Apoptosis in the lung: induction, clearance and detection

Henson, Peter M.; Tuder, Rubin M.

doi:10.1152/ajplung.00320.2007

Cited by 96 publications

(85 citation statements)

References 82 publications

(91 reference statements)

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“…In Prtn3 -/-mice, PR3 was also ablated in monocytes and macrophages, which may indirectly affect neutrophil accumulation by changing the inflammatory environment in the peritoneal cavity. Additionally, the proportion of apoptotic neutrophils may also be affected by engulfment and clearance of apoptotic neutrophils by phagocytes (i.e., efferocytosis) (26,27). Thus, to investigate whether PR3 is directly involved in neutrophil death in vivo, we conducted an adoptive transfer experiment ( Figure 9C).…”

Section: Discussionmentioning

confidence: 99%

Proteinase 3–dependent caspase-3 cleavage modulates neutrophil death and inflammation

Loison¹,

Zhu²,

Karatepe³

et al. 2014

J. Clin. Invest.

108

118

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Section: Discussionmentioning

confidence: 99%

Proteinase 3–dependent caspase-3 cleavage modulates neutrophil death and inflammation

Loison¹,

Zhu²,

Karatepe³

et al. 2014

J. Clin. Invest.

108

118

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“…P hagocytosis of apoptotic cells, also known as efferocytosis, occupies an important role in normal tissue homeostasis and regulation of immune responses (1)(2)(3). Rapid clearance of dying cells prevents leakage of potentially cytotoxic or antigenic contents into the extracellular milieu and the resultant initiation of inflammatory processes and tissue injury (4).…”

mentioning

confidence: 99%

PAI-1 inhibits neutrophil efferocytosis

Park

Liu²,

Lorne³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

102

105

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Phagocytosis of apoptotic cells, also called efferocytosis, is an essential feature of immune responses and critical for the resolution of inflammation. Plasma and tissue levels of plasminogen activator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis, are elevated in inflammatory conditions, including sepsis and acute lung injury, in which activated neutrophils accumulate in tissues and contribute to organ dysfunction. In this study, we explored the potential involvement of PAI-1 in modulating neutrophil efferocytosis. We found enhanced phagocytosis of viable PAI-1 deficient (PAI-1 ؊/؊ ) and of wild-type neutrophils treated with anti-PAI-1 antibodies. PAI-1 levels were decreased on the surface of apoptotic neutrophils and the enhanced phagocytosis of apoptotic wild-type neutrophils or of viable PAI-1 ؊/؊ neutrophils was diminished by preincubation with PAI-1. The increased phagocytosis associated with PAI-1 deficiency or blockade depended on both the lipoprotein receptor-related protein (LRP) and its ligand, calreticulin (CRT), because the LRP-mediated increase in phagocytosis of viable neutrophils induced by blockade of CD 47 was abrogated by PAI-1. CRT levels are increased on viable PAI-1 ؊/؊ neutrophils. While CRT colocalizes with PAI-1 on viable neutrophils, markedly diminished colocalization of PAI-1 and CRT was present on apoptotic neutrophils. Our data therefore indicate that PAI-1 serves as a novel ''don't eat me'' signal for viable and apoptotic neutrophils.calreticulin ͉ phagocytosis ͉ plasminogen activator inhibitor-1

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“…Apoptosis commitment features a similar phenotype of cellular rounding and partial detachment from the extracellular matrix, 33,34 leading to an increase in the cell height.The loss of cell height observed in the progression from early to late apoptosis can be attributed to the overall loss of cellular volume and content through the continual blebbing phenomenon and loss of membrane permeabilty. 35,36 Although both mitosis and apoptosis involve cell rounding due to partial detachment from the substrate, acoustic measurement of cell height may quickly discern cell growth from apoptosis, as cell undergoing the latter process will proceed to decrease cell height.…”

Section: Discussionmentioning

confidence: 99%

Properties of cells through life and death – an acoustic microscopy investigation

et al. 2015

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Current methods to evaluate the status of a cell are largely focused on fluorescent identification of molecular biomarkers. The invasive nature of these methods -requiring either fixation, chemical dyes, genetic alteration, or a combination of these -prevents subsequent analysis of samples. In light of this limitation, studies have considered the use of physical markers to differentiate cell stages. Acoustic microscopy is an ultrahigh frequency (>100 MHz) ultrasound technology that can be used to calculate the mechanical and physical properties of biological cells in realtime, thereby evaluating cell stage in live cells without invasive biomarker evaluation. Using acoustic microscopy, MCF-7 human breast adenocarcinoma cells within the G1, G2, and metaphase phases of the proliferative cell cycle, in addition to early and late programmed cell death, were examined. Physical properties calculated include the cell height, sound speed, acoustic impedance, cell density, adiabatic bulk modulus, and the ultrasonic attenuation. A total of 290 cells were measured, 58 from each cell phase, assessed using fluorescent and phase contrast microscopy. Cells actively progressing from G1 to metaphase were marked by a 28% decrease in attenuation, in contrast to the induction of apoptosis from G1, which was marked by a significant 81% increase in attenuation. Furthermore late apoptotic cells separated into 2 distinct groups based on ultrasound attenuation, suggesting that presently-unidentified sub-stages may exist within late apoptosis. A methodology has been implemented for the identification of cell stages without the use of chemical dyes, fixation, or genetic manipulation.

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Apoptosis in the lung: induction, clearance and detection

Cited by 96 publications

References 82 publications

Proteinase 3–dependent caspase-3 cleavage modulates neutrophil death and inflammation

Proteinase 3–dependent caspase-3 cleavage modulates neutrophil death and inflammation

PAI-1 inhibits neutrophil efferocytosis

Properties of cells through life and death – an acoustic microscopy investigation

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