Review Article: Apoptosis in the Kidney

Davis, Myrtle A.; Ryan, Dara H.

doi:10.1177/019262339802600615

Cited by 36 publications

(31 citation statements)

References 134 publications

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“…TNFR1, DR3 and DR4; (43)(44)(45)) and -independent (i.e. nitric oxide and drug toxicity) mechanisms (46,47) also play a role. Fas-FasL interactions in the kidney are complicated by the capacity of T cells to engage TECs as targets as well as potential TEC-TEC interactions.…”

Section: And Cd8mentioning

confidence: 99%

Renal Tubular Epithelial Cell Self-Injury Through Fas/Fas Ligand Interaction Promotes Renal Allograft Injury

Du¹,

Jiang²,

Guan³

et al. 2004

American Journal of Transplantation

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Section: And Cd8mentioning

confidence: 99%

Renal Tubular Epithelial Cell Self-Injury Through Fas/Fas Ligand Interaction Promotes Renal Allograft Injury

Du¹,

Jiang²,

Guan³

et al. 2004

American Journal of Transplantation

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“…The cell nuclei of whole-mount tissues stained with propidium iodide are easily analysable using confocal microscopy (Davis & Ryan, 1998). Apoptotic nuclei are smaller and more brightly stained than normal nuclei, and sometimes fragmented (Fig.…”

Section: Recognizing Apoptosis and Mitosismentioning

confidence: 99%

Apoptosis in the cortex of the developing mouse kidney

Foley

Bard

2002

Journal of Anatomy

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Published levels of apoptosis in developing rat kidney ( ∼ 2.5%) seem large for a tissue with no obvious need for continual cell death. This paper examines the levels and patterns of apoptosis and mitosis in the cortical region of the developing metanephros of the mouse, the standard mammalian model embryo. Using confocal microscopy on specimens stained with propidium iodide to highlight nuclear morphology, optical sections of wholemount kidneys to a depth of ∼ 50 µ m were analysed and mitotic, apoptotic and interphase nuclei counted in the various compartments. Of the ∼ 200 000 cells examined over E11.5-16.5, 2-3% were mitotic, confirming observations based on cryosections; the mitotic index peaked at E14.5, dropping to ∼ 0.5% by P14. The mean apoptotic index during this period was 0.28%; this figure from wholemounts was ∼ 10% of that earlier reported in cryosectioned rat kidneys.One possible explanation for the difference is that cryosectioning turns out to create small nuclear fragments that can stain strongly with propidium. Such fragments are not seen in wholemounts and do not stain with TUNEL.Wholemount mouse E11.5 tails and E16.5 lungs were also analysed and both their mitotic and their apoptotic indexes were similar to those in wholemount developing kidneys. These results show that the level of apoptosis in wholemount embryonic mouse kidney cortex is far less than previously reported in cryosectioned rat embryonic kidneys, and typical of that in other mouse embryonic tissues whose development seems not to require apoptosis.

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“…1 As part of our ongoing studies of cell injury and cell death in the kidney, we are exploring the detailed stages and mechanisms of apoptosis and comparing them with those of oncosis. As the prelethal changes of oncosis have been well characterized, we wished to carefully examine the changes of apoptosis before and after cell death.…”

mentioning

confidence: 99%

Studies on the Mechanisms and Kinetics of Apoptosis Induced by Microinjection of Cytochrome c in Rat Kidney Tubule Epithelial Cells (NRK-52E)

Chang

Phelps

Berezesky

et al. 2000

The American Journal of Pathology

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Recent reports substantiating the role of cytochrome c in the induction of apoptosis led us to examine the kinetics and mechanisms involved in this process as an extension of our ongoing studies of cell injury and cell death. Microinjection of cytochrome c into NRK-52E kidney cells produced rapid apoptosis, which usually began within 30 minutes and reached a maximum of 60 -70% by 3 hours. The changes that occurred included four phases: an initial shrinkage phase, an active phase, a spherical phase, and a necrotic phase. For morphological purposes, the progressive changes were followed by phase-contrast and fluorescence microscopy, transmission and scanning electron microscopy, and time-lapse video microscopy. Cells first showed shrinkage, then displayed multiple pseudopods, which rapidly extended and retracted, giving the cells a bosselated appearance. During this active phase there was chromatin condensation, mitochondria were swollen but retained membrane potential, and the endoplasmic reticulum was dilated. Within 2-4 hours, active-phase cells became spherical and smooth-surfaced but were still alive, the nuclei showed chromatin clumping, the mitochondria underwent high-amplitude swelling but retained membrane potential, the endoplasmic reticulum was highly dilated, and many large apical vacuoles were present. Elevation of [Ca 2؉ ] i was seen at the late spherical phase, shortly before cell death. Pretreatment with the caspase 3 inhibitor (Ac-DEVD-CHO) prevented apoptosis, whereas overexpression of Bcl-2 did not. Apoptosis is an important mechanism of cell death in the kidney during development and after many and diverse injuries.1 As part of our ongoing studies of cell injury and cell death in the kidney, we are exploring the detailed stages and mechanisms of apoptosis and comparing them with those of oncosis. As the prelethal changes of oncosis have been well characterized, we wished to carefully examine the changes of apoptosis before and after cell death. 2,3Cytochrome c release into the cytosol has been implicated as an intermediate event in the initiation of apoptosis after a variety of toxic and other stimuli and injury in several cell types 4 -9 ; it also serves as a useful model, inasmuch as we found that after microinjection, the early phase of apoptosis usually begins within 30 minutes. This means that the progression of changes in single injected cells can be followed by many important techniques. These include the use of time-lapse phase-contrast video microscopy, digital imaging fluorescence, and confocal microscopy to analyze mitochondrial membrane potential, mitochondrial permeability transition, cytosolic calcium concentration [Ca 2ϩ ] i , and cell death, as well as phase-contrast and electron microscopy for morphological characterization.The results clearly defined three principal prelethal stages or phases of apoptosis and characterized the morphology at the light and electron microscope levels. We also showed that ATP is required for the initiation of apoptosis, that the loss of mitocho...

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Review Article: Apoptosis in the Kidney

Cited by 36 publications

References 134 publications

Renal Tubular Epithelial Cell Self-Injury Through Fas/Fas Ligand Interaction Promotes Renal Allograft Injury

Renal Tubular Epithelial Cell Self-Injury Through Fas/Fas Ligand Interaction Promotes Renal Allograft Injury

Apoptosis in the cortex of the developing mouse kidney

Studies on the Mechanisms and Kinetics of Apoptosis Induced by Microinjection of Cytochrome c in Rat Kidney Tubule Epithelial Cells (NRK-52E)

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