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Preview: pubmed: Curr Op Hem[Jour]

pubmed: Curr Op Hem[Jour]



NCBI: db=pubmed; Term="Current Opinion in Hematology"[Jour]



 



Endothelial cell biology of Endoglin in hereditary hemorrhagic telangiectasia.
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Endothelial cell biology of Endoglin in hereditary hemorrhagic telangiectasia.

Curr Opin Hematol. 2018 Feb 12;:

Authors: Sugden WW, Siekmann AF

Abstract
PURPOSE OF REVIEW: Mutations in the Endoglin (Eng) gene, an auxiliary receptor in the transforming growth factor beta (TGFβ)-superfamily signaling pathway, are responsible for the human vascular disorder hereditary hemorrhagic telangiectasia (HHT) type 1, characterized in part by blood vessel enlargement. A growing body of work has uncovered an autonomous role for Eng in endothelial cells. We will highlight the influence of Eng on distinct cellular behaviors, such as migration and shape control, which are ultimately important for the assignment of proper blood vessel diameters.
RECENT FINDINGS: How endothelial cells establish hierarchically ordered blood vessel trees is one of the outstanding questions in vascular biology. Mutations in components of the TGFβ-superfamily of signaling molecules disrupt this patterning and cause arteriovenous malformations (AVMs). Eng is a TGFβ coreceptor enhancing signaling through the type I receptor Alk1. Recent studies identified bone morphogenetic proteins (BMPs) 9 and 10 as the primary ligands for Alk1/Eng. Importantly, Eng potentiated Alk1 pathway activation downstream of hemodynamic forces. New results furthermore revealed how Eng affects endothelial cell migration and cell shape control in response to these forces, thereby providing new avenues for our understanding of AVM cause.
SUMMARY: We will discuss the interplay of Eng and hemodynamic forces, such as shear stress, in relation to Alk1 receptor activation. We will furthermore detail how this signaling pathway influences endothelial cell behaviors important for the establishment of hierarchically ordered blood vessel trees. Finally, we will provide an outlook how these insights might help in developing new therapies for the treatment of HHT.

PMID: 29438260 [PubMed - as supplied by publisher]




Band 3 function and dysfunction in a structural context.
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Band 3 function and dysfunction in a structural context.

Curr Opin Hematol. 2018 Feb 12;:

Authors: Abbas YM, Toye AM, Rubinstein JL, Reithmeier RAF

Abstract
PURPOSE OF REVIEW: Current research on the human band 3 glycoprotein, the red cell chloride/bicarbonate anion exchanger (AE1), is highlighted and placed within a structural context.
RECENT FINDINGS: The determination of the crystal structure of the membrane domain of human band 3, the founding member of the solute carrier 4 (SLC4) family of bicarbonate transporters, is a major breakthrough toward understanding the mechanism of action of this membrane transport protein, its interaction with partner proteins, and how mutations linked to disease affect its ability to fold and function.
SUMMARY: Band 3 contains 14 transmembrane segments arranged in a 7+7 transmembrane inverted repeat topology common to all members of the SLC4 family and the unrelated SLC26 anion transporter family. A functional feature of this fold is the presence of a core and a gate domain: the core domain contains two short transmembrane helices (TM3 and 10) that face each other in the middle of the membrane with the positive N-terminal helix dipoles creating the anion-binding site, whereas the gate domain forms the dimer interface. During transport, the movement of these two domains relative to each other provides the intracellular and extracellular compartments with alternating access to the central anion-binding site.

PMID: 29438259 [PubMed - as supplied by publisher]




Contribution of resident and recruited macrophages in vascular physiology and pathology.
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Contribution of resident and recruited macrophages in vascular physiology and pathology.

Curr Opin Hematol. 2018 Feb 12;:

Authors: Zhang L

Abstract
PURPOSE OF REVIEW: Macrophages are generally believed to originate entirely from the bone marrow; however, this paradigm is challenged by the discovery of yolk-sac-derived resident macrophages. Here, we provide an overview of recent advances in the ontogeny and function of resident macrophages.
RECENT FINDINGS: Macrophage precursors from three distinct embryonic sources (yolk sac, fetal liver and bone marrow) are found to colonize various tissues via the blood circulation early during embryogenesis until shortly after birth. They differentiate into distinct long-lived resident macrophages in response to the expression of tissue-specific transcription factors. Resident macrophages are proficient at taking up tissue-specific cellular debris and consequently acquire tissue-specific imprints. They are primarily involved in homeostasis but can also support the functionality of various tissues. Under pathological settings, dysregulation of resident macrophages can promote disease progression.
SUMMARY: Resident macrophages maintain themselves via in-situ proliferation under steady state. Following injury, bone marrow monocytes can contribute to the resident macrophage pool in adult animal. Embryonically and postnatally derived resident macrophages are similar but not identical: the former are more efficient at efferocytosis, whereas the latter are more competent at host defense. Thus, specific targeting of these two different resident macrophage populations may lead to better therapeutic strategies.

PMID: 29438258 [PubMed - as supplied by publisher]




Recent insights into vascular development from studies in zebrafish.
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Recent insights into vascular development from studies in zebrafish.

Curr Opin Hematol. 2018 Feb 12;:

Authors: Matsuoka RL, Stainier DYR

Abstract
PURPOSE OF REVIEW: Zebrafish has provided a powerful platform to study vascular biology over the past 25 years, owing to their distinct advantages for imaging and genetic manipulation. In this review, we summarize recent progress in vascular biology with particular emphasis on vascular development in zebrafish.
RECENT FINDINGS: The advent of transcription activator-like effector nuclease and clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 genome-editing technologies has dramatically facilitated reverse genetic approaches in zebrafish, as in other models. Here, we highlight recent studies on vascular development in zebrafish which mainly employed forward or reverse genetics combined with high-resolution imaging. These studies have advanced our understanding of diverse areas in vascular biology, including transcriptional regulation of endothelial cell differentiation, endothelial cell signaling during angiogenesis and lymphangiogenesis, vascular bed-specific developmental mechanisms, and perivascular cell recruitment.
SUMMARY: The unique attributes of the zebrafish model have allowed critical cellular and molecular insights into fundamental mechanisms of vascular development. Knowledge acquired through recent zebrafish work further advances our understanding of basic mechanisms underlying vascular morphogenesis, maintenance, and homeostasis. Ultimately, insights provided by the zebrafish model will help to understand the genetic, cellular, and molecular underpinnings of human vascular malformations and diseases.

PMID: 29438257 [PubMed - as supplied by publisher]




Integrative view on how erythropoietin signaling controls transcription patterns in erythroid cells.
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Integrative view on how erythropoietin signaling controls transcription patterns in erythroid cells.

Curr Opin Hematol. 2018 Jan 30;:

Authors: Perreault AA, Venters BJ

Abstract
PURPOSE OF REVIEW: Erythropoietin (EPO) is necessary and sufficient to trigger dynamic transcriptional patterns that drive the differentiation of erythroid precursor cells into mature, enucleated red cells. Because the molecular cloning and Food and Drug Administration approval for the therapeutic use of EPO over 30 years ago, a detailed understanding of how EPO works has advanced substantially. Yet, the precise epigenetic and transcriptional mechanisms by which EPO signaling controls erythroid expression patterns remains poorly understood. This review focuses on the current state of erythroid biology in regards to EPO signaling from human genetics and functional genomics perspectives.
RECENT FINDINGS: The goal of this review is to provide an integrative view of the gene regulatory underpinnings for erythroid expression patterns that are dynamically shaped during erythroid differentiation. Here, we highlight vignettes connecting recent insights into a genome-wide association study linking an EPO mutation to anemia, a study linking EPO-signaling to signal transducer and activator of transcription 5 (STAT5) chromatin occupancy and enhancers, and studies that examine the molecular mechanisms driving topological chromatin organization in erythroid cells.
SUMMARY: The genetic, epigenetic, and gene regulatory mechanisms underlying how hormone signal transduction influences erythroid gene expression remains only partly understood. A detailed understanding of these molecular pathways and how they intersect with one another will provide the basis for novel strategies to treat anemia and potentially other hematological diseases. As new regulators and signal transducers of EPO-signaling continue to emerge, new clinically relevant targets may be identified that improve the specificity and effectiveness of EPO therapy.

PMID: 29389768 [PubMed - as supplied by publisher]