Promoting Primary Myoblast Differentiation Through Retinoid X Receptor Signaling

Author(s):  
Jihong Chen ◽  
Qiao Li
Endocrinology ◽  
2009 ◽  
Vol 150 (9) ◽  
pp. 4260-4269 ◽  
Author(s):  
Eiji Munetsuna ◽  
Yasushi Hojo ◽  
Minoru Hattori ◽  
Hirotaka Ishii ◽  
Suguru Kawato ◽  
...  

Abstract The hippocampus is essentially involved in learning and memory processes. Its functions are affected by various neuromodulators, including 17β-estradiol, testosterone, and retinoid. Brain-synthesized steroid hormones act as autocrine and paracrine modulators. The regulatory mechanism underlying brain steroidogenesis has not been fully elucidated. Synthesis of sex steroids in the gonads is stimulated by retinoic acids. Therefore, we examined the effects of retinoic acids on estradiol and testosterone biosynthesis in the rat hippocampus. We used cultured hippocampal slices from 10- to 12-d-old male rats to investigate de novo steroidogenesis. The infant rat hippocampus possesses mRNAs for steroidogenic enzymes and retinoid receptors. Slices were used after 24 h of preculture to obtain maximal steroidogenic activity because steroidogenesis in cultured slices decreases with time. The mRNA levels for P45017α, P450 aromatase and estrogen receptor-β in the slices were increased by treatment with 9-cis-retinoic acid but not by all-trans-isomer. The magnitude of stimulation and the shape of the dose-response curve for the mRNA level for P45017α were similar to those for cellular retinoid binding protein type 2, the transcription of which is activated by retinoid X receptor signaling. 9-cis-Retinoic acid also induced a 1.7-fold increase in the protein content of P45017α and a 2-fold increase in de novo synthesis of 17β-estradiol and testosterone. These steroids may be synthesized from a steroid precursor(s), such as pregnenolone or other steroids, or from cholesterol, as so-called neurosteroids. The stimulation of estradiol and testosterone synthesis by 9-cis-retinoic acid might be caused by activation of P45017α transcription via retinoid X receptor signaling.


2011 ◽  
Vol 286 (30) ◽  
pp. 26806-26812 ◽  
Author(s):  
Melanie Le May ◽  
Hymn Mach ◽  
Natascha Lacroix ◽  
Chenchen Hou ◽  
Jihong Chen ◽  
...  

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Lucas Fauquier ◽  
Karim Azzag ◽  
Marco Antonio Mendoza Parra ◽  
Aurélie Quillien ◽  
Manon Boulet ◽  
...  

1997 ◽  
Vol 230 (1) ◽  
pp. 50-60 ◽  
Author(s):  
Mary Shago ◽  
Grace Flock ◽  
Chung-Yee Leung Hagesteijn ◽  
Michael Woodside ◽  
Sergio Grinstein ◽  
...  

2020 ◽  
Vol 3 (1) ◽  
Author(s):  
Saadia Khilji ◽  
Munerah Hamed ◽  
Jihong Chen ◽  
Qiao Li

2016 ◽  
Vol 88 (4) ◽  
pp. 712-719 ◽  
Author(s):  
Kyungshin Shin ◽  
Sang-Gu Hwang ◽  
Ik Joon Choi ◽  
Young-Gyu Ko ◽  
Jaemin Jeong ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1673
Author(s):  
Lilya Lehka ◽  
Małgorzata Topolewska ◽  
Dominika Wojton ◽  
Olena Karatsai ◽  
Paloma Alvarez-Suarez ◽  
...  

We have previously postulated that unconventional myosin VI (MVI) could be involved in myoblast differentiation. Here, we addressed the mechanism(s) of its involvement using primary myoblast culture derived from the hindlimb muscles of Snell’s waltzer mice, the natural MVI knockouts (MVI-KO). We observed that MVI-KO myotubes were formed faster than control heterozygous myoblasts (MVI-WT), with a three-fold increase in the number of myosac-like myotubes with centrally positioned nuclei. There were also changes in the levels of the myogenic transcription factors Pax7, MyoD and myogenin. This was accompanied by changes in the actin cytoskeleton and adhesive structure organization. We observed significant decreases in the levels of proteins involved in focal contact formation, such as talin and focal adhesion kinase (FAK). Interestingly, the levels of proteins involved in intercellular communication, M-cadherin and drebrin, were also affected. Furthermore, time-dependent alterations in the levels of the key proteins for myoblast membrane fusion, myomaker and myomerger, without effect on their cellular localization, were observed. Our data indicate that in the absence of MVI, the mechanisms controlling cytoskeleton organization, as well as myoblast adhesion and fusion, are dysregulated, leading to the formation of aberrant myotubes.


2017 ◽  
Vol 130 (18) ◽  
pp. 3083-3093 ◽  
Author(s):  
Julie Perroud ◽  
Laurent Bernheim ◽  
Maud Frieden ◽  
Stephane Koenig

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