Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование
Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation. / Mazin, Mark E.; Yarushkin, Andrei A.; Pustylnyak, Yuliya A. и др.
в: Molecular Biology Reports, Том 49, № 5, 05.2022, стр. 4089-4093.Результаты исследований: Научные публикации в периодических изданиях › статья › Рецензирование
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TY - JOUR
T1 - Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation
AU - Mazin, Mark E.
AU - Yarushkin, Andrei A.
AU - Pustylnyak, Yuliya A.
AU - Prokopyeva, Elena A.
AU - Pustylnyak, Vladimir O.
N1 - Funding Information: This work was supported by Russian Science Foundation [Grant Number, 18-15-00021]. The authors acknowledge the Center for Collective Use "Proteomic Analysis" (supported by funding from the Ministry of Science and Higher Education of the Russian Federation, agreement No. 075-15-2021-691) for providing the necessary equipment to perform this study. Publisher Copyright: © 2022, The Author(s), under exclusive licence to Springer Nature B.V.
PY - 2022/5
Y1 - 2022/5
N2 - Background: The constitutive androstane receptor (CAR, NR1I3)-mediated mechanisms regulating hepatocyte proliferation and growth of the liver did not yet experience complete elucidation. We investigated whether STAT3 could be activated in vivo by NR1I3 signaling in mouse liver. Methods and results: Using Western blot analysis, immunofluorescence assays and real-time PCR we established the state of STAT3 activation when it comes to the mouse liver subsequent to treatment ofNR1I3 agonist,1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP). STAT3 nuclear relocation and hepatocyte growth were both induced by NR1I3-mediated phosphorylation of STAT3. Moreover, the NR1I3-STAT3 signaling pathway’s proliferation impact was facilitated, partly, by cMyc and Cyclin D1 upregulation. Conclusions: This work’s evidence demonstrates that NR1I3-pushed STAT3 activation contributes to TCPOBOP-induced liver growth and hepatocyte proliferation, at least in part, through its molecular targets cMyc and CyclinD1.
AB - Background: The constitutive androstane receptor (CAR, NR1I3)-mediated mechanisms regulating hepatocyte proliferation and growth of the liver did not yet experience complete elucidation. We investigated whether STAT3 could be activated in vivo by NR1I3 signaling in mouse liver. Methods and results: Using Western blot analysis, immunofluorescence assays and real-time PCR we established the state of STAT3 activation when it comes to the mouse liver subsequent to treatment ofNR1I3 agonist,1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP). STAT3 nuclear relocation and hepatocyte growth were both induced by NR1I3-mediated phosphorylation of STAT3. Moreover, the NR1I3-STAT3 signaling pathway’s proliferation impact was facilitated, partly, by cMyc and Cyclin D1 upregulation. Conclusions: This work’s evidence demonstrates that NR1I3-pushed STAT3 activation contributes to TCPOBOP-induced liver growth and hepatocyte proliferation, at least in part, through its molecular targets cMyc and CyclinD1.
KW - CAR
KW - Hepatocyte proliferation
KW - Liver
KW - Liver hyperplasia
KW - STAT3
KW - Animals
KW - Cell Proliferation
KW - Signal Transduction
KW - Mice, Inbred C57BL
KW - Receptors, Cytoplasmic and Nuclear/genetics
KW - Mice
KW - Hepatocytes/physiology
UR - http://www.scopus.com/inward/record.url?scp=85126758883&partnerID=8YFLogxK
U2 - 10.1007/s11033-022-07340-1
DO - 10.1007/s11033-022-07340-1
M3 - Article
C2 - 35305226
AN - SCOPUS:85126758883
VL - 49
SP - 4089
EP - 4093
JO - Molecular Biology Reports
JF - Molecular Biology Reports
SN - 0301-4851
IS - 5
ER -
ID: 35770224