Autophagic vacuoles in heart muscle and liver. A comparative morphometric study including circadian variations in meal-fed rats

Pfeifer, U; Strauss, Pirmin

doi:10.1016/0022-2828(81)90227-3

Cited by 79 publications

(38 citation statements)

References 40 publications

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“…Minimal levels of autophagy, meanwhile, occur early in the dark period of the cycle, soon after the animals begin to acquire food. 24,43 Similar rhythms of autophagy are also present in cardiomyocytes, with similar phasing to the autophagic cycling of hepatocytes. 43 The diurnal rhythm of autophagy in the peripheral tissues of adult mammals, much like the core circadian clock itself, is entrainable by food.…”

Section: Adult Mammals Undergo Diurnal Cycles Of Autophagymentioning

confidence: 73%

“…In rat hepatocytes, autophagy, as measured by both volume fraction and numerical density of autophagic vacuoles, peaks during the late light period in animals exposed to a 24-hour light/dark cycle. 24,43 This peak occurs near the end of the resting phase of the animal, just prior to the initiation of activity and the acquisition of food, which begins around the onset of darkness. Minimal levels of autophagy, meanwhile, occur early in the dark period of the cycle, soon after the animals begin to acquire food.…”

Section: Adult Mammals Undergo Diurnal Cycles Of Autophagymentioning

confidence: 99%

See 1 more Smart Citation

Diurnal rhythms of autophagy: Implications for cell biology and human disease

Sachdeva¹,

Thompson²

2008

Autophagy

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Section: Adult Mammals Undergo Diurnal Cycles Of Autophagymentioning

confidence: 73%

Section: Adult Mammals Undergo Diurnal Cycles Of Autophagymentioning

confidence: 99%

Diurnal rhythms of autophagy: Implications for cell biology and human disease

Sachdeva¹,

Thompson²

2008

Autophagy

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“…This finding stimulated interest in the physiological role of autophagy. One such subsequent study, by U Pfeifer et al, examined the degradation of long-lived proteins by autophagy, revealing the relationship between autophagy and the circadian rhythm [15,16]. In this work, the authors found that autophagy is inhibited by feeding and induced by fasting between meals, reinforcing that autophagy is tightly regulated by nutrient conditions.…”

Section: Before the Autophagy-related Genesmentioning

confidence: 80%

Historical landmarks of autophagy research

2013

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The year of 2013 marked the 50th anniversary of C de Duve's coining of the term "autophagy" for the degradation process of cytoplasmic constituents in the lysosome/vacuole. This year we regretfully lost this great scientist, who contributed much during the early years of research to the field of autophagy. Soon after the discovery of lysosomes by de Duve, electron microscopy revealed autophagy as a means of delivering intracellular components to the lysosome. For a long time after the discovery of autophagy, studies failed to yield any significant advances at a molecular level in our understanding of this fundamental pathway of degradation. The first breakthrough was made in the early 1990s, as autophagy was discovered in yeast subjected to starvation by microscopic observation. Next, a genetic effort to address the poorly understood problem of autophagy led to the discovery of many autophagy-defective mutants. Subsequent identification of autophagy-related genes in yeast revealed unique sets of molecules involved in membrane dynamics during autophagy. ATG homologs were subsequently found in various organisms, indicating that the fundamental mechanism of autophagy is well conserved among eukaryotes. These findings brought revolutionary changes to research in this field. For instance, the last 10 years have seen remarkable progress in our understanding of autophagy, not only in terms of the molecular mechanisms of autophagy, but also with regard to its broad physiological roles and relevance to health and disease. Now our knowledge of autophagy is dramatically expanding day by day. Here, the historical landmarks underpinning the explosion of autophagy research are described with a particular focus on the contribution of yeast as a model organism.

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“…Many of the affected tissues in LAMP-2-deficient mice are those that have a high degree of autophagy in normal animals. Using mainly rat tissues, active autophagy has been described at least in liver (Pfeifer and Strauss, 1981;Kovacs et al, 1982;de Waal et al, 1986), pancreas (Kovacs et al, 1988), muscle (Salminen and Vihko, 1984;Bahro et al, 1992), heart (Pfeifer and Strauss, 1981;Dammrich and Pfeifer, 1983), and kidney (Pfeifer and Scheller, 1975;Bahro et al, 1988). This suggests that active ongoing autophagy in normal conditions may be the prerequisite for the observed phenotype of autophagic vacuole accumulation in LAMP-2-deficient tissues.…”

Section: Discussionmentioning

confidence: 97%

Role of LAMP-2 in Lysosome Biogenesis and Autophagy

Eskelinen

Illert²,

Tanaka

et al. 2002

MBoC

321

260

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In LAMP-2–deficient mice autophagic vacuoles accumulate in many tissues, including liver, pancreas, muscle, and heart. Here we extend the phenotype analysis using cultured hepatocytes. In LAMP-2–deficient hepatocytes the half-life of both early and late autophagic vacuoles was prolonged as evaluated by quantitative electron microscopy. However, an endocytic tracer reached the autophagic vacuoles, indicating delivery of endo/lysosomal constituents to autophagic vacuoles. Enzyme activity measurements showed that the trafficking of some lysosomal enzymes to lysosomes was impaired. Immunoprecipitation of metabolically labeled cathepsin D indicated reduced intracellular retention and processing in the knockout cells. The steady-state level of 300-kDa mannose 6-phosphate receptor was slightly lower in LAMP-2–deficient hepatocytes, whereas that of 46-kDa mannose 6-phosphate receptor was decreased to 30% of controls due to a shorter half-life. Less receptor was found in the Golgi region and in vesicles and tubules surrounding multivesicular endosomes, suggesting impaired recycling from endosomes to the Golgi. More receptor was found in autophagic vacuoles, which may explain its shorter half-life. Our data indicate that in hepatocytes LAMP-2 deficiency either directly or indirectly leads to impaired recycling of 46-kDa mannose 6-phosphate receptors and partial mistargeting of a subset of lysosomal enzymes. Autophagic vacuoles may accumulate due to impaired capacity for lysosomal degradation

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Autophagic vacuoles in heart muscle and liver. A comparative morphometric study including circadian variations in meal-fed rats

Cited by 79 publications

References 40 publications

Diurnal rhythms of autophagy: Implications for cell biology and human disease

Diurnal rhythms of autophagy: Implications for cell biology and human disease

Historical landmarks of autophagy research

Role of LAMP-2 in Lysosome Biogenesis and Autophagy

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