferroportin, it regulates iron absorption in the duodenum and its release of stock cells. High hepcidin concentrations described in patients with CKD, especially in more advanced stages are attributed to decreased renal excretion and increased production...
July 2016: Jornal Brasileiro de Nefrologia: ʹorgão Oficial de Sociedades Brasileira e Latino-Americana de Nefrologia
Yuping Li, Ke Pan, Lin Chen, Jiao-Lin Ning, Xiaojun Li, Ting Yang, Niccolò Terrando, Jianteng Gu, Guocai Tao
BACKGROUND: Postoperative cognitive dysfunction (POCD) is a common complication after surgery, especially amongst elderly patients. Neuroinflammation and iron homeostasis are key hallmarks of several neurological disorders. In this study, we investigated the role of deferoxamine (DFO), a clinically used iron chelator, in a mouse model of surgery-induced cognitive dysfunction and assessed its neuroprotective effects on neuroinflammation, oxidative stress, and memory function. METHODS: A model of laparotomy under general anesthesia and analgesia was used to study POCD...
October 12, 2016: Journal of Neuroinflammation
Gaetano Bergamaschi, Antonio Di Sabatino, Alessandra Pasini, Cristina Ubezio, Filippo Costanzo, Davide Grataroli, Michela Masotti, Costanza Alvisi, Gino R Corazza
BACKGROUND & AIMS: Through inhibition of iron absorption and iron mobilization from tissue stores, hepcidin exerts a negative control on iron homeostasis. Hepcidin, in fact, promotes the degradation of ferroportin (Fpn1), the iron exporter molecule expressed on the membrane of hepatocytes and macrophages, thus preventing iron release from cells to plasma. Hepcidin effects on enterocytes, however, are less clear. Aim of the present study was to further investigate the regulation of iron absorption by hepcidin...
September 30, 2016: Clinical Nutrition: Official Journal of the European Society of Parenteral and Enteral Nutrition
Tomas Ganz
Hepcidin is an iron-regulating peptide hormone made in the liver. It controls the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte-recycling macrophages, and from iron-storing hepatocytes. Hepcidin acts by binding to and inactivating the sole cellular iron exporter, ferroportin, which delivers iron to plasma from all iron-transporting cells. In a classical endocrine feedback system, hepcidin production is stimulated by plasma iron and iron stores. Reflecting a likely role of hepcidin in innate immunity, hepcidin is also induced by inflammation...
2016: [Rinshō Ketsueki] the Japanese Journal of Clinical Hematology
Michela Asperti, Tanja Stuemler, Maura Poli, Magdalena Gryzik, Lena Lifshitz, Esther G Meyron-Holtz, Israel Vlodavsky, Paolo Arosio
Hepcidin is the key regulator of systemic iron availability that acts by controlling the degradation of the iron exporter ferroportin. It is expressed mainly in the liver and regulated by iron, inflammation, erythropoiesis and hypoxia. The various agents that control its expression act mainly via the BMP6/SMAD signaling pathway. Among them are exogenous heparins, which are strong hepcidin repressors with a mechanism of action not fully understood but that may involve the competition with the structurally similar endogenous Heparan Sulfates (HS)...
2016: PloS One
Don-Kyu Kim, Yong-Hoon Kim, Yoon Seok Jung, Ki-Sun Kim, Jae-Ho Jeong, Yong-Soo Lee, Jae-Min Yuk, Byung-Chul Oh, Hyon E Choy, Steven Dooley, Martina U Muckenthaler, Chul-Ho Lee, Hueng-Sik Choi
Small heterodimer partner (SHP) is a transcriptional corepressor regulating diverse metabolic processes. Here, we show that SHP acts as an intrinsic negative regulator of iron homeostasis. SHP-deficient mice maintained on a high-iron diet showed increased serum hepcidin levels, decreased expression of the iron exporter ferroportin as well as iron accumulation compared to WT mice. Conversely, overexpression of either SHP or AMP-activated protein kinase (AMPK), a metabolic sensor inducing SHP expression, suppressed BMP6-induced hepcidin expression...
September 30, 2016: Scientific Reports
Zi Xu, Weijia Sun, Yuheng Li, Shukuan Ling, Chenyang Zhao, Guohui Zhong, Dingsheng Zhao, Jinping Song, Hailin Song, Jinqiao Li, Linhao You, Guangjun Nie, Yanzhong Chang, Yingxian Li
Iron overload inhibits osteoblast function and promotes osteoclastogenesis. Hepcidin plays an important role in this process. The changes in iron content and the regulation of hepcidin under unloading-induced bone loss remain unknown. A hindlimb suspension model was adopted to simulate unloading-induced bone loss in mice. The results showed that iron deposition in both liver and bone was markedly increased in hindlimb unloaded mice, and was accompanied by the upregulation of osteoclast activity and downregulation of osteoblast activity...
September 26, 2016: Bone
Rafiou Agoro, Catherine Mura
Iron is essential in all organisms. In mammals systemic iron homeostasis relies on hepcidin, a peptide hormone with defensin properties, and its target, the cell iron exporter ferroportin. Hepcidin and ferroportin transcription are both upregulated by high iron levels, but are inversely regulated upon inflammation, leading to hypoferremia. Thus, host iron genes regulation may affect the innate immune responses against infectious microorganisms. Since macrophages, which are crucial innate immune cells, express both hepcidin and ferroportin, we explored in these cells their transcriptional regulation upon inflammation which is not completely understood...
October 2016: Blood Cells, Molecules & Diseases
Noriyuki Yamakawa, Kengo Oe, Naoichiro Yukawa, Kosaku Murakami, Ran Nakashima, Yoshitaka Imura, Hajime Yoshifuji, Koichiro Ohmura, Yasuo Miura, Naohisa Tomosugi, Hiroshi Kawabata, Akifumi Takaori-Kondo, Tsuneyo Mimori
Hereditary hemochromatosis (HH) is an inherited disorder usually seen in Northern Europeans, which results in iron overload syndrome. A few cases have also been reported in Japan. We herein report a Japanese man presenting with fever, arthritis, liver dysfunction, and hyperferritinemia who was diagnosed with type 4 HH. He was heterozygous for the 1520A>G (His507Arg) mutation in the ferroportin-1 gene (SLC40A1). He had a familial cataract as an infant, but hereditary hyperferritinemia cataract syndrome was excluded...
2016: Internal Medicine
Ke Pan, Xiaojun Li, Yan Chen, Dan Zhu, Yuping Li, Guocai Tao, Zhiyi Zuo
Postoperative cognitive dysfunction (POCD) is a common complication of elderly patients after surgery. The mechanisms of POCD have not been clarified. Iron accumulation is a feature of neurodegeneration. Recent reports showed that iron content was increased with impaired cognition induced by surgery. We sought to investigate whether iron chelation would attenuate POCD. In this study, male aged (18 months) Sprague-Dawley rats received 100 mg/kg deferoxamine or saline solution (0.9%) for 6 days before exploratory laparotomy...
December 2016: Neuropharmacology
Yusuke Kamihara, Kohichi Takada, Tsutomu Sato, Yutaka Kawano, Kazuyuki Murase, Yohei Arihara, Shohei Kikuchi, Naotaka Hayasaka, Makoto Usami, Satoshi Iyama, Koji Miyanishi, Yasushi Sato, Masayoshi Kobune, Junji Kato
Deregulated iron metabolism underlies the pathogenesis of many human cancers. Recently, low expression of ferroportin, which is the only identified non-heme iron exporter, has been associated with significantly reduced overall survival in multiple myeloma (MM); however, the altered iron metabolism in MM biology remains unclear. In this study we demonstrated, by live cell imaging, that MM cells have increased intracellular iron levels as compared with normal cells. In experiments to test the effect of iron chelation on the growth of MM cells, we found that deferasirox (DFX), an oral iron chelator used to treat iron overload in clinical practice, inhibits MM cell growth both in vivo and in vitro...
September 2, 2016: Oncotarget
Magdalena Dziegala, Monika Kasztura, Kamil Kobak, Jacek Bania, Waldemar Banasiak, Piotr Ponikowski, Ewa A Jankowska
The differential availability of iron during hypoxia is presumed to affect the functioning of cardiac and skeletal myocytes. Rat H9C2 cardiomyocytes and L6G8C5 myocytes were cultured for 48 h in normoxic or hypoxic conditions at the optimal, reduced or increased iron concentration. The mRNA expression levels of markers of apoptosis [B‑cell lymphoma‑2 (Bcl2; inhibition) and Bcl‑2‑activated X protein (Bax; induction)], atrophy (Atrogin), glycolysis (pyruvate kinase 2; PKM2) and iron metabolism [transferrin receptor 1 (TfR1; iron importer), ferroportin 1 (FPN1; iron exporter), ferritin heavy chain (FTH; iron storage protein) and hepcidin (HAMP; iron regulator)] were determined using reverse transcription‑quantitative polymerase chain reaction, and cell viability was measured using an tetrazolium reduction assay...
October 2016: Molecular Medicine Reports
Sundararaman Swaminathan
Gadolinium-based magnetic resonance (MR) contrast agents (GBCM) causes a devastating systemic fibrosing illness, nephrogenic systemic fibrosis (NSF), in patients with reduced kidney function. GBCM targets iron-recycling CD163- and ferroportin-expressing macrophages to release labile iron that mediates gadolinium toxicity and NSF. GBCA might similarly target iron-rich, ferroportin-expressing structures such as globus pallidus and cerebellar dentate nucleus in the brain to result in metal accumulation and potential toxicity...
August 28, 2016: Magnetic Resonance Imaging
Li-Na Lu, Zhong-Ming Qian, Ka-Chun Wu, Wing-Ho Yung, Ya Ke
Iron accumulates progressively in the brain with age; however, the cause is unknown. We hypothesized that iron accumulation may be associated with the age-induced changes in the expression of iron metabolism proteins in the brain. Here, we systematically investigated iron content and the expression of two major iron importers, transferrin receptor 1 (TfR1) and divalent metal transporter (DMT1), two iron exporters, ferroportin 1 (Fpn1) and ceruloplasmin (CP), and hepcidin, along with the pathological hallmarks of Parkinson's (PD) and Alzheimer's diseases (AD) in the brain of young (3 months), adult (12 months), and aged (24 months) rats...
August 30, 2016: Molecular Neurobiology
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