Effects of low doses of dietary lead on red blood cell production in male and female mice

2003 ◽  
Vol 137 (3) ◽  
pp. 193-199 ◽  
Author(s):  
I Iavicoli ◽  
G Carelli ◽  
E.J Stanek ◽  
N Castellino ◽  
E.J Calabrese
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Low Doses ◽  
Male And Female ◽  
Cell Production ◽  
Female Mice

scholarly journals Targeted Application of Human Genetic Variation Can Improve Red Blood Cell Production from Stem Cells

2016 ◽  
Vol 18 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Felix C. Giani ◽  
Claudia Fiorini ◽  
Aoi Wakabayashi ◽  
Leif S. Ludwig ◽  
Rany M. Salem ◽  
...  
Keyword(s):  
Stem Cells ◽  
Genetic Variation ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Human Genetic Variation ◽  
Cell Production

Chemical Modulation of 3-Methylindole Toxicosis in Mice: Effect on Bronchiolar and Olfactory Mucosal Injury

1986 ◽  
Vol 23 (5) ◽  
pp. 563-570 ◽  
Author(s):  
M. A. M. Turk ◽  
W. Flory ◽  
W. G. Henk
Keyword(s):  
Mucosal Injury ◽  
Low Doses ◽  
Mixed Function Oxidase ◽  
Male And Female ◽  
Oxidase System ◽  
Pulmonary Lesions ◽  
Epithelial Damage ◽  
Female Mice ◽  
Mixed Function Oxidase System ◽  
Chemical Modulation

C57BL/6N mice were treated to induce tolerance, to modulate the mixed function oxidase system or to deplete glutathione (GSH) before injection with 400 mg 3-methylindole (3MI)/kg. Effect of pretreatment was determined by histologic comparison of pulmonary and nasal lesions 24 hours after 3 MI. β-Naphthoflavone and 3MI pretreatment significantly decreased 3MI-induced bronchiolar epithelial damage in male and female mice, while phenobarbital protection was significant only in female mice. Only β-naphthoflavone decreased nasal olfactory epithelial damage. Pretreatment with piperonyl butoxide, SKF 525-A, or α-naphthoflavone had no significant effect on development of lesions. Diethylmaleate pretreatment significantly increased mortality and bronchiolar damage in both sexes. Significant differences between male and female mice were not detected in any group. The results suggest that pretreatment with low doses of 3MI or induction of cytochrome P-448 or P-450 protects against 3MI toxicosis while GSH depletion increases mortality and pulmonary lesions.

Lipocalin 2 functions as a negative regulator of red blood cell production in an autocrine fashion

2005 ◽  
Vol 19 (13) ◽  
pp. 1881-1883 ◽  
Author(s):  
Ken‐Ichi Miharada ◽  
Takashi Hiroyama ◽  
Kazuhiro Sudo ◽  
Toshiro Nagasawa ◽  
Yukio Nakamura
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Negative Regulator ◽  
Lipocalin 2 ◽  
Cell Production

Role for BH3-Only Protein NOXA In Growth-Factor Deprivation and Early Erythropoiesis

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 4235-4235
Author(s):  
Christian R. Geest ◽  
Felix M. Wensveen ◽  
Sten F.W.M. Libregts ◽  
Alex M. de Bruin ◽  
Ingrid A.M. Derks ◽  
...  
Keyword(s):  
Growth Factor ◽  
Blood Cell ◽  
Red Blood Cell ◽  
Erythroid Cell ◽  
Erythroid Progenitors ◽  
Erythroid Progenitor ◽  
Apoptosis Pathway ◽  
Cell Production ◽  
Growth Factor Deprivation ◽  
Redundant Role

Abstract Abstract 4235 Red blood cell production is a strictly regulated process and homeostatic maintenance of the erythropoietic system requires equilibrium between the rate of erythroid cell production and red blood cell destruction. Hematopoietic cytokines play a crucial role in regulating expansion, differentiation and survival of erythrocyte progenitors. Shortage of growth factors triggers the mitochondrial apoptosis pathway, which is critically dependent on Bcl-2 family members. However, the contribution of this mechanism in the regulation of erythropoiesis remains ill-defined. This prompted us to screen for candidate genes involved in this process in erythroid progenitors. We found that the expression of Noxa, a pro-apoptotic Bcl-2 family member, is upregulated during erythroid differentiation and following cytokine-withdrawal in erythroid progenitor cells. Knockdown or deletion of Noxa in IL-3 dependent human and murine erythroid progenitor cell lines increased Mcl-1 levels, which correlated with markedly decreased apoptosis following cytokine withdrawal. Importantly, Noxa ablation in mice increased extra-medullary erythropoiesis, resulting in enhanced numbers of early splenic erythroblasts and circulating reticulocytes. Noxa-deficient hematopoietic progenitors were more resistant to apoptosis induced by growth factor deprivation and displayed increased colony-forming potential. In addition, combined loss of Noxa and Bim resulted in enhanced resistance of erythroid progenitors to cytokine withdrawal compared to WT or single Bim knockouts, suggesting a non-redundant role for Noxa and Bim in regulating survival of erythroid progenitors in response to cytokine deprivation. Finally, in a model of acute haemolytic anaemia, deletion of Noxa enhanced subsequent hematocrit recovery. Together, these findings identify a non-redundant role for BH3-only protein Noxa in the regulation of erythroblast survival during early erythropoiesis. Therefore, Noxa may be a novel component to control red blood cell numbers and modulation of this pathway could be envisaged in therapeutic options for treatment of anaemia. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Erythropoietin in Brain Development and Beyond

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Mawadda Alnaeeli ◽  
Li Wang ◽  
Barbora Piknova ◽  
Heather Rogers ◽  
Xiaoxia Li ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cell ◽  
Cell Types ◽  
Erythropoietin Receptor ◽  
Adult Brain ◽  
Receptor Expression ◽  
Neural Cells ◽  
Erythroid Progenitor ◽  
Cell Production ◽  
Oxygen Carrying Capacity

Erythropoietin is known as the requisite cytokine for red blood cell production. Its receptor, expressed at a high level on erythroid progenitor/precursor cells, is also found on endothelial, neural, and other cell types. Erythropoietin and erythropoietin receptor expression in the developing and adult brain suggest their possible involvement in neurodevelopment and neuroprotection. During ischemic stress, erythropoietin, which is hypoxia inducible, can contribute to brain homeostasis by increasing red blood cell production to increase the blood oxygen carrying capacity, stimulate nitric oxide production to modulate blood flow and contribute to the neurovascular response, or act directly on neural cells to provide neuroprotection as demonstrated in culture and animal models. Clinical studies of erythropoietin treatment in stroke and other diseases provide insight on safety and potential adverse effects and underscore the potential pleiotropic activity of erythropoietin. Herein, we summarize the roles of EPO and its receptor in the developing and adult brain during health and disease, providing first a brief overview of the well-established EPO biology and signaling, its hypoxic regulation, and role in erythropoiesis.

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