Wild-type macrophages reverse disease in heme oxygenase 1-deficient mice

Kovtunovych, Gennadiy; Ghosh, Manik C.; Ollivierre, Wade H.; Weitzel, R. Patrick; Eckhaus, Michael; Tisdale, John F.; Yachie, Akihiro; Rouault, Tracey A.

doi:10.1182/blood-2014-02-554162

Cited by 55 publications

(52 citation statements)

References 39 publications

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“…Of note, heme itself can trigger the differentiation of monocytes into iron recycling macrophages by activating the heme-binding transcriptional repressor BACH1 (Btb and Cnc Homology 1) and subsequent induction of a SPI-C-transcription factor-regulated cell differentiation program (Haldar et al, 2014). Because dietary iron absorption alone cannot sustain erythropoiesis (see below), the recycling of heme iron by HMOX1 (Kovtunovych et al, 2014) and its release by FPN (Zhang et al, 2011) in macrophages are critical for sustaining physiological erythropoiesis.…”

Section: Rolling Out the Red Carpet: Iron Metabolism In Erythroid Cellsmentioning

confidence: 99%

A Red Carpet for Iron Metabolism

Muckenthaler

Rivella

Hentze

et al. 2017

Cell

1,009

993

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200 billion red blood cells (RBCs) are produced every day, requiring more than 2 × 3 1015 iron atoms every second to maintain adequate erythropoiesis. These numbers translate into 20 mL of blood being produced each day, containing 6 g of hemoglobin and 20 mg of iron. These impressive numbers illustrate why the making and breaking of RBCs is at the heart of iron physiology, providing an ideal context to discuss recent progress in understanding the systemic and cellular mechanisms that underlie the regulation of iron homeostasis and its disorders.

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Section: Rolling Out the Red Carpet: Iron Metabolism In Erythroid Cellsmentioning

confidence: 99%

A Red Carpet for Iron Metabolism

Muckenthaler

Rivella

Hentze

et al. 2017

Cell

1,009

993

View full text Add to dashboard Cite

show abstract

“…In fact, the specialized function of RPMɸs is unique among splenic Mɸs, such that an additional transcription factor, SpiC, is required for the development of these cells (55). Since dietary iron absorption is insufficient to sustain erythropoiesis, RPMɸ recycling of heme iron by HO-1 and its release by Fpn is critical (37,56,57).…”

Section: Introductionmentioning

confidence: 99%

Regulation of tissue iron homeostasis: the macrophage “ferrostat”

Winn¹,

Volk²,

Hasty³

2020

JCI Insight

127

113

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“…The root cause for some symptoms of HO-1 deficiency has been attributed directly to the depletion of tissue macrophages (i.e., in the spleen, liver, and bone marrow) [16]. More interestingly, transplantation of WT macrophages into HO-1 KO (HO-1 2/2 ) mice resulted in a transient engraftment of WT macrophages in the liver and spleen, which subsequently reversed the disease process [17]. All of these findings suggest the importance of HO-1 in macrophage development and function.…”

Section: Introductionmentioning

confidence: 99%

Infiltration of myeloid cells in the pregnant uterus is affected by heme oxygenase-1

Zhao

Kalish

Wong

et al. 2016

Journal of Leukocyte Biology

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Infiltrating myeloid cells in pregnant uteri play critical roles in the establishment of the placenta and maintenance of normal pregnancies. Their recruitment and proliferation are primarily mediated by the interactions of cytokines and chemokines secreted locally with their corresponding receptors. Heme oxygenase-1 (HO-1) has various physiologic properties that contribute to placental vascular development, with deficiencies in HO-1 associated with pregnancy disorders. Here, we investigated the effect of HO-1 on myeloid cell infiltration into pregnant uteri using a partial HO-1-deficient (Het, HO-1) mouse model. With the use of flow cytometry, HO-1 was found predominantly expressed in circulating and uterine myeloid cells, specifically neutrophils and monocytes/macrophages. In pregnant Het uteri, the numbers of neutrophils and monocytes/macrophages were significantly reduced compared with pregnant wild-type (WT; HO-1) uteri. With the use of BrdU in vivo assays, HO-1 deficiency did not affect cell proliferation or blood cell populations. With the use of PCR arrays, gene expression of cytokines (Csf1, Csf3), chemokines (Ccl1, Ccl2, Ccl6, Ccl8, Ccl11, Ccl12, Cxcl4, Cxcl9, Cxcl12), and their receptors (Ccr1, Ccr2, Ccr3, Ccr5) were also reduced significantly in Het compared with pregnant WT uteri. Moreover, with the use of flow cytometry, myeloid CSF1R and CCR2 expression in blood and uteri from both pregnant and nonpregnant mice was characterized, and a deficiency in HO-1 significantly reduced CCR2 expression in infiltrating uterine monocytes/macrophages and dendritic cells (DCs). These data reveal that HO-1 regulates not only cytokine/chemokine production in pregnant uteri but also myeloid cell receptor numbers, suggesting a role of HO-1 in the recruitment and maintenance of myeloid cells in pregnant uteri and subsequent effects on placental vascular formation.

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Wild-type macrophages reverse disease in heme oxygenase 1-deficient mice

Cited by 55 publications

References 39 publications

A Red Carpet for Iron Metabolism

A Red Carpet for Iron Metabolism

Regulation of tissue iron homeostasis: the macrophage “ferrostat”

Infiltration of myeloid cells in the pregnant uterus is affected by heme oxygenase-1

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