scholarly journals Changes in the Structure and Function of the Multicatalytic Proteinase (Proteasome) during Programmed Cell Death in the Intersegmental Muscles of the Hawkmoth, Manduca sexta

1995 ◽  
Vol 169 (2) ◽  
pp. 436-447 ◽  
Author(s):  
Margaret E.E. Jones ◽  
Marcy F. Haire ◽  
Peter-M. Kloetzel ◽  
Donald L. Mykles ◽  
Lawrence M. Schwartz
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Manduca Sexta ◽  
Structure And Function ◽  
Multicatalytic Proteinase ◽  
And Function

scholarly journals Calpain inhibition preserves myocardial structure and function following myocardial infarction

2009 ◽  
Vol 297 (5) ◽  
pp. H1744-H1751 ◽  
Author(s):  
Santhosh K. Mani ◽  
Sundaravadivel Balasubramanian ◽  
Juozas A. Zavadzkas ◽  
Laura B. Jeffords ◽  
William T. Rivers ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Left Ventricular ◽  
Structure And Function ◽  
Left Ventricular Ejection ◽  
Tunel Staining ◽  
Ventricular Ejection Fraction ◽  
Myocardial Structure ◽  
And Function

Cardiac pathology, such as myocardial infarction (MI), activates intracellular proteases that often trigger programmed cell death and contribute to maladaptive changes in myocardial structure and function. To test whether inhibition of calpain, a Ca2+-dependent cysteine protease, would prevent these changes, we used a mouse MI model. Calpeptin, an aldehydic inhibitor of calpain, was intravenously administered at 0.5 mg/kg body wt before MI induction and then at the same dose subcutaneously once per day. Both calpeptin-treated ( n = 6) and untreated ( n = 6) MI mice were used to study changes in myocardial structure and function after 4 days of MI, where end-diastolic volume (EDV) and left ventricular ejection fraction (EF) were measured by echocardiography. Calpain activation and programmed cell death were measured by immunohistochemistry, Western blotting, and TdT-mediated dUTP nick-end labeling (TUNEL). In MI mice, calpeptin treatment resulted in a significant improvement in EF [EF decreased from 67 ± 2% pre-MI to 30 ± 4% with MI only vs. 41 ± 2% with MI + calpeptin] and attenuated the increase in EDV [EDV increased from 42 ± 2 μl pre-MI to 73 ± 4 μl with MI only vs. 55 ± 4 μl with MI + calpeptin]. Furthermore, calpeptin treatment resulted in marked reduction in calpain- and caspase-3-associated changes and TUNEL staining. These studies indicate that calpain contributes to MI-induced alterations in myocardial structure and function and that it could be a potential therapeutic target in treating MI patients.

scholarly journals Extensive and diverse patterns of cell death sculpt neural networks in insects

2019 ◽  
Author(s):  
Sinziana Pop ◽  
Chin-Lin Chen ◽  
Connor J Sproston ◽  
Shu Kondo ◽  
Pavan Ramdya ◽  
...  
Keyword(s):  
Neural Networks ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Neural Activity ◽  
Structure And Function ◽  
Evolutionary Adaptation ◽  
Cell Numbers ◽  
The Many ◽  
And Function ◽  
Evolutionary Role

ABSTRACTChanges to the structure and function of neural networks are thought to underlie the evolutionary adaptation of animal behaviours. Among the many developmental phenomena that generate change programmed cell death appears to play a key role. We show that cell death occurs continuously throughout insect neurogenesis and happens soon after neurons are born. Focusing on two dipterans which have lost flight during evolution we reveal that reductions in populations of flight interneurons are likely caused by increased cell death during development.Mimicking an evolutionary role for increasing cell numbers, we artificially block programmed cell death in the medial neuroblast lineage in Drosophila melanogaster, which results in the production of ‘undead’ neurons with complex arborisations and distinct neurotransmitter identities. Activation of these ‘undead’ neurons and recordings of neural activity in behaving animals demonstrate that they are functional. Our findings suggest that the evolutionary modulation of death-based patterning could generate novel network configurations.

Metabolic events during programmed cell death in insect labial glands

1994 ◽  
Vol 72 (11-12) ◽  
pp. 597-601 ◽  
Author(s):  
Reginald Halaby ◽  
Zahra Zakeri ◽  
Richard A. Lockshin
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Acid Phosphatase ◽  
Programmed Cell Death ◽  
Manduca Sexta ◽  
Adenosine Triphosphate ◽  
Mitochondrial Respiration ◽  
Second Messengers ◽  
Labial Gland ◽  
Dying Cells

The labial gland of Manduca sexta is a valuable system to study the mechanisms of programmed cell death since the death of the gland is nearly synchronous and, except for the anterior duct, involves all of the tissue. The gland degenerates in 5 days during pupation. Our previous work documents a drop in total protein synthesis as the gland degenerates. To evaluate potential causes of this altered protein synthesis, we monitored several parameters of metabolism in dying cells: levels of adenosine triphosphate to estimate the energy resources of the gland; reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide to assess mitochondrial respiration; levels of acid phosphatase to assay lysosomal enzyme activity; and concentrations of cyclic nucleotides and inositol triphosphate to monitor signaling. While protein synthesis fell precipitously on day 0, total adenosine triphosphate and mitochondrial respiration were unchanged until the cells underwent massive collapse on day 3. Lysosomal acid phosphatase increased during early metamorphosis, and ultimately the bulk of the cytoplasm was destroyed in autophagic vacuoles. Changes in the concentrations of second messengers were modest and late. The relationships between the metabolism and the collapse of the labial gland are under investigation.Key words: programmed cell death, Manduca sexta, energetics, lysosomes, second messengers, protein synthesis.

scholarly journals Acheron, a novel member of the Lupus Antigen family, is induced during the programmed cell death of skeletal muscles in the moth Manduca sexta

Gene ◽  
2007 ◽  
Vol 393 (1-2) ◽  
pp. 101-109 ◽  
Author(s):  
Christos Valavanis ◽  
Zhaohui Wang ◽  
Danhui Sun ◽  
Michael Vaine ◽  
Lawrence M. Schwartz
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Manduca Sexta ◽  
Skeletal Muscles
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