Studies on medullary and extramedullary erythropoiesis in the adult mouse

Ce, Bozzini; Rendo, ME Barrio; Devoto, F.C.H.; Ce, Epper

doi:10.1152/ajplegacy.1970.219.3.724

Cited by 69 publications

(39 citation statements)

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“…Furthermore, the prevalence of eosinophilic cells within the red pulp and marginal sinus, which was prominent at 7 weeks of age, restored to wild-type pattern (data not shown). Therefore, in agreement with the significant function of the postnatal spleen as an erythropoietic organ in the mouse (Brodsky et al, 1966;Bozzini et al, 1970), the transient nature of the increase in spleen size and histological changes in Pcm heterozygotes probably reflects augmented splenic erythropoiesis because of Epo stimulation.…”

Section: Impaired Red Pulp Function In Pcm Heterozygous Spleensupporting

confidence: 74%

“…Here, we show that Pcm heterozygous spleens demonstrate changes consistent with elevated Epo levels, including a transient increase in spleen weight and red pulp hyperplasia, which temporally coincide with the transient polycythemia. In contrast, similar to genetically asplenic or splenectomized mice, the spleen rudiment in Pcm homozygotes should not respond to factors stimulating erythropoiesis (Bozzini et al, 1970;Lozzio, 1972). Therefore, despite elevated Epo levels, functional asplenia and severe perinatal iron deficiency probably represent the limiting factors toward the diminished rate of productive erythropoiesis during postnatal development in Pcm homozygotes, resulting in the lower peak hematocrit as compared with heterozygous mutants.…”

Section: Discussionmentioning

confidence: 98%

“…In the mouse, the red pulp constitutes a significant erythropoietic organ during normal development as well as in response to hypoxia, phlebotomy, or exogenous Epo administration (Brodsky et al, 1966;Bozzini et al, 1970). Pcm heterozygotes demonstrate an Epo-dependent polycythemia at 7 weeks of age (Mok et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

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Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

et al. 2004

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Regulatory interferences at the iron transporter ferroportin 1 (Fpn1) cause transient defects in iron homeostasis and erythropoiesis in polycythaemia(Pcm) mutant mice. The present study identified decreased Fpn1 expression in placental syncytiotrophoblast cells at late gestation as the mechanism of neonatal iron deficiency in Pcm mutants. Tissue specificity of embryonic Fpn1 dysregulation was evident from concomitant decreases in Fpn1 mRNA and protein expression in placenta and liver, as opposed to upregulation of Fpn1 protein despite decreased transcript levels in spleen, implicating post-transcriptional regulation of Fpn1. Dysregulation of Fpn1 and decreased iron levels in Pcm mutant spleens correlated with apoptotic cell death in the stroma, resulting in a semidominant spleen regression. At 7 weeks of age, a transient increase in spleen size in Pcm heterozygotes reflected a transient erythropoietin-mediated polycythemia. Structurally, Pcm mutant spleens displayed a severe defect in red pulp formation, including disruption of the sinusoidal endothelium, as well as discrete defects in white pulp organization during postnatal development. Reduced functional competence of the Pcmmutant spleen was manifested by an impaired response to chemically induced hemolytic anemia. Thus, aberrant Fpn1 regulation and iron homeostasis interferes with development of the spleen stroma during embryogenesis,resulting in a novel defect in spleen architecture postnatally.

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Section: Impaired Red Pulp Function In Pcm Heterozygous Spleensupporting

confidence: 74%

Section: Discussionmentioning

confidence: 98%

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Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

et al. 2004

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“…The spleen contributed considerably to the expansion of erythropoiesis, up to 50% of the total expansion of the tissue TfR mass and up to 19-fold over its own baseline activity, whereas the bone marrow attained its physiologic limit much sooner [22,23]. This already was reported in situations of hypoxia or hemolysis-or phlebotomy-induced anemia [24][25][26]. The mass of liver TfR remained constant in most experimental conditions studied here, except after phlebotomies.…”

Section: Discussionsupporting

confidence: 52%

Serum soluble transferrin receptor concentration is an accurate estimate of the mass of tissue receptors

R'Zik

Béguin

2001

Experimental Hematology

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Objective. Serum levels of the soluble transferrin receptor (sTfR) vary depending on the erythropoietic activity and iron status. In vitro, sTfR shed in the incubation medium correlates well with cellular TfR, but this relationship has never been established in vivo. To determine the value of serum sTfR as a quantitative marker of the body mass of tissue TfR, we designed experiments to examine the correlation between serum sTfR and tissue TfR in rats with various degrees of erythropoietic activity or iron status. Materials and Methods. We studied changes in erythropoietic activity in normal rats as well as in animals experiencing hemolysis, phlebotomy-induced iron deficiency, transfusion-or thiamphenicol-induced erythroid aplasia, or inflammation. At the end of follow-up, ferrokinetic studies were performed and animals were sacrificed. Organs were isolated and homogenized to determine the total mass of tissue TfR from the sum of tissue solubilized TfR in the bone marrow, spleen, liver, and blood cells (direct method). An indirect method was developed to derive the corporeal mass of tissue TfR from a representative marrow sample. Results. As expected, serum sTfR and total mass of tissue TfR varied as a function of iron status and erythropoiesis. Relative erythroid expansion in the spleen was greater than in the bone marrow. With the exception of phlebotomized animals, the indirect method correlated very well with direct measurements of the total mass of tissue TfR ( r ϭ 0.97, p Ͻ 0.0001). There was a close relationship between the total mass of tissue TfR and the total mass of serum sTfR ( r ϭ 0.79, p Ͻ 0.0001). Serum sTfR represented approximately 5-6% of the total mass of tissue TfR in most experimental situations, but this ratio was twice as high during iron-restricted erythropoiesis. In addition, the ratio could be higher or lower in nonsteady-state situations, because changes in tissue TfR occurred faster than those of serum sTfR. Conclusions. Serum sTfR represents a constant proportion of the total mass of tissue TfR over a wide range of erythropoietic activity. However, iron deficiency results in a higher proportion of serum sTfR, and the pace of change in serum sTfR levels is slower than that of tissue TfR mass.

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“…Thus it is likely that the bone marrow at 60 days is as active in erythropoietic activity as the spleen at birth. In laboratory animals, erythropoietic activity in the bone marrow and spleen has been examined under various experimental conditions, such as hypoxia, bleeding and administration of erythropoietin (BRUCE and Mc-CULLOCH, 1964;KUBANEK et al, 1968;BozziNi et al, 1970), starvation and ref eeding (FRUHMAN, 1966), pregnancy (FRUHMAN, 1968, adrenalectomy and hydrocortisone injection (POSPISIL et al, 1970;PosPISIL and ZAKOPALOVA, 1971), administration of bacterial endotoxin (TWENTYMAN, 1972) and estradiol injection (SANDBERG and BJORKHOLM, 1974). Erythropoiesis in the spleen is generally known to be more sensitive to experimental agents than that in the marrow.…”

Section: Discussionmentioning

confidence: 99%

Morphometric analysis of postnatal erythropoiesis in the spleen and bone marrow of the mouse.

Sasaki

Matsumura

Ito

1982

Arch. Histol. Jap., Arch. Histol. Jpn

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Studies on medullary and extramedullary erythropoiesis in the adult mouse

Cited by 69 publications

References 0 publications

Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

Serum soluble transferrin receptor concentration is an accurate estimate of the mass of tissue receptors

Morphometric analysis of postnatal erythropoiesis in the spleen and bone marrow of the mouse.

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