Adenosine signaling promotes hematopoietic stem and progenitor cell emergence

Jing, Lili; Tamplin, Owen J.; Chen, Michael; Deng, Qing; Patterson, Shenia; Kim, Peter Geon; Durand, Ellen M.; McNeil, Ashley; Green, Julie M.; Matsuura, Shinobu; Ablain, Julien; Brandt, Margot; Schlaeger, Thorsten M.; Huttenlocher, Anna; Daley, George Q.; Ravid, Katya; Zon, Leonard I.

doi:10.1084/jem.20141528

Cited by 73 publications

(57 citation statements)

References 49 publications

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“…To determine if the Cxcr2 ligand, Cxcl8a, is involved in neutrophil resolution we examined neutrophil behavior in the cxcl8a TALEN mutant previously generated in our lab (Jing et al, 2015). The mutant contains a deletion of 2 amino acids (Figure S7A) in the 30S loop, thought to be involved in ligand stability and conformational changes during signaling (Helmer et al, 2015; Joseph et al, 2013; Liou et al, 2014).…”

Section: Resultsmentioning

confidence: 99%

Chemokine Signaling and the Regulation of Bidirectional Leukocyte Migration in Interstitial Tissues

et al. 2017

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Summary Motile cells navigate through complex tissue environments that include both attractive and repulsive cues. In response to tissue wounding, neutrophils, primary cells of the innate immune response, exhibit bidirectional migration that is orchestrated by chemokines and their receptors. Although progress has been made in identifying signals that mediate the recruitment phase, the mechanisms that regulate neutrophil reverse migration remain largely unknown. Here, we visualize bidirectional neutrophil migration to sterile wounds in zebrafish larvae and identify specific roles for the chemokine receptors Cxcr1 and Cxcr2 in neutrophil recruitment to sterile injury and infection. Notably, we also identify Cxcl8a/Cxcr2 as a specific ligand-receptor pair that orchestrates neutrophil chemokinesis in interstitial tissues during neutrophil reverse migration and resolution of inflammation. Taken together, our findings identify distinct receptors that mediate bidirectional leukocyte motility during interstitial migration depending on the context and type of tissue damage in vivo.

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Section: Resultsmentioning

confidence: 99%

Chemokine Signaling and the Regulation of Bidirectional Leukocyte Migration in Interstitial Tissues

et al. 2017

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“…2 d). HSC specification in the AGM requires cxcl8 expression and so this experiment was repeated with heat shock induction at 48 and 60 hpf, a period of time after peak HSC specification but still during the initial wave of CHT colonization (Jing et al, 2015). HSPC colonization of the CHT was enhanced by cxcr1 under these conditions as well (4.3 ± 0.9 vs. 11.8 ± 3.1 HSPCs per CHT, P = 0.023, Fig.…”

Section: Resultsmentioning

confidence: 99%

CXCR1 remodels the vascular niche to promote hematopoietic stem and progenitor cell engraftment

Blaser

Moore

Hagedorn

et al. 2017

Journal of Experimental Medicine

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“…Relative to the FL and BM, the AGM is enriched in IL-3 and IL-6 signaling pathways, 3,24 which in concert with other pathways such as Notch signaling, participate in hematopoietic emergence. 19,43 The AGM is enriched for shear-stress-mediated PGE2 and protein kinase A/cAMP-responsive element-binding protein signaling, [44][45][46] which can activate IL-6. [47][48][49] Subsequently, through exposure to IFN-a during maturation in the FL, AGM HSCs acquire expanded potential for engraftment in adults.…”

Section: Discussionmentioning

confidence: 99%

Interferon-α signaling promotes embryonic HSC maturation

Kim

Canver

Rhee

et al. 2016

Blood

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In the developing mouse embryo, the first hematopoietic stem cells (HSCs) arise in the aorta-gonad-mesonephros (AGM) and mature as they transit through the fetal liver (FL). Compared with FL and adult HSCs, AGM HSCs have reduced repopulation potential in irradiated adult transplant recipients but mechanisms underlying this deficiency in AGM HSCs are poorly understood. By co-expression gene network analysis, we deduced that AGM HSCs show lower levels of interferon-a (IFN-a)/Jak-Stat1-associated gene expression than FL HSCs. Treatment of AGM HSCs with IFN-a enhanced long-term hematopoietic engraftment and donor chimerism. Conversely, IFN-a receptor-deficient AGMs (Ifnar1 2/2 ), had significantly reduced donor chimerism. We identify adenine-thymine-rich interactive domain-3a (Arid3a), a factor essential for FL and B lymphopoiesis, as a key transcriptional co-regulator of IFN-a/Stat1 signaling. Arid3a occupies the genomic loci of Stat1 as well as several IFN-a effector genes, acting to regulate their expression. Accordingly, Arid3a 2/2 AGM HSCs had significantly reduced transplant potential, which was rescued by IFN-a treatment. Our results implicate the inflammatory IFN-a/ Jak-Stat pathway in the developmental maturation of embryonic HSCs, whose manipulation may lead to increased potency of reprogrammed HSCs for transplantation. (Blood. 2016;128(2):204-216)

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Adenosine signaling promotes hematopoietic stem and progenitor cell emergence

Abstract: Jing and colleagues show that adenosine signaling plays an important evolutionary role in the first step of hematopoietic stem cell generation in the embryonic aorta.

Cited by 73 publications

References 49 publications

Chemokine Signaling and the Regulation of Bidirectional Leukocyte Migration in Interstitial Tissues

Chemokine Signaling and the Regulation of Bidirectional Leukocyte Migration in Interstitial Tissues

CXCR1 remodels the vascular niche to promote hematopoietic stem and progenitor cell engraftment

Interferon-α signaling promotes embryonic HSC maturation

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