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Intraspinal administration of interleukin-7 promotes neuronal apoptosis and limits functional recovery through JAK/STAT5 pathway following spinal cord injury.
- Source :
-
Biochemical & Biophysical Research Communications . Jun2019, Vol. 514 Issue 3, p1023-1029. 7p. - Publication Year :
- 2019
-
Abstract
- It has been previously reported that the blockade of interleukin-7 receptor (IL-7R) promotes functional recovery following spinal cord injury (SCI), however, the direct function and molecular mechanism of IL-7 involved in this pathogenic process are unclear. Here, we report that, contrary to IL-7R blockade, the intraspinal administration of IL-7 limits functional recovery following SCI. In addition, IL-7 treatment promotes neuronal apoptosis in spinal cord lesions, which may be attributed to exacerbated focal inflammatory response, as shown by increased accumulation of activated microglia/macrophage and production of proinflammatory mediators. Moreover, IL-7 treatment activates JAK/STAT5 pathway following SCI. At last, more importantly, the pharmacological inhibition of STAT5 abrogates the effects of IL-7 treatment on functional recovery, neuronal apoptosis and focal inflammatory response, suggesting that the effects of IL-7 treatment following SCI are dependent on activating the JAK/STAT5 pathway. Overall, this study reveals the JAK/STAT5 pathway-dependent detrimental role of IL-7 following SCI, and also implies that targeting the IL-7/JAK/STAT5 axis may represent a potential therapeutic approach for SCI treatment. • Intraspinal administration of IL-7 limits functional recovery following SCI. • Intraspinal administration of IL-7 promotes focal inflammatory response. • Intraspinal administration of IL-7 promotes neuronal apoptosis in spinal cord lesions. • Intraspinal administration of IL-7 activates JAK/STAT5 pathway following SCI. [ABSTRACT FROM AUTHOR]
- Subjects :
- *SPINAL cord injuries
*INTERLEUKIN-7
*APOPTOSIS
*SPINAL cord
*THERAPEUTICS
Subjects
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 514
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 136711886
- Full Text :
- https://doi.org/10.1016/j.bbrc.2019.04.159