PTH and PTHrP Actions on Kidney and Bone

Bisello, Alessandro; Friedman, Peter A.

doi:10.1016/b978-0-12-373884-4.00050-1

“…Note that the magnitude of Ca 2+ concentrations in the blood lumen is several orders greater than that of the cytoplasmic Ca 2+ concentration 52 . As a consequence, the lumen Ca 2+ concentration is taken as a homogeneous and infinitely large reservoir of Ca 2+ (term in Eq.…”

Section: Resultsmentioning

confidence: 97%

Endothelial calcium dynamics elicited by ATP release from red blood cells

Nayak,

Das,

Misbah

2024

Sci Rep

0

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Red blood cells (RBCs) exhibit an interesting response to hydrodynamic flow, releasing adenosine triphosphate (ATP). Subsequently, these liberated ATP molecules initiate a crucial interaction with endothelial cells (ECs), thereby setting off a cascade involving the release of calcium ions (Ca$$^{2+}$$ 2 + ). Ca$$^{2+}$$ 2 + exerts control over a plethora of cellular functions, and acts as a mediator for dilation and contraction of blood vessel walls. This study focuses on the relationship between RBC dynamics and Ca$$^{2+}$$ 2 + dynamics, based on numerical simulations under Poiseuille flow within a linear two-dimensional channel. It is found that the concentration of ATP depends upon a variety of factors, including RBC density, channel width, and the vigor of the flow. The results of our investigation reveals several features. Firstly, the peak amplitude of Ca$$^{2+}$$ 2 + per EC escalates in direct proportion to the augmentation of RBC concentration. Secondly, increasing the flow strength induces a reduction in the time taken to reach the peak of Ca$$^{2+}$$ 2 + concentration, under the condition of a constant channel width. Additionally, when flow strength remains constant, an increase in channel width corresponds to an elevation in calcium peak amplitude, coupled with a decrease in peak time. This implies that Ca$$^{2+}$$ 2 + signals should transition from relatively unconstrained channels to more confined pathways within real vascular networks. This notion gains support from our examination of calcium propagation in a linear channel. In this scenario, the localized Ca$$^{2+}$$ 2 + release initiates a propagating wave that gradually encompasses the entire channel. Notably, our computed propagation speed agrees with observations.

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“…Later in this paper we will come back to this point. Note that the magnitude of Ca 2+ concentrations in the blood lumen is several orders greater than that of the cytoplasmic Ca 2+ concentration 47 . As a consequence, the lumen Ca 2+ concentration is taken as a homogeneous and infinitely large reservoir of Ca 2+ (term in equation ( 27)).…”

Section: Resultsmentioning

confidence: 97%

Endothelial Calcium Dynamics Elicited by ATP Release from Red Blood Cells

Nayak,

Das,

Misbah

2023

Preprint

0

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Red blood cells (RBCs) exhibit an interesting response to hydrodynamic flow, releasing adenosine triphosphate (ATP). Subsequently, these liberated ATP molecules initiate a crucial interaction with endothelial cells (ECs), thereby setting off a cascade involving the release of calcium ions (Ca2+). Ca2+ exerts control over a plethora of cellular functions, and acts as a mediator for dilation and contraction of blood vessel walls. This study focuses on the relationship between RBC dynamics and Ca2+ dynamics, based on numerical simulations under Poiseuille flow within a linear two-dimensional channel. It is found that the concentration of ATP depends upon a variety of factors, including RBC density, channel width, and the vigor of the flow. The results of our investigation reveals several features. Firstly, the peak amplitude of Ca2+ per EC escalates in direct proportion to the augmentation of RBC concentration. Secondly, increasing the flow strength induces a reduction in the time taken to reach the peak of Ca2+ concentration, under the condition of a constant channel width. Additionally, when flow strength remains constant, an increase in channel width corresponds to an elevation in calcium peak amplitude, coupled with a decrease in peak time. This implies that Ca2+ signals should transition from relatively unconstrained channels to more confined pathways within real vascular networks. This notion gains support from our examination of calcium propagation in a linear channel. In this scenario, localized calcium release initiates a propagating wave that gradually encompasses the entire channel. Notably, our computed propagation speed agrees with observations.

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“…Low calcium is one of the stimuli inducing T3SS expression and secretion (Perry et al 1997). The low concentration of calcium in M9, i.e., 0.1 mM, compared to 1 mM of free ionized calcium in human plasma (Bisello et al 2008), even in the presence of the calcium ion chelator acid-citrate-dextrose (ACD) serving as anti-coagulant, may thus be a trigger. Another signal sensed by Y. pestis RNA thermometers to activate expression of the T3SS regulon is the human host temperature of 37°C (Perry et al 1997).…”

Section: Resultsmentioning

confidence: 99%

Dual proteomic signature of immune cells andYersinia pestisupon blood infection

Lê-Bury

¹

,

Douché

²

,

Gianetto

³

et al. 2023

Preprint

1

0

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Emerging and reemerging infectious diseases represent major public health concerns. The urgent need for infection control measures requires deep understanding of molecular pathogenesis. Global approaches to study biological systems such as mass-spectrometry based proteomics benefited from groundbreaking physical and bioinformatical technological developments over recent years. However, dual proteomic study of highly pathogenic microorganisms and their hosts in complex matrices encountered during infection remains challenging due to high protein dynamic range of samples and requirements imposed in biosafety level 3 or 4 laboratories. Here, we constructed a dual proteomic pipeline of Yersinia pestis in human blood and plasma, mirroring bacteremic phase of plague. We provide the most complete Y. pestis proteome revealing a major reshaping of important bacterial pathways such as methionine biosynthesis and iron acquisition in human plasma. Remarkably, proteomic profiling in human blood highlights a greater Yersinia outer proteins intoxication of monocytes than neutrophils. Our study unravels global expression changes and points to a specific pathogenic signature during infection, paving the way for future exploration of proteomes in the complex context of host-pathogen interactions.

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PTH and PTHrP Actions on Kidney and Bone

Cited by 11 publications

References 677 publications

Endothelial calcium dynamics elicited by ATP release from red blood cells

Endothelial calcium dynamics elicited by ATP release from red blood cells

Endothelial Calcium Dynamics Elicited by ATP Release from Red Blood Cells

Dual proteomic signature of immune cells andYersinia pestisupon blood infection

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