Mitochondrial Dysfunction and Adipogenic Reduction by Prohibitin Silencing in 3T3-L1 Cells

Hdl Handle:
http://hdl.handle.net/10675.2/706
Title:
Mitochondrial Dysfunction and Adipogenic Reduction by Prohibitin Silencing in 3T3-L1 Cells
Authors:
Liu, Dong; Lin, Yiming; Kang, Ting; Huang, Bo; Xu, Wei; Garcia-Barrio, Minerva; Olatinwo, Moshood; Matthews, Roland; Chen, Yuqing Eugene; Thompson, Winston E.
Abstract:
Increase in mitochondrial biogenesis has been shown to accompany brown and white adipose cell differentiation. Prohibitins (PHBs), comprised of two evolutionarily conserved proteins, prohibitin-1 (PHB1) and prohibitin-2 (PHB2), are present in a high molecular-weight complex in the inner membrane of mitochondria. However, little is known about the effect of mitochondrial PHBs in adipogenesis. In the present study, we demonstrate that the levels of both PHB1 and PHB2 are significantly increased during adipogenesis of 3T3-L1 preadipocytes, especially in mitochondria. Knockdown of PHB1 or PHB2 by oligonucleotide siRNA significantly reduced the expression of adipogenic markers, the accumulation of lipids and the phosphorylation of extracellular signal-regulated kinases. In addition, fragmentation of mitochondrial reticulum, loss of mitochondrial cristae, reduction of mitochondrial content, impairment of mitochondrial complex I activity and excessive production of ROS were observed upon PHB-silencing in 3T3-L1 cells. Our results suggest that PHBs are critical mediators in promoting 3T3-L1 adipocyte differentiation and may be the potential targets for obesity therapies.
Editors:
McNeil, Paul L.
Citation:
PLoS One. 2012 Mar 30; 7(3):e34315
Issue Date:
30-Mar-2012
URI:
http://hdl.handle.net/10675.2/706
DOI:
10.1371/journal.pone.0034315
PubMed ID:
22479600
PubMed Central ID:
PMC3316679
Type:
Article
ISSN:
1932-6203
Appears in Collections:
Department of Cellular Biology and Anatomy Faculty Papers

Full metadata record

DC FieldValue Language
dc.contributor.authorLiu, Dongen_US
dc.contributor.authorLin, Yimingen_US
dc.contributor.authorKang, Tingen_US
dc.contributor.authorHuang, Boen_US
dc.contributor.authorXu, Weien_US
dc.contributor.authorGarcia-Barrio, Minervaen_US
dc.contributor.authorOlatinwo, Moshooden_US
dc.contributor.authorMatthews, Rolanden_US
dc.contributor.authorChen, Yuqing Eugeneen_US
dc.contributor.authorThompson, Winston E.en_US
dc.contributor.editorMcNeil, Paul L.-
dc.date.accessioned2012-10-26T16:40:49Z-
dc.date.available2012-10-26T16:40:49Z-
dc.date.issued2012-03-30en_US
dc.identifier.citationPLoS One. 2012 Mar 30; 7(3):e34315en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid22479600en_US
dc.identifier.doi10.1371/journal.pone.0034315en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/706-
dc.description.abstractIncrease in mitochondrial biogenesis has been shown to accompany brown and white adipose cell differentiation. Prohibitins (PHBs), comprised of two evolutionarily conserved proteins, prohibitin-1 (PHB1) and prohibitin-2 (PHB2), are present in a high molecular-weight complex in the inner membrane of mitochondria. However, little is known about the effect of mitochondrial PHBs in adipogenesis. In the present study, we demonstrate that the levels of both PHB1 and PHB2 are significantly increased during adipogenesis of 3T3-L1 preadipocytes, especially in mitochondria. Knockdown of PHB1 or PHB2 by oligonucleotide siRNA significantly reduced the expression of adipogenic markers, the accumulation of lipids and the phosphorylation of extracellular signal-regulated kinases. In addition, fragmentation of mitochondrial reticulum, loss of mitochondrial cristae, reduction of mitochondrial content, impairment of mitochondrial complex I activity and excessive production of ROS were observed upon PHB-silencing in 3T3-L1 cells. Our results suggest that PHBs are critical mediators in promoting 3T3-L1 adipocyte differentiation and may be the potential targets for obesity therapies.en_US
dc.rightsLiu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectBiochemistryen_US
dc.subjectBioenergeticsen_US
dc.subjectCytochemistryen_US
dc.subjectCell Membraneen_US
dc.subjectDevelopmental Biologyen_US
dc.subjectMolecular Cell Biologyen_US
dc.subjectCellular Structuresen_US
dc.subjectMedicineen_US
dc.subjectNutritionen_US
dc.titleMitochondrial Dysfunction and Adipogenic Reduction by Prohibitin Silencing in 3T3-L1 Cellsen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3316679en_US
dc.contributor.corporatenameDepartment of Cellular Biology and Anatomy-
dc.contributor.corporatenameCollege of Graduate Studies-

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