Literature DB >> 27984179

Immunohistochemical analysis of huntingtin-associated protein 1 in adult rat spinal cord and its regional relationship with androgen receptor.

Md Nabiul Islam1, Yukio Takeshita1, Akie Yanai1, Amami Imagawa1, Mir Rubayet Jahan1, Greggory Wroblewski1, Joe Nemoto1, Ryutaro Fujinaga1, Koh Shinoda2.   

Abstract

Huntingtin-associated protein 1 (HAP1) is a neuronal interactor with causatively polyglutamine (polyQ)-expanded huntingtin in Huntington's disease and also associated with pathologically polyQ-expanded androgen receptor (AR) in spinobulbar muscular atrophy (SBMA), being considered as a protective factor against neurodegenerative apoptosis. In normal brains, it is abundantly expressed particularly in the limbic-hypothalamic regions that tend to be spared from neurodegeneration, whereas the areas with little HAP1 expression, including the striatum, thalamus, cerebral neocortex and cerebellum, are targets in several neurodegenerative diseases. While the spinal cord is another major neurodegenerative target, HAP1-immunoreactive (ir) structures have yet to be determined there. In the current study, HAP1 expression was immunohistochemically evaluated in light and electron microscopy through the cervical, thoracic, lumbar, and sacral spinal cords of the adult male rat. Our results showed that HAP1 is specifically expressed in neurons through the spinal segments and that more than 90% of neurons expressed HAP1 in lamina I-II, lamina X, and autonomic preganglionic regions. Double-immunostaining for HAP1 and AR demonstrated that more than 80% of neurons expressed both in laminae I-II and X. In contrast, HAP1 was specifically lacking in the lamina IX motoneurons with or without AR expression. The present study first demonstrated that HAP1 is abundantly expressed in spinal neurons of the somatosensory, viscerosensory, and autonomic regions but absent in somatomotor neurons, suggesting that the spinal motoneurons are, due to lack of putative HAP1 protectivity, more vulnerable to stresses in neurodegenerative diseases than other HAP1-expressing neurons probably involved in spinal sensory and autonomic functions.
Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  huntingtin-associated protein 1; immunohistochemistry; motoneurons; neurodegenerative diseases; neuroprotection; stigmoid body

Mesh:

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Year:  2016        PMID: 27984179     DOI: 10.1016/j.neuroscience.2016.10.053

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  3 in total

1.  Immunohistochemical expression and neurochemical phenotypes of huntingtin-associated protein 1 in the myenteric plexus of mouse gastrointestinal tract.

Authors:  Abu Md Mamun Tarif; Md Nabiul Islam; Mir Rubayet Jahan; Akie Yanai; Kanako Nozaki; Koh-Hei Masumoto; Koh Shinoda
Journal:  Cell Tissue Res       Date:  2021-10-19       Impact factor: 5.249

2.  Loss of Hap1 selectively promotes striatal degeneration in Huntington disease mice.

Authors:  Qiong Liu; Siying Cheng; Huiming Yang; Louyin Zhu; Yongcheng Pan; Liang Jing; Beisha Tang; Shihua Li; Xiao-Jiang Li
Journal:  Proc Natl Acad Sci U S A       Date:  2020-08-03       Impact factor: 11.205

3.  Huntingtin-associated protein 1 plays an essential role in the pathogenesis of type 2 diabetes by regulating the translocation of GLUT4 in mouse adipocytes.

Authors:  Yan-Ju Gong; Ying Feng; Gui-Zhi Yang; Xue Zhou; Yuan-Yuan Cao; Jia Zhao; Wei Wu; Ya-Yun Zheng; Jia-Rui Wu; Xin Li
Journal:  BMJ Open Diabetes Res Care       Date:  2020-10
  3 in total

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