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  1. Article ; Online: A novel promoter of endothelial dysfunction in African Americans: Relevance to sickle cell anaemia.

    Hebbel, Robert P / Milbauer, Liming / Wei, Peng

    British journal of haematology

    2023  Volume 203, Issue 2, Page(s) e71–e73

    MeSH term(s) Humans ; Black or African American/genetics ; Anemia, Sickle Cell/genetics ; Vascular Diseases
    Language English
    Publishing date 2023-07-23
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.18993
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  2. Article ; Online: Multiple inducers of endothelial NOS (eNOS) dysfunction in sickle cell disease.

    Hebbel, Robert P / Vercellotti, Gregory M

    American journal of hematology

    2021  Volume 96, Issue 11, Page(s) 1505–1517

    Abstract: A characteristic aspect of the robust, systemic inflammatory state in sickle cell disease is dysfunction of endothelial nitric oxide synthase (eNOS). We identify 10 aberrant endothelial cell inputs, present in the specific sickle context, that are known ... ...

    Abstract A characteristic aspect of the robust, systemic inflammatory state in sickle cell disease is dysfunction of endothelial nitric oxide synthase (eNOS). We identify 10 aberrant endothelial cell inputs, present in the specific sickle context, that are known to have the ability to cause eNOS dysfunction. These are: endothelial arginase depletion, asymmetric dimethylarginine, complement activation, endothelial glycocalyx degradation, free fatty acids, inflammatory mediators, microparticles, oxidized low density lipoproteins, reactive oxygen species, and Toll-like receptor 4 signaling ligands. The effect of true eNOS dysfunction on clinical testing using flow-mediated dilation can be simulated by two known examples of endothelial dysfunction mimicry (hemoglobin consumption of NO; and oxidation of smooth muscle cell soluble guanylate cyclase). This lends ambiguity to interpretation of such clinical testing. The presence of these multiple perturbing factors argues that a therapeutic approach targeting only a single injurious endothelial input (or either example of mimicry) would not be sufficiently efficacious. This would seem to argue for identifying therapeutics that directly protect eNOS function or application of multiple therapeutic approaches.
    MeSH term(s) Anemia, Sickle Cell/metabolism ; Anemia, Sickle Cell/pathology ; Animals ; Humans ; Lipoproteins, LDL/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Toll-Like Receptor 4/metabolism
    Chemical Substances Lipoproteins, LDL ; Reactive Oxygen Species ; Toll-Like Receptor 4 ; oxidized low density lipoprotein ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
    Language English
    Publishing date 2021-08-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.26308
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  3. Article ; Online: Blood endothelial cells: utility from ambiguity.

    Hebbel, Robert P

    The Journal of clinical investigation

    2017  Volume 127, Issue 5, Page(s) 1613–1615

    Abstract: In the mid-1990s, my research group began to devise a method to establish endothelial cell cultures from human peripheral blood, with an ultimate goal of examining interindividual heterogeneity of endothelial biology. The initial work, published in the ... ...

    Abstract In the mid-1990s, my research group began to devise a method to establish endothelial cell cultures from human peripheral blood, with an ultimate goal of examining interindividual heterogeneity of endothelial biology. The initial work, published in the JCI in 2000, described the method enabling successful attainment of blood outgrowth endothelial cells (BOEC). Truly endothelial, BOEC are progeny of a transplantable cell that originates in bone marrow, a putative endothelial progenitor. Our subsequent experimental work focused upon practical applications of BOEC: their use for gene therapy, tissue engineering, assessment of mutant gene effect, and discovery of heterogeneity in endothelial biology.
    MeSH term(s) Bone Marrow Cells/cytology ; Bone Marrow Cells/metabolism ; Cell Culture Techniques/methods ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Genetic Therapy/methods ; Humans ; Stem Cells/cytology ; Stem Cells/metabolism ; Tissue Engineering/methods
    Language English
    Publishing date 2017-05-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI93649
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  4. Article ; Online: SARS-CoV-2 severity in African Americans - A role for Duffy Null?

    Hebbel, Robert P / Vercellotti, Gregory M

    Haematologica

    2020  Volume 105, Issue 12, Page(s) 2892

    MeSH term(s) African Americans/genetics ; Betacoronavirus ; Biological Specimen Banks ; COVID-19 ; Cardiovascular Diseases ; Coronavirus Infections ; Humans ; Pandemics ; Pneumonia, Viral ; SARS Virus ; SARS-CoV-2 ; Socioeconomic Factors ; United Kingdom ; Vitamin D
    Chemical Substances Vitamin D (1406-16-2)
    Keywords covid19
    Language English
    Publishing date 2020-12-01
    Publishing country Italy
    Document type Journal Article ; Comment
    ZDB-ID 2333-4
    ISSN 1592-8721 ; 0017-6567 ; 0390-6078
    ISSN (online) 1592-8721
    ISSN 0017-6567 ; 0390-6078
    DOI 10.3324/haematol.2020.269415
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  6. Article ; Online: Ischemia-reperfusion injury in sickle cell anemia: relationship to acute chest syndrome, endothelial dysfunction, arterial vasculopathy, and inflammatory pain.

    Hebbel, Robert P

    Hematology/oncology clinics of North America

    2014  Volume 28, Issue 2, Page(s) 181–198

    Abstract: Ischemia-reperfusion (I/R) physiology, also called reperfusion injury, instigates vascular and tissue injury in human disease states. This review describes why sickle cell anemia should be conceptualized in this fashion and how I/R physiology explains ... ...

    Abstract Ischemia-reperfusion (I/R) physiology, also called reperfusion injury, instigates vascular and tissue injury in human disease states. This review describes why sickle cell anemia should be conceptualized in this fashion and how I/R physiology explains the genesis of characteristic aspects of vascular pathobiology and clinical disease in sickle cell anemia. The nature of I/R and its relevance to sickle cell anemia are discussed, with an emphasis on the acute chest syndrome, endothelial dysfunction with aberrant vasoregulation, circle of Willis vasculopathy, and inflammatory pain. Viewing sickle disease from this perspective elucidates defining pathophysiology and identifies a host of novel potential therapeutic targets.
    MeSH term(s) Acute Chest Syndrome/physiopathology ; Anemia, Sickle Cell/physiopathology ; Animals ; Endothelium, Vascular/physiopathology ; Humans ; Inflammation/physiopathology ; Models, Biological ; Pain/physiopathology ; Reperfusion Injury/physiopathology ; Vascular Diseases/physiopathology
    Language English
    Publishing date 2014-04
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 93115-9
    ISSN 1558-1977 ; 0889-8588
    ISSN (online) 1558-1977
    ISSN 0889-8588
    DOI 10.1016/j.hoc.2013.11.005
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  7. Article ; Online: The multifaceted role of ischemia/reperfusion in sickle cell anemia.

    Hebbel, Robert P / Belcher, John D / Vercellotti, Gregory M

    The Journal of clinical investigation

    2020  Volume 130, Issue 3, Page(s) 1062–1072

    Abstract: Sickle cell anemia is a unique disease dominated by hemolytic anemia and vaso-occlusive events. The latter trigger a version of ischemia/reperfusion (I/R) pathobiology that is singular in its origin, cyclicity, complexity, instability, perpetuity, and ... ...

    Abstract Sickle cell anemia is a unique disease dominated by hemolytic anemia and vaso-occlusive events. The latter trigger a version of ischemia/reperfusion (I/R) pathobiology that is singular in its origin, cyclicity, complexity, instability, perpetuity, and breadth of clinical consequences. Specific clinical features are probably attributable to local I/R injury (e.g., stroke syndromes) or remote organ injury (e.g., acute chest syndrome) or the systematization of inflammation (e.g., multifocal arteriopathy). Indeed, by fashioning an underlying template of endothelial dysfunction and vulnerability, the robust inflammatory systematization no doubt contributes to all sickle pathology. In this Review, we highlight I/R-targeting therapeutics shown to improve microvascular blood flow in sickle transgenic mice undergoing I/R, and we suggest how such insights might be translated into human therapeutic strategies.
    MeSH term(s) Anemia, Sickle Cell/genetics ; Anemia, Sickle Cell/metabolism ; Anemia, Sickle Cell/physiopathology ; Animals ; Disease Models, Animal ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Inflammation/classification ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/physiopathology ; Mice ; Mice, Transgenic ; Reperfusion Injury/classification ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Reperfusion Injury/physiopathology
    Language English
    Publishing date 2020-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI133639
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  8. Article ; Online: Sickle hemoglobin oxygen affinity-shifting strategies have unequal cerebrovascular risks.

    Hebbel, Robert P / Hedlund, Bo E

    American journal of hematology

    2017  Volume 93, Issue 3, Page(s) 321–325

    MeSH term(s) 2,3-Diphosphoglycerate/blood ; Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/drug therapy ; Benzaldehydes/adverse effects ; Benzaldehydes/pharmacology ; Benzaldehydes/therapeutic use ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Disorders/chemically induced ; Cerebrovascular Disorders/etiology ; Erythrocytes, Abnormal/metabolism ; Hematocrit ; Hematologic Agents/adverse effects ; Hematologic Agents/pharmacology ; Hematologic Agents/therapeutic use ; Hemoglobin, Sickle/chemistry ; Hemoglobin, Sickle/metabolism ; Hemolysis/drug effects ; Humans ; Hypoxia/prevention & control ; Microcirculation/drug effects ; Models, Biological ; Organ Specificity ; Oxygen/blood ; Oxyhemoglobins/metabolism ; Polymerization/drug effects ; Protein Binding ; Pyrazines/adverse effects ; Pyrazines/pharmacology ; Pyrazines/therapeutic use ; Pyrazoles/adverse effects ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Risk Assessment
    Chemical Substances Benzaldehydes ; Hematologic Agents ; Hemoglobin, Sickle ; Oxyhemoglobins ; Pyrazines ; Pyrazoles ; 2,3-Diphosphoglycerate (138-81-8) ; oxyhemoglobin S (37203-69-3) ; voxelotor (3ZO554A4Q8) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2017-12-06
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.24975
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  9. Article ; Online: Microparticles in sickle cell anaemia: promise and pitfalls.

    Hebbel, Robert P / Key, Nigel S

    British journal of haematology

    2016  Volume 174, Issue 1, Page(s) 16–29

    Abstract: Blood from patients with sickle cell disease contains microparticles (MP) derived from multiple cell sources, including red cells, platelets, monocytes and endothelial cells. MPs are of great interest because of their disease associations, their status ... ...

    Abstract Blood from patients with sickle cell disease contains microparticles (MP) derived from multiple cell sources, including red cells, platelets, monocytes and endothelial cells. MPs are of great interest because of their disease associations, their status as promising biomarkers, and the intercellular communications they mediate. To illustrate the likelihood of their relevance in sickle cell disease, we discuss the nature of MP, their profiling in sickle disease, some caveats relevant to their detection, their roles in supporting coagulation and the disparate influences they may exert upon the pathobiology of sickle cell disease.
    MeSH term(s) Anemia, Sickle Cell/blood ; Biomarkers ; Blood Coagulation ; Cell-Derived Microparticles/physiology ; Humans
    Chemical Substances Biomarkers
    Language English
    Publishing date 2016-07
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.14112
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  10. Article ; Online: Reconstructing sickle cell disease: a data-based analysis of the "hyperhemolysis paradigm" for pulmonary hypertension from the perspective of evidence-based medicine.

    Hebbel, Robert P

    American journal of hematology

    2011  Volume 86, Issue 2, Page(s) 123–154

    Abstract: The "hyperhemolytic paradigm" (HHP) posits that hemolysis in sickle disease sequentially and causally establishes increased cell-free plasma Hb, consumption of NO, a state of NO biodeficiency, endothelial dysfunction, and a high prevalence of pulmonary ... ...

    Abstract The "hyperhemolytic paradigm" (HHP) posits that hemolysis in sickle disease sequentially and causally establishes increased cell-free plasma Hb, consumption of NO, a state of NO biodeficiency, endothelial dysfunction, and a high prevalence of pulmonary hypertension. The basic science underpinning this concept has added an important facet to the complexity of vascular pathobiology in sickle disease, and clinical research has identified worrisome clinical issues. However, this critique identifies and explains a number of significant concerns about the various HHP component tenets. In addressing these issues, this report presents: a very brief history of the HHP, an integrated synthesis of mechanisms underlying sickle hemolysis, a review of the evidentiary value of hemolysis biomarkers, an examination of evidence bearing on existence of a hyperhemolytic subgroup, and a series of questions that should naturally be applied to the HHP if it is examined using critical thinking skills, the fundamental basis of evidence-based medicine. The veracity of different HHP tenets is found to vary from true, to weakly supported, to demonstrably false. The thesis is developed that the HHP has misidentified the mechanism and clinical significance of its findings. The extant research questions identified by these analyses are delineated, and a conservative, evidence-based approach is suggested for application in clinical medicine.
    MeSH term(s) Anemia, Sickle Cell/blood ; Anemia, Sickle Cell/genetics ; Anemia, Sickle Cell/metabolism ; Anemia, Sickle Cell/physiopathology ; Animals ; Biomarkers/blood ; Blood Flow Velocity ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/physiopathology ; Evidence-Based Medicine ; Hemoglobin, Sickle/chemistry ; Hemoglobin, Sickle/metabolism ; Hemolysis ; Humans ; Hypertension, Pulmonary/diagnosis ; Hypertension, Pulmonary/etiology ; Nitric Oxide/metabolism ; Severity of Illness Index ; Tricuspid Valve
    Chemical Substances Biomarkers ; Hemoglobin, Sickle ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2011-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.21952
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