Internal Disintegration Model of Cytotoxic Lymphocyte‐Induced Target Damage

Russell, John H.

doi:10.1111/j.1600-065x.1983.tb01074.x

Cited by 213 publications

(84 citation statements)

References 32 publications

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“…The hepatocytes that show early changes of apoptosis have also been found to have lymphocytes closely ajoining to their surfaces [27] and these lymphocytes were revealed to be mainly composed of cytotoxic T-lymphocytes (CTL) [28,29]. Some reports have shown that the death of CTL targets is apoptotic during viral infections, autoimmune reactions, and graft rejection [30].…”

Section: Discussionmentioning

confidence: 99%

Expression of p53, p21 (Waf1/Cip1/Sdi1) and Fas antigen in collagen vascular and granulomatous lung diseases

Kunitake

Kuwano²,

Miyazaki³

et al. 1998

Eur Respir J

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Fas is expressed in various cells and transduces the cell death signal. p21 is a mediator of p53-dependent G1 arrest associated with deoxyribonucleic acid (DNA) damage. The upregulation of p53 and p21 associated with DNA damage in idiopathic pulmonary fibrosis has been described previously. In this study, p53, p21, and Fas expression and DNA damage were examined in interstitial pneumonia associated with collagen vascular diseases (CVD-IP). DNA damage was assessed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end-labelling (TUNEL) and p53, p21 and Fas proteins were detected by immunohistochemistry in 13 cases of CVD-IP, 13 of sarcoidosis, seven of hypersensitivity pneumonitis (HP) and eight control patients with normal lung parenchyma. TUNEL-positive signals were found in bronchiolar or alveolar epithelial cells in 11 of 13 (85%) specimens of CVD-IP, but not in sarcoidosis, HP or controls, except for a case of chronic HP with pulmonary fibrosis. p53, p21 and Fas were detected in bronchiolar or alveolar epithelial cells in nine (69%), 10 (77%) and 12 (92%) of 13 specimens of CVD-IP, respectively, but not in sarcoidosis, HP or controls, except for a case of chronic HP. These results suggest that the upregulation of p53, p21 and Fas in bronchiolar and alveolar epithelial cells associated with deoxyribonucleic acid damage may participate in the process of pulmonary fibrosis in interstitial pneumonia associated with collagen vascular diseases and chronic hypersensitivity pneumonitis.

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Section: Discussionmentioning

confidence: 99%

Expression of p53, p21 (Waf1/Cip1/Sdi1) and Fas antigen in collagen vascular and granulomatous lung diseases

Kunitake

Kuwano²,

Miyazaki³

et al. 1998

Eur Respir J

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“…It was absent in many neurons displaying early cytoplas mic changes associated with necrosis. The labeling in tensity in the ICC neurons decreased and by 15 days after ischemia, it was often weak and confined to neuronal cytoplasm, a localization representing a presumed leak of broken DNA strands from the nucleus into the cytoplasm of the dead cell (Russell, 1983;Rink, 1995).…”

Section: Discussionmentioning

confidence: 99%

DNA Fragmentation Follows Delayed Neuronal Death in CA1 Neurons Exposed to Transient Global Ischemia in the Rat

Petito

Torres-Muñoz

Roberts

et al. 1997

J Cereb Blood Flow Metab

144

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Summary: Apoptosis is an active, gene-directed process of cell death in which early fragmentation of nuclear DNA pre cedes morphological changes in the nucleus and, later, in the cytoplasm, In ischemia, biochemical studies have detected oli gonucleosomes of apoptosis whereas sequential morphological studies show changes consistent with necrosis rather than ap optosis, To resolve this apparent discrepancy, we subjected rats to 10 minutes of transient forebrain ischemia followed by I to 14 days of reperfusion, Parameters evaluated in the CAl region of the hippocampus included morphology, in situ end labeling (ISEL) of fr'l-gmented DNA, and expression of p53, Neurons were indistinguishable from controls at postischemic day I but displayed cytoplasmic basophilia or focal condensations at day 2; some neurons were slightly swollen and a few appearedThe neuronal response to brain ischemia depends on the severity and duration of the ischemic insult as well as on intrinsic neuronal factors that impart selective vulner ability to specific brain regions (Scholz, 1953), Brief periods of global ischemia kill vulnerable neurons in the CAl region of the hippocampus whereas longer intervals of vascular occlusion kill neurons in the cerebral cortex and corpus striatum as well (Ito et aI., 1975; Pulsinelli et aI., 1982a), Although seemingly undamaged, neurons in other brain regions such as the CA3 region of the hip pocampus or the paramedian cerebral cortex undergo transient alterations as evidenced by reversible changes 967normaL In situ end labeling was absent At days 3 and 5, approximately 40 to 60% of CAl neurons had shrunken eosin ophilic cytoplasm and pyknotic nuclei, but only half of these were ISEL By day 14, many of the necrotic neurons had been removed by phagocytes; those remaining retained mild ISEL Neither p53 protein nor mRNA were identified in control or postischemic brain by in situ hybridization with riboprobes or by northern blot analysis, These results show that DNA frag mentation occurs after the development of delayed neuronal death in CA I neurons subjected to 10 minutes of global isch emia, They suggest that mechanisms other than apoptosis may mediate the irreversible changes in the CAl neurons in this model. Key Words: Global ischemia-Apoptosis Necrosis-Delayed neuronal death-In situ end labeling-Rat in their subcellular organelles (Petito and Pulsinelli, 1984a,b), The postischemic interval required for the ap parent development of selective neuronal necrosis is in versely proportional to the severity or duration of the ischemic insult-the so-called maturation phenomena described by Ito et al. (Ito et at, 1975), This interval is especially prolonged in the CAl neurons of the hippo campus (Ito et aI., 1975; Pulsinelli et aI, 1982a). The term delayed neuronal death has been applied to this process (Kirino, 1982).During the past few years, the concept of cell death via apoptosis has become increasingly important. This mechanism of cell death is mediated by regulated path ways involving defined gene product...

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“…Chromatin fragmentation in aging neutrophils. In direct relationship to stereotyped morphological changes, cells undergoing programmed cell death exhibited chromatin fragmentation in a characteristic internucleosomal pattern thought to represent endogenous endonuclease activation, the amount of DNA in each fragment being a multiple of -180 bp (24,25,(28)(29)(30)(31). In view of the morphological changes seen in aging PMN, evidence of chromatin fragmentation was sought in PMN isolated from blood and aged in the standard fashion.…”

Section: Methodsmentioning

confidence: 99%

Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.

Savill¹,

Wyllie²,

Henson³

et al. 1989

J. Clin. Invest.

1,435

1,088

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Internal Disintegration Model of Cytotoxic Lymphocyte‐Induced Target Damage

Cited by 213 publications

References 32 publications

Expression of p53, p21 (Waf1/Cip1/Sdi1) and Fas antigen in collagen vascular and granulomatous lung diseases

Expression of p53, p21 (Waf1/Cip1/Sdi1) and Fas antigen in collagen vascular and granulomatous lung diseases

DNA Fragmentation Follows Delayed Neuronal Death in CA1 Neurons Exposed to Transient Global Ischemia in the Rat

Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.

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