JNK/c-Jun signaling pathway mediates arginine vasopressin neuron regeneration by promoting cytoskeleton reconstruction in rats with electrical lesions of the pituitary stalk.
10.12122/j.issn.1673-4254.2019.09.16
- Author:
Kai LI
1
;
Zhanpeng FENG
1
;
Yichao OU
1
;
Mingfeng ZHOU
1
;
Junjie PENG
1
;
Haodong GONG
2
;
Guangsen WU
1
;
Yawei LIU
1
;
Songtao QI
1
Author Information
1. Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
2. First Clinical Medical College, Southern Medical University, Guangzhou 510515, China.
- Publication Type:Journal Article
- Keywords:
Rats;
arginine vasopressin;
doublecortin;
pituitary stalk electrical lesions;
supraoptic nucleus
- MeSH:
Animals;
Apoptosis;
Arginine Vasopressin;
pharmacology;
Cytoskeleton;
metabolism;
MAP Kinase Signaling System;
Neurons;
cytology;
Pituitary Gland;
cytology;
injuries;
Proto-Oncogene Proteins c-jun;
metabolism;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Regeneration;
Tubulin;
metabolism
- From:
Journal of Southern Medical University
2019;39(9):1099-1106
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the mechanism by which doublecortin promotes the recovery of cytoskeleton in arginine vasopressin (AVP) neurons in rats with electrical lesions of the pituitary stalk (PEL).
METHODS:Thirty-two SD rats were randomized into PEL group with electrical lesions of the pituitary stalk through the floor of the skull base (=25) and sham operation group (=7), and the daily water consumption (DWC), daily urine volume (DUV) and urine specific gravity (USG) of the rats were recorded. Four rats on day 1 and 7 rats on each of days 3, 7 and 14 after PEL as well as the sham-operated rats were sacrificed for detection of the expressions of β-Tubulin (Tuj1), doublecortin and caspase- 3 in the AVP neurons of the supraoptic nucleus using immunofluorescence assay and Western blotting.
RESULTS:After PEL, the rats exhibited a typical triphasic pattern of diabetes insipidus, with the postoperative days 1-2 as the phase one, days 3-5 as the phase two, and days 6-14 as the phase three. Immunofluorescent results indicated the repair of the AVP neurons evidenced by significantly increased doublecortin expressions in the AVP neurons following PEL; similarly, the expression of Tuj1 also increased progressively after PEL, reaching the peak level on day 7 after PEL. The apoptotic rates of the AVP neurons exhibited a reverse pattern of variation, peaking on postoperative day 3 followed by progressive reduction till day 14. Western blotting showed that the expressions of c-Jun and p-c-Jun were up-regulated significantly on day 3 ( < 0.05) and 7 ( < 0.01) after PEL, while an upregulated p-JNK expression was detected only on day 3 ( < 0.05), as was consistent with the time-courses of neuronal recovery and apoptosis after PEL.
CONCLUSIONS:JNK/c-Jun pathway is activated after PEL to induce apoptosis of AVP neurons in the acute phase and to promote the repair of neuronal cytoskeleton by up-regulation of doublecortin and Tuj1 expressions.
