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Statements

Subject Item
n2:RIV%2F00216208%3A11110%2F14%3A10272412%21RIV15-MSM-11110___
rdf:type
skos:Concept n19:Vysledek
rdfs:seeAlso
http://dx.doi.org/10.1210/en.2014-1008
dcterms:description
The bulbocavernosus (BC) is a sexually dimorphic muscle observed only in males. Androgen receptor knockout mouse studies show the loss of BC formation. This suggests that androgen signaling plays a vital role in its development. Androgen has been known to induce muscle hypertrophy through satellite cell activation and myonuclei accretion during muscle regeneration and growth. To identify the mechanism of sexual dimorphism during BC embryonic development, the timing of morphological differences was first established. The BC was morphologically different between male and female mice at embryonic day (E) 16.5. Differences in the myogenic process were detected at E15.5. The male BC possesses a higher number of proliferating undifferentiated myoblasts. To identify the role of androgen signaling, muscle-specific androgen receptor (AR) mutation was introduced, which resulted in no observable phenotypes. Hence, the expression of AR in the BC was examined and found that the AR did not colocalize with any muscle markers such as Myogenic differentiation 1, Myogenin, and paired box transcription factor 7. The mesenchyme surrounding the BC expressed AR and the BC started to express AR at E15.5. AR mutation on the nonmyocytic cells using spalt-like transcription factor 1 (Sall1) Cre driver mouse was performed, which resulted in defective BC formation. The number of proliferating undifferentiated myoblasts was reduced in the Sall1 Cre:AR(L-/Y) mutant embryos, and the adult mutants were devoid of BC. The transition of myoblasts from proliferation to differentiation is mediated by cyclin-dependent kinase inhibitors. An increased expression of p21 was observed in the BC myoblast of the Sall1 Cre:AR(L-/Y) mutant and wild-type female. Altogether this study suggests that the nonmyocytic AR may paracrinely regulate the proliferation of myoblast possibly through inhibiting p21 expression in myoblasts of the BC. The bulbocavernosus (BC) is a sexually dimorphic muscle observed only in males. Androgen receptor knockout mouse studies show the loss of BC formation. This suggests that androgen signaling plays a vital role in its development. Androgen has been known to induce muscle hypertrophy through satellite cell activation and myonuclei accretion during muscle regeneration and growth. To identify the mechanism of sexual dimorphism during BC embryonic development, the timing of morphological differences was first established. The BC was morphologically different between male and female mice at embryonic day (E) 16.5. Differences in the myogenic process were detected at E15.5. The male BC possesses a higher number of proliferating undifferentiated myoblasts. To identify the role of androgen signaling, muscle-specific androgen receptor (AR) mutation was introduced, which resulted in no observable phenotypes. Hence, the expression of AR in the BC was examined and found that the AR did not colocalize with any muscle markers such as Myogenic differentiation 1, Myogenin, and paired box transcription factor 7. The mesenchyme surrounding the BC expressed AR and the BC started to express AR at E15.5. AR mutation on the nonmyocytic cells using spalt-like transcription factor 1 (Sall1) Cre driver mouse was performed, which resulted in defective BC formation. The number of proliferating undifferentiated myoblasts was reduced in the Sall1 Cre:AR(L-/Y) mutant embryos, and the adult mutants were devoid of BC. The transition of myoblasts from proliferation to differentiation is mediated by cyclin-dependent kinase inhibitors. An increased expression of p21 was observed in the BC myoblast of the Sall1 Cre:AR(L-/Y) mutant and wild-type female. Altogether this study suggests that the nonmyocytic AR may paracrinely regulate the proliferation of myoblast possibly through inhibiting p21 expression in myoblasts of the BC.
dcterms:title
Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle
skos:prefLabel
Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle Nonmyocytic androgen receptor regulates the sexually dimorphic development of the embryonic bulbocavernosus muscle
skos:notation
RIV/00216208:11110/14:10272412!RIV15-MSM-11110___
n3:aktivita
n13:V
n3:aktivity
V
n3:cisloPeriodika
7
n3:dodaniDat
n8:2015
n3:domaciTvurceVysledku
n10:1223402
n3:druhVysledku
n9:J
n3:duvernostUdaju
n16:S
n3:entitaPredkladatele
n11:predkladatel
n3:idSjednocenehoVysledku
32818
n3:idVysledku
RIV/00216208:11110/14:10272412
n3:jazykVysledku
n7:eng
n3:klicovaSlova
muscle; bulbocavernosus; embryonic; development; dimorphic; sexually; regulates; receptor; androgen; Nonmyocytic
n3:klicoveSlovo
n4:regulates n4:muscle n4:androgen n4:Nonmyocytic n4:embryonic n4:dimorphic n4:sexually n4:development n4:receptor n4:bulbocavernosus
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[13F1B229B7F2]
n3:nazevZdroje
Endocrinology
n3:obor
n14:EA
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
10
n3:rokUplatneniVysledku
n8:2014
n3:svazekPeriodika
155
n3:tvurceVysledku
Nishinakamura, Ryuichi Ipulan, Lerrie Ann Omori, Akiko Suzuki, Kentaro Valášek, Petr Imai, Yuuki Murashima, Aki Yamada, Gen Sakamoto, Yuki Nakagata, Naomi
n3:wos
000342343400015
s:issn
0013-7227
s:numberOfPages
15
n17:doi
10.1210/en.2014-1008
n18:organizacniJednotka
11110