Identification of four human cDNAs that are differentially expressed by early hematopoietic progenitors

Zhang, Xinmin; Dormady, Shane P.; Basch, Ross S.

doi:10.1016/s0301-472x(00)00539-7

Cited by 30 publications

(24 citation statements)

References 49 publications

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“…1). Together with the previous observations that sLR11 is produced only by immature SMCs and not in mature SMCs in atherosclerotic arteries (21) and that high levels of LR11 mRNA are expressed in human CD34 ϩ CD38 Ϫ immature hematopoietic progenitors (26), sLR11 released from immature cells may strengthen cell attachment to other stromal cells or extracellular matrices. In this context, preliminary results suggest that sLR11 is a potent enhancer of TNF-␣-induced attachment of hematological cells to stromal cells in response to G-CSF treatment.…”

Section: Discussionsupporting

confidence: 65%

“…Recent studies in humans and animals have shown that sLR11 is produced by myeloid cells after G-CSF treatment and that the released sLR11 plays an important role in the G-CSF-induced leukocyte mobilization from BM to the circulation. 4 Zhang et al reported high levels of LR11 mRNA in human CD34 ϩ CD38 Ϫ immature hematopoietic precursors (26). Both LR11 mRNA and cell surface protein levels are elevated in immature leukemic cells, in turn leading to increased levels of sLR11 in acute leukemias (27).…”

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confidence: 99%

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The Soluble Form of LR11 Protein Is a Regulator of Hypoxia-induced, Urokinase-type Plasminogen Activator Receptor (uPAR)-mediated Adhesion of Immature Hematological Cells

Nishii

Nakaseko

Jiang

et al. 2013

Journal of Biological Chemistry

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Background: Serum levels of the soluble LR11 fragment (sLR11) increase in patients with acute leukemia. Results: Hypoxia-induced factor (HIF)-1␣ activation increases LR11 levels, and sLR11 enhances adhesion of HSPCs to BM stromal cells via a uPAR-mediated pathway. Conclusion: sLR11 regulates hypoxia-induced attachment of HSPCs. Significance: sLR11 may stabilize the hematological pool size by controlling HSPC attachment to the BM niche.

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Section: Discussionsupporting

confidence: 65%

mentioning

confidence: 99%

The Soluble Form of LR11 Protein Is a Regulator of Hypoxia-induced, Urokinase-type Plasminogen Activator Receptor (uPAR)-mediated Adhesion of Immature Hematological Cells

Nishii

Nakaseko

Jiang

et al. 2013

Journal of Biological Chemistry

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“…This gene encodes a mitogen-activated protein kinase 3 phosphatase implicated in cell proliferation (36,37). Interestingly, this gene is preferentially expressed in CD34 ϩ CD38 Ϫ HSC compared with CD34 ϩ CD38 ϩ cells (38), similar to c-fos (see above), suggesting that Wnt signaling in early progenitor cells in the thymus induces similar target genes as those expressed in HSC.…”

Section: Discussionmentioning

confidence: 95%

Wnt Target Genes Identified by DNA Microarrays in Immature CD34+ Thymocytes Regulate Proliferation and Cell Adhesion

Staal

Weerkamp

Baert

et al. 2004

The Journal of Immunology

101

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The thymus is seeded by very small numbers of progenitor cells that undergo massive proliferation before differentiation and rearrangement of TCR genes occurs. Various signals mediate proliferation and differentiation of these cells, including Wnt signals. Wnt signals induce the interaction of the cytoplasmic cofactor β-catenin with nuclear T cell factor (TCF) transcription factors. We identified target genes of the Wnt/β-catenin/TCF pathway in the most immature (CD4−CD8−CD34+) thymocytes using Affymetrix DNA microarrays in combination with three different functional assays for in vitro induction of Wnt signaling. A relatively small number (∼30) of genes changed expression, including several proliferation-inducing transcription factors such as c-fos and c-jun, protein phosphatases, and adhesion molecules, but no genes involved in differentiation to mature T cell stages. The adhesion molecules likely confine the proliferating immature thymocytes to the appropriate anatomical sites in the thymus. For several of these target genes, we validated that they are true Wnt/β-catenin/TCF target genes using real-time quantitative PCR and reporter gene assays. The same core set of genes was repressed in Tcf-1-null mice, explaining the block in early thymocyte development in these mice. In conclusion, Wnt signals mediate proliferation and cell adhesion, but not differentiation of the immature thymic progenitor pool.

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“…17,19,25 Considering the difficulties involved in trying to identify the major source of cells that regulate circulating sLR11 levels, we analyzed LR11 expression in rat monocrotaline and mouse hypoxia models. Levels of LR11 protein increased in both models, indicating that LR11 expression increased in the present models of PAH under hypoxia and under treatment with monocrotaline (data not shown).…”

Section: Cd38mentioning

confidence: 99%

Deletion of LR11 Attenuates Hypoxia-Induced Pulmonary Arterial Smooth Muscle Cell Proliferation With Medial Thickening in Mice

Jiang

Konishi

Nurwidya

et al. 2016

ATVB

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Objective-We aimed to determine whether LR11 (low-density lipoprotein receptor with 11 binding repeats) is a potential key regulator of smooth muscle cell (SMC) proliferation during the progression of hypoxia-induced medial thickening in mice and whether sLR11 (soluble LR11) can serve as a biomarker in patients with pulmonary arterial hypertension. Approach and Results-The role of LR11 in pulmonary arterial hypertension was investigated using mouse and cell models of induced hypoxia. The expression of LR11 and of hypoxia-inducible factor-1α was significantly increased in lung tissues from C57Bl/6 mice after 3 weeks of exposure to hypoxia compared with normoxia. Serum sLR11 levels were also increased. Physiological and histochemical analyses showed that increased right ventricular systolic pressure, right ventricular hypertrophy, and medial thickening induced under hypoxia in wild-type mice were attenuated in LR11−/− mice. The proliferation rates stimulated by hypoxia or platelet-derived growth factor-BB were attenuated in SMC derived from LR11 −/− mice, compared with those from wild-type mice. Exogenous sLR11 protein increased the proliferation rates of SMC from wild-type mice. The expression of LR11 and hypoxia-inducible factor-1α was increased in cultured SMC under hypoxic conditions, and hypoxia-inducible factor-1α knockdown almost abolished the induction of LR11. Serum sLR11 levels were significantly higher in patients with, rather than without, pulmonary arterial hypertension. sLR11 levels positively correlated with pulmonary vascular resistance and mean pulmonary arterial pressure. Conclusions-LR11 regulated SMC proliferation during the progression of hypoxia-induced medial thickening in mice.The findings obtained from mice, together with those in humans, indicate that sLR11 could serve as a novel biomarker that reflects the pathophysiology of proliferating medial SMC in pulmonary arterial hypertension. (Arterioscler Thromb

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Identification of four human cDNAs that are differentially expressed by early hematopoietic progenitors

Cited by 30 publications

References 49 publications

The Soluble Form of LR11 Protein Is a Regulator of Hypoxia-induced, Urokinase-type Plasminogen Activator Receptor (uPAR)-mediated Adhesion of Immature Hematological Cells

The Soluble Form of LR11 Protein Is a Regulator of Hypoxia-induced, Urokinase-type Plasminogen Activator Receptor (uPAR)-mediated Adhesion of Immature Hematological Cells

Wnt Target Genes Identified by DNA Microarrays in Immature CD34+ Thymocytes Regulate Proliferation and Cell Adhesion

Deletion of LR11 Attenuates Hypoxia-Induced Pulmonary Arterial Smooth Muscle Cell Proliferation With Medial Thickening in Mice

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