Znf202 Affects High Density Lipoprotein Cholesterol Levels and Promotes Hepatosteatosis in Hyperlipidemic Mice

CLJ Vrins; R Out; P van Santbrink; A van der Zee; Tokameh Mahmoudi; M (Martine) Groenendijk; LM Havekes; TJC Van Berkel; KW van Dijk; EAL Biessen

doi:10.1371/journal.pone.0057492

Znf202 Affects High Density Lipoprotein Cholesterol Levels and Promotes Hepatosteatosis in Hyperlipidemic Mice

CLJ Vrins
, R Out
, P van Santbrink
, A van der Zee
, Tokameh Mahmoudi
, M (Martine) Groenendijk
, LM Havekes
, TJC Van Berkel
, KW van Dijk
, EAL Biessen

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

17 Citations (Scopus)

51 Downloads (Pure)

Abstract

Background: The zinc finger protein Znf202 is a transcriptional suppressor of lipid related genes and has been linked to hypoalphalipoproteinemia. A functional role of Znf202 in lipid metabolism in vivo still remains to be established. Methodology and Principal Findings: We generated mouse Znf202 expression vectors, the functionality of which was established in several in vitro systems. Next, effects of adenoviral znf202 overexpression in vivo were determined in normoas well as hyperlipidemic mouse models. Znf202 overexpression in mouse hepatoma cells mhAT3F2 resulted in downregulation of members of the Apoe/c1/c2 and Apoa1/c3/a4 gene cluster. The repressive activity of Znf202 was firmly confirmed in an apoE reporter assay and Conclusion/Significance: Znf202 overexpression in vivo reveals an important role of this transcriptional regulator in liver lipid homeostasis, while firmly establishing the proposed key role in the control of HDL levels.

Original language	Undefined/Unknown
Journal	PLoS One (print)
Volume	8
Issue number	2
DOIs	https://doi.org/10.1371/journal.pone.0057492
Publication status	Published - 2013

Research programs

EMC MGC-02-21-01

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http://hdl.handle.net/1765/40857

Cite this

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title = "Znf202 Affects High Density Lipoprotein Cholesterol Levels and Promotes Hepatosteatosis in Hyperlipidemic Mice",

abstract = "Background: The zinc finger protein Znf202 is a transcriptional suppressor of lipid related genes and has been linked to hypoalphalipoproteinemia. A functional role of Znf202 in lipid metabolism in vivo still remains to be established. Methodology and Principal Findings: We generated mouse Znf202 expression vectors, the functionality of which was established in several in vitro systems. Next, effects of adenoviral znf202 overexpression in vivo were determined in normoas well as hyperlipidemic mouse models. Znf202 overexpression in mouse hepatoma cells mhAT3F2 resulted in downregulation of members of the Apoe/c1/c2 and Apoa1/c3/a4 gene cluster. The repressive activity of Znf202 was firmly confirmed in an apoE reporter assay and Conclusion/Significance: Znf202 overexpression in vivo reveals an important role of this transcriptional regulator in liver lipid homeostasis, while firmly establishing the proposed key role in the control of HDL levels.",

author = "CLJ Vrins and R Out and \{van Santbrink\}, P and \{van der Zee\}, A and Tokameh Mahmoudi and Groenendijk, \{M (Martine)\} and LM Havekes and \{Van Berkel\}, TJC and \{van Dijk\}, KW and EAL Biessen",

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doi = "10.1371/journal.pone.0057492",

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volume = "8",

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T1 - Znf202 Affects High Density Lipoprotein Cholesterol Levels and Promotes Hepatosteatosis in Hyperlipidemic Mice

AU - Vrins, CLJ

AU - Out, R

AU - van Santbrink, P

AU - van der Zee, A

AU - Mahmoudi, Tokameh

AU - Groenendijk, M (Martine)

AU - Havekes, LM

AU - Van Berkel, TJC

AU - van Dijk, KW

AU - Biessen, EAL

PY - 2013

Y1 - 2013

N2 - Background: The zinc finger protein Znf202 is a transcriptional suppressor of lipid related genes and has been linked to hypoalphalipoproteinemia. A functional role of Znf202 in lipid metabolism in vivo still remains to be established. Methodology and Principal Findings: We generated mouse Znf202 expression vectors, the functionality of which was established in several in vitro systems. Next, effects of adenoviral znf202 overexpression in vivo were determined in normoas well as hyperlipidemic mouse models. Znf202 overexpression in mouse hepatoma cells mhAT3F2 resulted in downregulation of members of the Apoe/c1/c2 and Apoa1/c3/a4 gene cluster. The repressive activity of Znf202 was firmly confirmed in an apoE reporter assay and Conclusion/Significance: Znf202 overexpression in vivo reveals an important role of this transcriptional regulator in liver lipid homeostasis, while firmly establishing the proposed key role in the control of HDL levels.

AB - Background: The zinc finger protein Znf202 is a transcriptional suppressor of lipid related genes and has been linked to hypoalphalipoproteinemia. A functional role of Znf202 in lipid metabolism in vivo still remains to be established. Methodology and Principal Findings: We generated mouse Znf202 expression vectors, the functionality of which was established in several in vitro systems. Next, effects of adenoviral znf202 overexpression in vivo were determined in normoas well as hyperlipidemic mouse models. Znf202 overexpression in mouse hepatoma cells mhAT3F2 resulted in downregulation of members of the Apoe/c1/c2 and Apoa1/c3/a4 gene cluster. The repressive activity of Znf202 was firmly confirmed in an apoE reporter assay and Conclusion/Significance: Znf202 overexpression in vivo reveals an important role of this transcriptional regulator in liver lipid homeostasis, while firmly establishing the proposed key role in the control of HDL levels.

U2 - 10.1371/journal.pone.0057492

DO - 10.1371/journal.pone.0057492

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