Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 235, Issue 5, Pages 4605-4617Publisher
WILEY
DOI: 10.1002/jcp.29338
Keywords
casitas b-lineage lymphoma; epidermal growth factor; epidermal growth factor receptor; miR-22-3p; primary sensory neuron; spinal cord injury
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Funding
- Medical Science and Technology Youth Cultivation Project of the Chinese People's Liberation Army [13QNP017, 16QNP074]
- International Cooperation Program of National Natural Science Foundation of China [81620108018]
- General Program of Natural Science Foundation of Hebei Province of China [H2017101030]
- National Natural Science Foundation of China [81472070, 81772342, 81930070]
- Key Program of Medical Science Foundation of Hebei province of China [20190189]
- Tianjin key research and development plan, key projects for science and technology [19YFZCSY00660]
- Research and Development of Science and Technology Program - Chengde Government [201606A062, 201701A125, 201701A127]
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Spinal cord injury (SCI) is a devastating disease. Strategies that enhance the intrinsic regenerative ability are very important for the recovery of SCI to radically prevent the occurrence of sensory disorders. Epidermal growth factor (EGF) showed a limited effect on the growth of primary sensory neuron neurites due to the degradation of phosphorylated-epidermal growth factor receptor (p-EGFR) in a manner dependent on Casitas B-lineage lymphoma (CBL) (an E3 ubiquitin-protein ligase). MiR-22-3p predicted from four databases could target CBL to inhibit the expression of CBL, increase p-EGFR levels and neurites length via STAT3/GAP43 pathway rather than Erk1/2 axis. EGF, EGFR, and miR-22-3p were downregulated sharply after injury. In vivo miR-22-3p Agomir application could regulate CBL/p-EGFR/p-STAT3/GAP43/p-GAP43 axis, and restore spinal cord sensory conductive function. This study clarified the mechanism of the limited promotion effect of EGF on adult primary sensory neuron neurite and targeting miR-22-3p could be a novel strategy to treat sensory dysfunction after SCI.
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