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Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation. / Mazin, Mark E.; Yarushkin, Andrei A.; Pustylnyak, Yuliya A. et al.

In: Molecular Biology Reports, Vol. 49, No. 5, 05.2022, p. 4089-4093.

Research output: Contribution to journal › Article › peer-review

Harvard

Mazin, ME, Yarushkin, AA, Pustylnyak, YA, Prokopyeva, EA & Pustylnyak, VO 2022, 'Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation', Molecular Biology Reports, vol. 49, no. 5, pp. 4089-4093. https://doi.org/10.1007/s11033-022-07340-1

APA

Mazin, M. E., Yarushkin, A. A., Pustylnyak, Y. A., Prokopyeva, E. A., & Pustylnyak, V. O. (2022). Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation. Molecular Biology Reports, 49(5), 4089-4093. https://doi.org/10.1007/s11033-022-07340-1

Vancouver

Mazin ME, Yarushkin AA, Pustylnyak YA, Prokopyeva EA, Pustylnyak VO. Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation. Molecular Biology Reports. 2022 May;49(5):4089-4093. Epub 2022 Mar 19. doi: 10.1007/s11033-022-07340-1

Author

Mazin, Mark E. ; Yarushkin, Andrei A. ; Pustylnyak, Yuliya A. et al. / Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation. In: Molecular Biology Reports. 2022 ; Vol. 49, No. 5. pp. 4089-4093.

BibTeX

@article{7a9ccd1df2ca465394705dc0ff5e5436,
title = "Promotion of NR1I3-mediated liver growth is accompanied by STAT3 activation",
abstract = "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{\textquoteright}s proliferation impact was facilitated, partly, by cMyc and Cyclin D1 upregulation. Conclusions: This work{\textquoteright}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.",
keywords = "CAR, Hepatocyte proliferation, Liver, Liver hyperplasia, STAT3, Animals, Cell Proliferation, Signal Transduction, Mice, Inbred C57BL, Receptors, Cytoplasmic and Nuclear/genetics, Mice, Hepatocytes/physiology",
author = "Mazin, {Mark E.} and Yarushkin, {Andrei A.} and Pustylnyak, {Yuliya A.} and Prokopyeva, {Elena A.} and Pustylnyak, {Vladimir O.}",
note = "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: {\textcopyright} 2022, The Author(s), under exclusive licence to Springer Nature B.V.",
year = "2022",
month = may,
doi = "10.1007/s11033-022-07340-1",
language = "English",
volume = "49",
pages = "4089--4093",
journal = "Molecular Biology Reports",
issn = "0301-4851",
publisher = "Springer Netherlands",
number = "5",

}

RIS

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