Novel Evidence that Purinergic Signaling - Nlrp3 Inflammasome Axis Regulates Circadian Rhythm of Hematopoietic Stem/Progenitor Cells Circulation in Peripheral Blood

Adamiak, Mateusz; Ciechanowicz, Andrzej; Skoda, Marta; Cymer, Monika; Tracz, Michał; Xu, Bing; Ratajczak, Mariusz Z.

doi:10.1007/s12015-020-09953-0

Cited by 20 publications

(21 citation statements)

References 32 publications

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“…The researchers first illustrated that the MBL-initiated ComC and coagulation cascade (CoaC) are involved in triggering the mobilization of HSPCs [ 95 ]. ATP is released extracellularly primarily through the pannexin-1 channel and activates the MBL-ComC (CoaC) pathway as a DAMP via purinergic receptors [ 95 , 96 , 97 ]. The researchers then proposed that the ATP-induced NLRP3 inflammasome acts as a neutralizer that connects purinergic signaling with the activation of the ComC, which is required for the egress of HSPCs from the BM into the PB [ 98 ].…”

Section: Extracellular Signals Activate the Inflammasome Through Pmentioning

confidence: 99%

Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities

Yang

et al. 2021

Molecules

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Hematopoietic stem cells (HSCs) regularly produce various blood cells throughout life via their self-renewal, proliferation, and differentiation abilities. Most HSCs remain quiescent in the bone marrow (BM) and respond in a timely manner to either physiological or pathological cues, but the underlying mechanisms remain to be further elucidated. In the past few years, accumulating evidence has highlighted an intermediate role of inflammasome activation in hematopoietic maintenance, post-hematopoietic transplantation complications, and senescence. As a cytosolic protein complex, the inflammasome participates in immune responses by generating a caspase cascade and inducing cytokine secretion. This process is generally triggered by signals from purinergic receptors that integrate extracellular stimuli such as the metabolic factor ATP via P2 receptors. Furthermore, targeted modulation/inhibition of specific inflammasomes may help to maintain/restore adequate hematopoietic homeostasis. In this review, we will first summarize the possible relationships between inflammasome activation and homeostasis based on certain interesting phenomena. The cellular and molecular mechanism by which purinergic receptors integrate extracellular cues to activate inflammasomes inside HSCs will then be described. We will also discuss the therapeutic potential of targeting inflammasomes and their components in some diseases through pharmacological or genetic strategies.

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Section: Extracellular Signals Activate the Inflammasome Through Pmentioning

confidence: 99%

Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities

Yang

et al. 2021

Molecules

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“…Immunosurveillance is maintained by the constant flow of hematopoietic stem cells (HPSCs) from the bone marrow and recirculation in the blood and lymph via a bioactive phosphoshingolipid, Spingosine-1 phosphate (S1P), which acts as a chemoattractant of HPSCs (Massberg et al, 2007 ). The number of HPSCs has been shown to be highly circadian, with the majority of HPSCs circulating in peripheral blood in the early morning hours (Golan et al, 2018 ; Adamiak et al, 2020 ; Ratajczak et al, 2020 ). Both S1P levels and the activated C5 complement pathway are reportedly circadian and play a role in the diurnal chemotaxis of HPSC egression of stem cells from bone marrow to the peripheral blood circulation to maintain immunosurveillance.…”

Section: Co-regulatory Roles Of Complement and Sleep On Immunosurveilmentioning

confidence: 99%

Circadian Clock and Complement Immune System—Complementary Control of Physiology and Pathology?

Shivshankar

Fekry

Eckel‐Mahan

et al. 2020

Front. Cell. Infect. Microbiol.

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Mammalian species contain an internal circadian (i.e., 24-h) clock that is synchronized to the day and night cycles. Large epidemiological studies, which are supported by carefully controlled studies in numerous species, support the idea that chronic disruption of our circadian cycles results in a number of health issues, including obesity and diabetes, defective immune response, and cancer. Here we focus specifically on the role of the complement immune system and its relationship to the internal circadian clock system. While still an incompletely understood area, there is evidence that dysregulated proinflammatory cytokines, complement factors, and oxidative stress can be induced by circadian disruption and that these may feed back into the oscillator at the level of circadian gene regulation. Such a feedback cycle may contribute to impaired host immune response against pathogenic insults. The complement immune system including its activated anaphylatoxins, C3a and C5a, not only facilitate innate and adaptive immune response in chemotaxis and phagocytosis, but they can also amplify chronic inflammation in the host organism. Consequent development of autoimmune disorders, and metabolic diseases associated with additional environmental insults that activate complement can in severe cases, lead to accelerated tissue dysfunction, fibrosis, and ultimately organ failure. Because several promising complement-targeted therapeutics to block uncontrolled complement activation and treat autoimmune diseases are in various phases of clinical trials, understanding fully the circadian properties of the complement system, and the reciprocal regulation by these two systems could greatly improve patient treatment in the long term.

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“…In addition, other mechanisms of AIM2 transcriptional regulation may exist. For example, it was shown that the mRNA expression of most inflammasomes, including AIM2, is affected by the circadian rhythm in mice, showing higher levels in peripheral blood granulocytes during the morning hours and decreasing gradually through the late evening hours [ 24 ].…”

Section: Brief Overview Of Aim2 Inflammasome Activation and Regulamentioning

confidence: 99%

The Emerging Relevance of AIM2 in Liver Disease

Lozano-Ruiz

González‐Navajas

2020

IJMS

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Absent in melanoma 2 (AIM2) is a cytosolic receptor that recognizes double-stranded DNA (dsDNA) and triggers the activation of the inflammasome cascade. Activation of the inflammasome results in the maturation of inflammatory cytokines, such as interleukin (IL)-1 β and IL-18, and a form of cell death known as pyroptosis. Owing to the conserved nature of its ligand, AIM2 is important during immune recognition of multiple pathogens. Additionally, AIM2 is also capable of recognizing host DNA during cellular damage or stress, thereby contributing to sterile inflammatory diseases. Inflammation, either in response to pathogens or due to sterile cellular damage, is at the center of the most prevalent and life-threatening liver diseases. Therefore, during the last 15 years, the study of inflammasome activation in the liver has emerged as a new research area in hepatology. Here, we discuss the known functions of AIM2 in the pathogenesis of different hepatic diseases, including non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH), hepatitis B, liver fibrosis, and hepatocellular carcinoma (HCC).

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Novel Evidence that Purinergic Signaling - Nlrp3 Inflammasome Axis Regulates Circadian Rhythm of Hematopoietic Stem/Progenitor Cells Circulation in Peripheral Blood

Cited by 20 publications

References 32 publications

Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities

Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities

Circadian Clock and Complement Immune System—Complementary Control of Physiology and Pathology?

The Emerging Relevance of AIM2 in Liver Disease

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