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Gap-junctional communication is required for mitotic clonal expansion during adipogenesis.
Obesity (Silver Spring). 2007 Mar; 15(3):572-82.O

Abstract

OBJECTIVE

Gap-junctional communication (GJC) plays critical roles in cell growth and differentiation. Several studies have demonstrated the involvement of GJC in myogenesis and osteogenesis; however, the role of GJC in adipogenesis has not been fully studied. Thus, we investigated the role of GJC in adipogenesis.

RESEARCH METHODS AND PROCEDURES

3T3-L1 preadipocytes were differentiated in the presence of gap junction inhibitor, 18-alpha-glycyrrhetinic acid (AGA), and accumulation of cytoplasmic triglycerides was measured. 3T3-L1 cells were transfected with 100 nM small interfering RNA duplexes targeting connexin (Cx) 43. The mRNA levels of CCAAT/enhancer-binding protein (C/EBP) alpha, peroxisome proliferator-activated receptor gamma, glucose transporter 4, C/EBPbeta, and Cx43 were measured by real-time polymerase chain reaction. The protein levels of C/EBPbeta were quantitated by Western blotting. The cell proliferation was measured by counting cell numbers, and DNA synthesis was measured by bromodeoxyuridine incorporation.

RESULTS

AGA inhibited adipocyte differentiation dose-dependently. The lipid accumulation and the mRNA levels of C/EBPalpha, peroxisome proliferator-activated receptor gamma, and glucose transporter 4 were markedly reduced in AGA-treated adipocytes. The mRNA levels of C/EBPbeta did not decrease; however, C/EBPbeta [liver-enriched transcriptional activator protein (LAP)] expression and the C/EBPbeta (LAP)-to-C/EBP [liver-enriched transcriptional inhibitory protein (LIP)] ratio were reduced by AGA treatment. The increase in both cell number and DNA synthesis, which occurs during mitotic clonal expansion, was reduced by AGA in a dose-dependent fashion. The major component of gap junctions in 3T3-L1 cells was Cx43. Down-regulation of Cx43 using small interfering RNA reduced the expression of C/EBPbeta (LAP) and inhibited adipogenesis.

DISCUSSION

Our data suggest that GJC plays some important roles in adipogenesis through inhibiting mitotic clonal expansion and modulating C/EBPbeta (LAP) expression.

Authors+Show Affiliations

Yanagiya T
Laboratory for Obesity, Research Group for Disease-Causing Mechanism, SNP Research Center, RIKEN, 1-7-22, Suehiro, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan.
Tanabe A
No affiliation info available
Hotta K
No affiliation info available

MeSH

3T3-L1 CellsAdipocytesAdipogenesisAnimalsCell CommunicationCell ProliferationConnexin 43Gap JunctionsGlycyrrhetinic AcidMaleMiceMice, Inbred C57BLMitosisRNA, Small Interfering

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17372306

Citation

Yanagiya, Takahiro, et al. "Gap-junctional Communication Is Required for Mitotic Clonal Expansion During Adipogenesis." Obesity (Silver Spring, Md.), vol. 15, no. 3, 2007, pp. 572-82.
Yanagiya T, Tanabe A, Hotta K. Gap-junctional communication is required for mitotic clonal expansion during adipogenesis. Obesity (Silver Spring). 2007;15(3):572-82.
Yanagiya, T., Tanabe, A., & Hotta, K. (2007). Gap-junctional communication is required for mitotic clonal expansion during adipogenesis. Obesity (Silver Spring, Md.), 15(3), 572-82.
Yanagiya T, Tanabe A, Hotta K. Gap-junctional Communication Is Required for Mitotic Clonal Expansion During Adipogenesis. Obesity (Silver Spring). 2007;15(3):572-82. PubMed PMID: 17372306.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gap-junctional communication is required for mitotic clonal expansion during adipogenesis. AU - Yanagiya,Takahiro, AU - Tanabe,Atsushi, AU - Hotta,Kikuko, PY - 2007/3/21/pubmed PY - 2007/5/16/medline PY - 2007/3/21/entrez SP - 572 EP - 82 JF - Obesity (Silver Spring, Md.) JO - Obesity (Silver Spring) VL - 15 IS - 3 N2 - OBJECTIVE: Gap-junctional communication (GJC) plays critical roles in cell growth and differentiation. Several studies have demonstrated the involvement of GJC in myogenesis and osteogenesis; however, the role of GJC in adipogenesis has not been fully studied. Thus, we investigated the role of GJC in adipogenesis. RESEARCH METHODS AND PROCEDURES: 3T3-L1 preadipocytes were differentiated in the presence of gap junction inhibitor, 18-alpha-glycyrrhetinic acid (AGA), and accumulation of cytoplasmic triglycerides was measured. 3T3-L1 cells were transfected with 100 nM small interfering RNA duplexes targeting connexin (Cx) 43. The mRNA levels of CCAAT/enhancer-binding protein (C/EBP) alpha, peroxisome proliferator-activated receptor gamma, glucose transporter 4, C/EBPbeta, and Cx43 were measured by real-time polymerase chain reaction. The protein levels of C/EBPbeta were quantitated by Western blotting. The cell proliferation was measured by counting cell numbers, and DNA synthesis was measured by bromodeoxyuridine incorporation. RESULTS: AGA inhibited adipocyte differentiation dose-dependently. The lipid accumulation and the mRNA levels of C/EBPalpha, peroxisome proliferator-activated receptor gamma, and glucose transporter 4 were markedly reduced in AGA-treated adipocytes. The mRNA levels of C/EBPbeta did not decrease; however, C/EBPbeta [liver-enriched transcriptional activator protein (LAP)] expression and the C/EBPbeta (LAP)-to-C/EBP [liver-enriched transcriptional inhibitory protein (LIP)] ratio were reduced by AGA treatment. The increase in both cell number and DNA synthesis, which occurs during mitotic clonal expansion, was reduced by AGA in a dose-dependent fashion. The major component of gap junctions in 3T3-L1 cells was Cx43. Down-regulation of Cx43 using small interfering RNA reduced the expression of C/EBPbeta (LAP) and inhibited adipogenesis. DISCUSSION: Our data suggest that GJC plays some important roles in adipogenesis through inhibiting mitotic clonal expansion and modulating C/EBPbeta (LAP) expression. SN - 1930-7381 UR - https://www.unboundmedicine.com/medline/citation/17372306/Gap_junctional_communication_is_required_for_mitotic_clonal_expansion_during_adipogenesis_ L2 - https://doi.org/10.1038/oby.2007.547 DB - PRIME DP - Unbound Medicine ER -