Hypoxia induces transcriptomic changes in bone marrow cells leading to increased erythropoiesis [TFPI]
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ABSTRACT:
PROVIDER: PRJNA933339 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23388113_1.fastq.gz | Fastqsanger.gz | |||
| SRR23388113_2.fastq.gz | Fastqsanger.gz | |||
| SRR23388114_1.fastq.gz | Fastqsanger.gz | |||
| SRR23388114_2.fastq.gz | Fastqsanger.gz | |||
| SRR23388115_1.fastq.gz | Fastqsanger.gz |
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Project description:Erythropoiesis takes place mostly in bone marrow and ends in blood. Previous studies have shown that hypoxia has direct effects on the bone marrow, which could promotes erythropoiesis by modulating erythroid progenitor maturation. However, how bone marrow microenvironment participates in erythropoiesis under hypoxia still need further clarification. In this study, we analyzed transcriptional changes of bone marrow cells of mice exposed to 5000 m altitude hypoxia for 1 week. We profiled the top 20 up-regulated secreted factor genes after treatment with hypoxia, and found TFPI was one of the secreted factor genes with the highest expression.
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Project description:Hypoxia is associated with increased erythropoietin (EPO) release to drive erythropoiesis. However, a prolonged sojourn at high altitude results in an increase in EPO levels followed by a decrease, although erythropoiesis remains elevated at a stable level. The role of hypoxia and related EPO adjustments are not fully understood and contributed to the formulation of the theory of neocytolysis. In this study, we aimed to exclusively evaluate the role of oxygen on erythropoiesis comparing in vitro erythroid differentiation performed at atmospheric oxygen, with a lower oxygen concentration (3% O2) and with cultures of erythroid precursors isolated from peripheral blood after a 19-day sojourn at high altitude (3450 m). Results highlight an accelerated erythroid maturation at low oxygen and more concave morphology of reticulocytes. No differences in deformability were observed in the formed reticulocytes in the tested conditions. Moreover, hematopoietic stem and progenitor cells isolated from blood affected by hypoxia at high altitude did not result in a different erythroid development, suggesting no retention of high altitude signature but rather an immediate adaptation to oxygen concentration. This adaptation was observed during in vitro erythropoiesis at 3% oxygen, displaying a significantly increased glycolytic metabolic profile. These hypoxia-induced effects on in vitro erythropoiesis fail to provide an intrinsic explanation to the concept of neocytolysis.
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Project description:Paternal hypoxia exposure primes offspring for increased hypoxia resistance
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Project description:Erythropoiesis occurs first in the yolk sac as a transit “primitive” form, then is gradually re-placed by the “definitive” form in the fetal liver (FL) during fetal development and in the bone marrow (BM) postnatal. While it is well known that differences exist between primitive and de-finitive erythropoiesis, the similarities and differences between FL and BM definitive erythropoi-esis have not been studied. Here we performed comprehensive comparisons of erythroid progen-itors and precursors at all maturational stages sorted from E16.5 FL and adult BM. Transcriptome comparison revealed that genes with increased expression in FL BFU-E were en-riched in cell division. Interestingly, the expression levels of glucocorticoid receptor Nr3c1, Myc and Myc downstream target Ccna2, were significantly higher in FL BFU-E, indicating the role of Nr3c1-Myc-Ccna2 axis in the enhanced proliferation/cell division of FL BFU-E cells. At the CFU-E stage, the expression of genes associated with hemoglobin biosynthesis were much higher in FL CFU-E, indicating more hemoglobin production. During terminal erythropoiesis, overall temporal patterns in gene expression were conserved between FL and BM. While biological pro-cesses related to translation, TCA and hypoxia response were upregulated in FL erythroblasts, that related to antiviral signal pathway were upregulated in BM erythroblasts. Our findings un-covered previously unrecognized differences between FL and BM definitive erythropoiesis and provide novel insights into erythropoiesis.
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Project description:The hypoxia signaling pathway controls hypoxia adaptation and tolerance of organisms, which is regulated by multiple mechanisms. Viral infection elicits various pathophysiological responses in the host. However, whether viral infection can affect the hypoxia response is still largely unknown. In this study, we found that Spring viraemia of carp virus (SVCV) infection in zebrafish caused symptoms similar to those in zebrafish under hypoxic conditions. Further assays indicated that SVCV infection activated the hypoxia signaling pathway in zebrafish. In addition, SVCV infection caused increased glycolysis and ROS levels in cells. Mechanistically, SVCV-G protein interacted with hif1α-a/b and attenuated their K48-linked polyubiquitination, leading to their stabilization and subsequent enhancement of target gene expression. Moreover, treatment with the HIF1α-specific inhibitor PX478 enhanced the antiviral ability against SVCV infection in zebrafish and zebrafish cells. This study reveals a relationship between SVCV infection and the hypoxia signaling pathway in fish, and provides a strategy for reducing the damage of viral disease in the aquaculture industry.
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