Cell line models for differentiation: preadipocytes and adipocytes

Poulos, Sylvia P.; Dodson, Michael V.; Hausman, Gary

doi:10.1258/ebm.2010.010063

Cited by 242 publications

(221 citation statements)

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“…Taken together, leptin acts in an autocrine/paracrine manner via the PI3K/Akt signaling pathway, contributing to sustain adipocyte inflammation through the synthesis and release of the alarmin TNC. Data are based on the immortalized cell line 3T3-L1 since the preadipose cell line 3T3-L1 is one of the most common in vitro models used in the study of adipocyte biology due to its potential to differentiate from fibroblasts to adipocytes 58 . However, 3T3-L1 adipocytes display features of multiple adipocyte lineages, and this should be taken into consideration when interpreting data from experiments using this cell line 59 .…”

Section: Discussionmentioning

confidence: 99%

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

et al. 2018

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Background/Objectives: Obesity is related to a dynamic extracellular matrix (ECM) remodeling, which involves the synthesis and degradation of different proteins, such as tenascin C (TNC) in the adipose tissue (AT). Given the functional relationship between leptin and inducible nitric oxide synthase (iNOS), our aim was to analyze the impact of the absence of the iNOS gene in AT inflammation and ECM remodeling in ob/ob mice. Subjects/Methods: The expression of genes involved in inflammation and ECM remodeling was evaluated in 10-week-old male double knockout (DBKO) mice simultaneously lacking the ob and iNOS genes as well as in ob/ob mice classified into three groups [control, leptin-treated (1 mg kg −1 day −1 ) and pair-fed]. Results: Leptin deficiency increased inflammation and fibrosis in AT. As expected, leptin treatment improved the obesity phenotype. iNOS deficiency in ob/ob mice improved insulin sensitivity, AT inflammation, and ECM remodeling, as evidenced by lower AT macrophage infiltration and collagen deposition, a downregulation of proinflammatory and profibrogenic genes Tnf, Emr1, Hif1a, Col6a1, Col6a3, and Tnc, as well as lower circulating TNC levels. Interestingly, leptin upregulated TNC expression and release in 3T3-L1 adipocytes, and iNOS knockdown in 3T3-L1 fat cells produced a significant decrease in basal and leptin-induced Tnc expression. Conclusions: Ablation of iNOS in leptin-deficient mice improved AT inflammation and ECM remodeling-related genes, attenuating fibrosis, and metabolic dysfunction. The activation of iNOS by leptin is necessary for the synthesis and secretion of TNC in adipocytes, suggesting an important role of this alarmin in the development of AT inflammation and fibrosis.

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Section: Discussionmentioning

confidence: 99%

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

et al. 2018

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“…Adipogenesis is the process by which preadipocytes differentiate into mature adipocytes. Preadipocyte proliferation and differentiation have been widely studied with a well-characterized and reliable in vitro model using the 3T3-L1 preadipocyte cell line, which was isolated from Swiss 3T3 mouse embryos (Green & Meuth 1974;Poulos et al 2010). In this study, we investigated the effects of porcine PID1 on 3T3-L1 preadipocyte proliferation and differentiation.…”

Section: Discussionmentioning

confidence: 99%

Porcine phosphotyrosine interaction domain containing 1 modulates 3T3-L1 preadipocyte proliferation and differentiation

et al. 2013

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Abstract:The phosphotyrosine interaction domain containing 1 (PID1) gene was firstly isolated from obese subjects and involved in obesity-associated insulin resistance. In the present study, Duroc×Landrace×Yorkshire (DLY) pig PID1 cDNA was cloned. The entire open reading frame of the cloned porcine PID1 is 654 bp. The predicted protein is composed of 217 amino acids residues with a molecular mass of 24,774 Da. Over-expression of porcine PID1 significantly accelerated the proliferation of 3T3-L1 preadipocyte, but inhibited preadipocyte differentiation by decreasing the numerous fat droplets appeared and down-regulating the mRNA expression levels of peroxisome proliferators-activated receptor-γ, CCAAT/enhancer binding protein α, fat acid synthase and lipoprotein lipase. Together, these results suggest that porcine PID1 plays a role in regulating adipose development.

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“…Sufficient (isolatable) adipose tissue is present in all adipose depots of cattle for cell isolation and comparative evaluation (Dodson et al, 2010b) and a broadening database of research tools is rapidly being developed for bovine adipose research models. Furthermore, previous studies have indicated that the physiology of adipocytes derived from cattle may be different from other well-understood adipocyte models (such as 3T3-L1) (Fernyhough et al, 2007;Taniguchi et al, 2008a,b;Dodson et al, 2010a,c;Poulos et al, 2010). Bovine adipocytes with potential dominance are the cell model of studying adipogenesis and lipid metabolism for improving animal production and serving human health.…”

Section: Introductionmentioning

confidence: 99%

Adenovirus-mediated interference of FABP4 regulates mRNA expression of ADIPOQ, LEP and LEPR in bovine adipocytes

Wei¹,

Liu²,

Wang³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Fatty acid binding protein 4 (FABP4) is an important adipocyte gene, with roles in fatty acid transport and fat deposition in animals as well as human metabolic syndrome. However, little is known about the functional regulation of FABP4 at the cellular level in bovine. We designed and selected an effective shRNA (small hairpin RNA) against bovine FABP4, constructed a corresponding adenovirus (AD-FABP4), and then detected its influence on mRNA expression of four differentiation-related genes (PPARᵧ, CEBPA, CEBPB, and SREBF1) and three lipid metabolism-related genes (ADIPOQ, LEP and LEPR) of adipocytes. The FABP4 mRNA content, derived from bovine adipocytes, decreased by 41% (P < 0.01) after 24 h and 66% (P < 0.01) 495©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 12 (1): 494-505 (2013) shRNA interference of FABP4 in bovine adipocytes after 72 h of AD-FABP4 infection. However, lower mRNA content of FABP4 did not significantly alter levels of differentiation-related gene expression at 24 h following AD-FABP4 treatment of bovinederived preadipocytes (P = 0.54, 0.78, 0.89, and 0.94, respectively). Meanwhile, knocking down (partially silencing) FABP4 significantly decreased ADIPOQ (P < 0.05) and LEP (P < 0.01) gene expression after 24 h of AD-FABP4 treatment, decreased ADIPOQ (P < 0.01) and LEP (P < 0.01) gene expression, but increased LEPR mRNA expression (P < 0.01) after a 72-h treatment of bovine preadipocytes. We conclude that FABP4 plays a role in fat deposition and metabolic syndrome by regulating lipid metabolism-related genes (such as ADIPOQ, LEP and LEPR), without affecting the ability of preadipocytes to differentiate into adipocytes.

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Cell line models for differentiation: preadipocytes and adipocytes

Cited by 242 publications

References 69 publications

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

Targeted disruption of the iNOS gene improves adipose tissue inflammation and fibrosis in leptin-deficient ob/ob mice: role of tenascin C

Porcine phosphotyrosine interaction domain containing 1 modulates 3T3-L1 preadipocyte proliferation and differentiation

Adenovirus-mediated interference of FABP4 regulates mRNA expression of ADIPOQ, LEP and LEPR in bovine adipocytes

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