Involvement of c-Jun-JNK Pathways in the Regulation of Programmed Cell Death of Developing Chick Embryo Spinal Cord Motoneurons

2006 ◽  
Vol 29 (6) ◽  
pp. 438-451 ◽  
Author(s):  
Joan Ribera ◽  
Victoria Ayala ◽  
Celia Casas
1999 ◽  
Vol 19 (24) ◽  
pp. 10803-10812 ◽  
Author(s):  
Jerònia Lladó ◽  
Jordi Calderó ◽  
Joan Ribera ◽  
Olga Tarabal ◽  
Ronald W. Oppenheim ◽  
...  

2006 ◽  
Vol 21 (1) ◽  
pp. 194-205 ◽  
Author(s):  
Ghanashyam D. Ghadge ◽  
Lijun Wang ◽  
Kamal Sharma ◽  
Anna Liza Monti ◽  
Vytas Bindokas ◽  
...  

2011 ◽  
Vol 55 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Anna Gibson ◽  
Neil Robinson ◽  
Andrea Streit ◽  
Guojun Sheng ◽  
Claudio D. Stern

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0142280 ◽  
Author(s):  
Marc Pirson ◽  
Stéphanie Debrulle ◽  
André Clippe ◽  
Frédéric Clotman ◽  
Bernard Knoops

Development ◽  
1976 ◽  
Vol 35 (3) ◽  
pp. 649-665
Author(s):  
Marie-Paule Pautou

Morphogenesis of the chick embryo foot as studied by Janus green B-induced malformations Janus green was injected into the amnioticsac of 6·5-day-old chick embryos at a single dose of 8·5 or 15 μg; the dye causes respectively 55 and 82 % malformations of the feet. Toes are affected by partial or total soft tissue syndactyly, hypophalangy and infrequently by hyperphalangy. Lateral toes are more severely and more frequently affected by syndactyly and hypophalangy than medium ones. Hyperphalangy is found exclusively in toes I and II and causes the formation of one excess phalanx at most Syndactylous toes are joined by an overdeveloped digital membrane. Hypophalangic toes have a truncated (non-pointed) distaltip. Two phalanges are lacking at most. These malformations are due to two distinct phases of the Janus green action. The first one, which is early and fast, inhibits interdigital programmed cell death, causing in term the non-regression of the inter digital membranes and thus syndactyly. The second one, which is late and slow, blocks the apical growth; this leads to hypophalangy.


1998 ◽  
Vol 5 (4) ◽  
pp. E1 ◽  
Author(s):  
Evelyne Emery ◽  
Philipp Aldana ◽  
Mary Bartlett Bunge ◽  
William Puckett ◽  
Anu Srinivasan ◽  
...  

Object Apoptosis is a form of programmed cell death seen in a variety of developmental and disease states, including traumatic injuries. The main objective of this study was to determine whether apoptosis is observed after human spinal cord injury (SCI). The spatial and temporal expression of apoptotic cells as well as the nature of the cells involved in programmed cell death were also investigated. Methods The authors examined the spinal cords of 15 patients who died between 3 hours and 2 months after a traumatic SCI. Apoptotic cells were found at the edges of the lesion epicenter and in the adjacent white matter, particularly in the ascending tracts, by using histological (cresyl violet, hematoxylin and eosin) and nuclear staining (Hoechst 33342). The suspected presence of apoptotic cells was supported by staining with the terminal deoxynucleotidyl transferase-mediated biotinylated-deoxyuridinetriphosphate nick-end labeling technique and confirmed by immunostaining for the processed form of caspase-3 (CPP-32), a member of the interleukin-1-beta-converting enzyme/Caenorhabditis elegans D 3 family of proteases that plays an essential role in programmed cell death. Apoptosis in this series of human SCIs was a prominent pathological finding in 14 of the 15 spinal cords examined when compared with five uninjured control spinal cords. To determine the type of cells undergoing apoptosis, the authors immunostained specimens with a variety of antibodies, including glial fibrillary acidic protein, 2,′3′-cyclic nucleotide 3′-phosphohydrolase (CNPase), and CD45/68. Oligodendrocytes stained with CNPase and a number of apoptotic nuclei colocalized with positive staining for this antibody. Conclusions These results support the hypothesis that apoptosis occurs in human SCIs and is accompanied by the activation of CPP-32 of the cysteine protease family. This mechanism of cell death contributes to the secondary injury processes seen after human SCI and may have important clinical implications for the further development of protease inhibitors to prevent programmed cell death.


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