Some Endocrine and Metabolic Consequences of the Stress Following High Level Spinal Cord Section

Author(s):  
Kalina I. Vaptzarova ◽  
Panteley G. Popov
2009 ◽  
Vol 110 (5) ◽  
pp. 1409-1421 ◽  
Author(s):  
Kurt M. Lucin ◽  
Virginia M. Sanders ◽  
Phillip G. Popovich

Development ◽  
1990 ◽  
Vol 110 (4) ◽  
pp. 1159-1168 ◽  
Author(s):  
R. Vogels ◽  
W. de Graaff ◽  
J. Deschamps

This study reports the expression pattern of the murine homeobox-containing gene Hox-2.3 during development. Using in situ hybridization, we first detect Hox-2.3 transcripts in the allantois primordium at 7.5 days post coitum (p.c.). One day later transcripts are found in embryonic ectoderm and mesoderm. In 9.5- and 10.5- day embryos Hox-2.3 expression is observed in the central nervous system (CNS) from a rostral boundary in the upper spinal cord to the caudal end. Within this anteroposterior domain, Hox-2.3 expression is also found in the peripheral nervous system, in the mesoderm and in the hindgut epithelium. The rostral boundary in the mesoderm is located at the level of the 11th somite and thus shifted posteriorwards compared to the rostral boundary in the neural tube. During subsequent development, the initially broad expression pattern in the somitic, lateral plate and intermediate mesoderm becomes restricted to structures in the urogenital system. In adults, the spinal cord and the derivatives of the Wolffian and Mullerian ducts continue to express the gene at a high level. The described temporal and tissue-specific changes in expression of Hox-2.3 are suggestive of several levels of regulation as reported for Drosophila homeotic genes and argue for more than one role of the gene during development and in adults.


2019 ◽  
Vol 311 ◽  
pp. 173-181 ◽  
Author(s):  
Anne Järve ◽  
Mihail Todiras ◽  
Xiaoming Lian ◽  
Rafael Filippelli-Silva ◽  
Fatimunnisa Qadri ◽  
...  

Development ◽  
2001 ◽  
Vol 128 (12) ◽  
pp. 2255-2268 ◽  
Author(s):  
Cynthia Lance-Jones ◽  
Natalia Omelchenko ◽  
Anya Bailis ◽  
Stephen Lynch ◽  
Kamal Sharma

We have used Hoxd10 expression as a primary marker of the lumbosacral region to examine the early programming of regional characteristics within the posterior spinal cord of the chick embryo. Hoxd10 is uniquely expressed at a high level in the lumbosacral cord, from the earliest stages of motor column formation through stages of motoneuron axon outgrowth. To define the time period when this gene pattern is determined, we assessed Hoxd10 expression after transposition of lumbosacral and thoracic segments at early neural tube stages. We present evidence that there is an early prepattern for Hoxd10 expression in the lumbosacral neural tube; a prepattern that is established at or before stages of neural tube closure. Cells within more posterior lumbosacral segments have a greater ability to develop high level Hoxd10 expression than the most anterior lumbosacral segments or thoracic segments. During subsequent neural tube stages, this prepattern is amplified and stabilized by environmental signals such that all lumbosacral segments acquire the ability to develop high levels of Hoxd10, independent of their axial environment. Results from experiments in which posterior neural segments and/or paraxial mesoderm segments were placed at different axial levels suggest that signals setting Hoxd10 expression form a decreasing posterior-to-anterior gradient. Our experiments do not, however, implicate adjacent paraxial mesoderm as the only source of graded signals. We suggest, instead, that signals from more posterior embryonic regions influence Hoxd10 expression after the early establishment of a regional prepattern. Concurrent analyses of patterns of LIM proteins and motor column organization after experimental surgeries suggest that the programming of these characteristics follows similar rules.


2019 ◽  
Vol 20 (15) ◽  
pp. 3762 ◽  
Author(s):  
James Hong ◽  
Alex Chang ◽  
Yang Liu ◽  
Jian Wang ◽  
Michael G. Fehlings

Spinal cord injury (SCI) is associated with an increased susceptibility to infections, such as pneumonia, which is the leading cause of death in these patients. This phenomenon is referred to as SCI immune deficiency syndrome (SCI-IDS), and has been shown to be more prevalent after high-level transection in preclinical SCI models. Despite the high prevalence of contusion SCIs, the effects of this etiology have not been studied in the context of SCI-IDS. Compared to transection SCIs, which involve a complete loss of supraspinal input and lead to the disinhibition of spinally-generated activity, contusion SCIs may cause significant local deafferentation, but only a partial disruption of sympathetic tone below the level of injury. In this work, we investigate the effects of thoracic (T6-7) and cervical (C6-7) moderate–severe contusion SCIs on the spleen by characterizing splenic norepinephrine (NE) and cortisol (CORT), caspase-3, and multiple inflammation markers at 3- and 7-days post-SCI. In contrary to the literature, we observe an increase in splenic NE and CORT that correspond to an increase in caspase-3 after thoracic SCI relative to cervical SCI. Further, we found differences in expression of leptin, eotaxin, IP-10, and IL-18 that implicate alterations in splenocyte recruitment and function. These results suggest that incomplete SCI drastically alters the level-dependence of SCI-IDS.


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