Oxygen tension–mediated erythrocyte membrane interactions regulate cerebral capillary hyperemia

Zhou, Sitong; Giannetto, Michael; DeCourcey, James; Kang, Hyunmo; Kang, Ning; Li, Yizeng; Zheng, Shan Suo; Zhao, Hetince; Simmons, William J.; Wei, Helen; Bodine, David M.; Smith, Nathan A.; Wan, Jiandi

doi:10.1126/sciadv.aaw4466

Cited by 35 publications

(24 citation statements)

References 55 publications

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“…Wei et al (2016) provided evidence that the transient decrease in tissue O 2 tension resulting from neuronal-evoked increases in metabolic activity (Devor et al, 2011) increases red blood cell deformability and velocity in capillaries. The authors proposed that O 2 release-induced displacement of ankyrin from band 3 weakens spectrin-actin cytoskeleton interactions (Stefanovic et al, 2013;Zhou et al, 2019), thereby increasing erythrocytes deformability (Wei et al, 2016), a phenomenon later confirmed using both ex vivo (microfluidics) and in vivo (two-photon imaging) approaches (Zhou et al, 2019).…”

Section: Neurovascular Couplingmentioning

confidence: 95%

Vasculo-Neuronal Coupling and Neurovascular Coupling at the Neurovascular Unit: Impact of Hypertension

et al. 2020

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Components of the neurovascular unit (NVU) establish dynamic crosstalk that regulates cerebral blood flow and maintain brain homeostasis. Here, we describe accumulating evidence for cellular elements of the NVU contributing to critical physiological processes such as cerebral autoregulation, neurovascular coupling, and vasculoneuronal coupling. We discuss how alterations in the cellular mechanisms governing NVU homeostasis can lead to pathological changes in which vascular endothelial and smooth muscle cell, pericyte and astrocyte function may play a key role. Because hypertension is a modifiable risk factor for stroke and accelerated cognitive decline in aging, we focus on hypertension-associated changes on cerebral arteriole function and structure, and the molecular mechanisms through which these may contribute to cognitive decline. We gather recent emerging evidence concerning cognitive loss in hypertension and the link with vascular dementia and Alzheimer's disease. Collectively, we summarize how vascular dysfunction, chronic hypoperfusion, oxidative stress, and inflammatory processes can uncouple communication at the NVU impairing cerebral perfusion and contributing to neurodegeneration.

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Section: Neurovascular Couplingmentioning

confidence: 95%

Vasculo-Neuronal Coupling and Neurovascular Coupling at the Neurovascular Unit: Impact of Hypertension

et al. 2020

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“…Specifically, the reversible association of deoxyHb with band 3 in the RBC membrane, increased intracellular glycolysis, and G i protein activation are all linked to this conformational change and have been shown to be required for deoxygenation-induced ATP release (Jagger et al 2001;Olearczyk et al 2004b;Chu et al 2016). In addition, the association of deoxyHb with band 3 increases RBC deformability by displacing band 3 from the cytoskeletal protein ankyrin (Stefanovic et al 2013;Chu et al 2016;Zhou et al 2019), which is closely associated with deoxygenation-induced increases in RBC capillary velocity (Zhou et al 2019), and also facilitates an increase in glycolysis by displacing a complex of glycolytic enzymes from band 3 (Campanella et al 2005(Campanella et al , 2008Chu & Low, 2006;Lewis et al 2009;Puchulu-Campanella et al 2013;Chu et al 2016). Increases in intracellular ATP also produce fluctuations, or 'flickering' , of the RBC membrane (Park et al 2010), which could activate mechanosensitive proteins such as G i proteins or Piezo1 channels (Gudi et al 1998;Cinar et al 2015) and facilitate the subsequent release of ATP.…”

Section: Mechanisms Of Impaired Deoxygenation-induced Atp Release Fromentioning

confidence: 99%

Reduced deformability contributes to impaired deoxygenation‐induced ATP release from red blood cells of older adult humans

Racine

Dinenno

2019

The Journal of Physiology

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Red blood cells (RBCs) release ATP in response to deoxygenation, which can increase blood flow to help match oxygen supply with tissue metabolic demand. r This release of ATP is impaired in RBCs from older adults, but the underlying mechanisms are unknown. r In this study, improving RBC deformability in older adults restored deoxygenation-induced ATP release, whereas decreasing RBC deformability in young adults reduced ATP release to the level of that of older adults. r In contrast, treating RBCs with a phosphodiesterase 3 inhibitor did not affect ATP release in either age group, possibly due to intact intracellular signalling downstream of deoxygenation as indicated by preserved cAMP and ATP release responses to pharmacological G i protein activation in RBCs from older adults. r These findings are the first to demonstrate that the age-related decrease in RBC deformability is a primary mechanism of impaired deoxygenation-induced ATP release, which may have implications for treating impaired vascular control with advancing age.

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“…Spatial compartmentalization of processes and resources in RBCs was discovered (Hoffman et al, 2009;Chu et al, 2012). Complex dynamics precise orchestration of processes occurring in the circulating RBCs in response to the changes in micro-and macro-environment (hormonal and mechanical stimulation, changes in local or ambient oxygen availability, temperature, circadian rhythm-related processes and others) is becoming evident (e.g., O'Neill and Reddy, 2011;Cahalan et al, 2015;Zhou et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Heterogeneity of Red Blood Cells: Causes and Consequences

et al. 2020

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Mean values of hematological parameters are currently used in the clinical laboratory settings to characterize red blood cell properties. Those include red blood cell indices, osmotic fragility test, eosin 5-maleimide (EMA) test, and deformability assessment using ektacytometry to name a few. Diagnosis of hereditary red blood cell disorders is complemented by identification of mutations in distinct genes that are recognized "molecular causes of disease." The power of these measurements is clinically wellestablished. However, the evidence is growing that the available information is not enough to understand the determinants of severity of diseases and heterogeneity in manifestation of pathologies such as hereditary hemolytic anemias. This review focuses on an alternative approach to assess red blood cell properties based on heterogeneity of red blood cells and characterization of fractions of cells with similar properties such as density, hydration, membrane loss, redox state, Ca 2+ levels, and morphology. Methodological approaches to detect variance of red blood cell properties will be presented. Causes of red blood cell heterogeneity include cell age, environmental stress as well as shear and metabolic stress, and multiple other factors. Heterogeneity of red blood cell properties is also promoted by pathological conditions that are not limited to the red blood cells disorders, but inflammatory state, metabolic diseases and cancer. Therapeutic interventions such as splenectomy and transfusion as well as drug administration also impact the variance in red blood cell properties. Based on the overview of the studies in this area, the possible applications of heterogeneity in red blood cell properties as prognostic and diagnostic marker commenting on the power and selectivity of such markers are discussed.

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Oxygen tension–mediated erythrocyte membrane interactions regulate cerebral capillary hyperemia

Cited by 35 publications

References 55 publications

Vasculo-Neuronal Coupling and Neurovascular Coupling at the Neurovascular Unit: Impact of Hypertension

Vasculo-Neuronal Coupling and Neurovascular Coupling at the Neurovascular Unit: Impact of Hypertension

Reduced deformability contributes to impaired deoxygenation‐induced ATP release from red blood cells of older adult humans

Heterogeneity of Red Blood Cells: Causes and Consequences

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