Differential redox potential profiles during adipogenesis and osteogenesis

Imhoff, Barry R.; Hansen, Jason M.

doi:10.2478/s11658-010-0042-0

Cited by 54 publications

(43 citation statements)

References 23 publications

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“…This finding is in accordance with previous studies in other models of adipocyte differentiation (9,11,13), and thus validates the ST2 cell line as a model of adipogenesis in which to study redox-related phenomena and to investigate factors that may underlie their regulation.…”

Section: Resultssupporting

confidence: 92%

“…The present data are in agreement with previous studies showing that ROS levels increase during adipocyte differentiation in another cellular model of adipogenesis (3T3-L1 cells) (11,12), and that the glutathione redox potential shifts towards a more oxidized state during adipogenesis in human mesenchymal stem cells (13). The role of cellular redox status changes during adipogenesis has also been highlighted by a study showing that GSH depletion in 3T3-L1 cells promoted adipogenesis by enhancing the mitotic clonal expansion (MCE) phase and by activating the transcription factor C/EBPβ, whereas GSH supplementation (with GSHest, a permeable compound able to increase the intracellular GSH levels) inhibited adipogenesis Figure 4.…”

Section: Discussionsupporting

confidence: 93%

“…ROS levels increase during adipogenesis in models such as 3T3-L1 cell line (11,12), and indeed seem to facilitate adipocyte differentiation (9). Consistently, the intracellular redox-sensitive couples such as the glutathione (GSH/GSSG) and cysteine (Cys/CySS) systems shift towards more oxidized states during adipogenesis (13).…”

Section: Introductionmentioning

confidence: 87%

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Nrf2 activation diminishes during adipocyte differentiation of ST2 cells

Habeos¹

2011

Int J Mol Med

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Abstract. Adipocyte differentiation (adipogenesis) is a highly controlled process known to be affected, among other factors, by the redox status of the cell. Nrf2 (NFE2-related factor 2) is a transcription factor that orchestrates the expression of a battery of antioxidant and detoxification genes under both basal and stress conditions. The present study investigated the activation of Nrf2 during adipocyte differentiation using as a model the mouse bone marrow-derived ST2 cell line. Treatment of ST2 cells with a differentiation cocktail containing IBMX, indomethacin, hydrocortisone and insulin induced differentiation into adipocytes over 5 days. During adipogenesis, the intracellular glutathione redox potential, which is an indicator of oxidative stress levels, became steadily more oxidized, as shown by real-time measurement in differentiating ST2 cells stably transfected with a redox-sensitive Grx1-roGFP2 fusion protein.The nuclear abundance of Nrf2 was assessed by Western immunoblotting and its DNA binding activity by EMSA (electrophoretic mobility shift assay) performed on nuclear protein extracts prepared every 24 h. The nuclear abundance of Nrf2 continuously decreased during adipogenesis in ST2 cells. Its DNA binding activity reached a nadir during the first two days of differentiation, after which it increased slightly without approaching its initial level. The pattern of Nrf2 DNA binding corresponded to its transcriptional activity as assessed in ST2 cells stably transfected with a reporter construct bearing a Nrf2 bind site upstream of the luciferase gene. In conclusion, the activation of Nrf2 decreased significantly during adipogenesis. The observed changes might lead to increased oxidative stress levels that could facilitate the differentiation process. These findings could shed new light on the pathogenesis of obesity, in which the adipose tissue and oxidative stress play prominent roles.

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Section: Resultssupporting

confidence: 92%

Section: Discussionsupporting

confidence: 93%

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Nrf2 activation diminishes during adipocyte differentiation of ST2 cells

Habeos¹

2011

Int J Mol Med

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“…Adipogenic differentiation of hMSCs is a complex process that requires the precise regulation of cellular interactions with multiple differentiation factors and components of the extracellular matrix [19]. Therefore, various signaling pathways, adhesion molecules, and transcription factors play important roles in this process [20].…”

Section: Discussionmentioning

confidence: 99%

Gene expression profiling of human bone marrow-derived mesenchymal stem cells during adipogenesis

Yan

et al. 2015

Folia Histochem Cytobiol.

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Introduction. Adipogenesis comprises multiple processes by which mesenchymal stem cells differentiate into adipocytes. To increase our knowledge of the mechanism underlying adipogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs), we performed full-genome gene expression microarray and gene ontology analyses of induced differentiation of hMSCs. Material and methods. Adipogenic differentiation of hMSCs was induced by an adipogenic medium, and total RNA was extracted from undifferentiated hMSCs (day 0) and differentiated adipocytes (day 14). Then microarray hybridization of RNA samples was performed. The GeneChip Operating Software was used to analyze the hybridization data to identify differentially expressed genes, which were performed Gene Ontology categorization and pathway analysis. Pathway-act-network and genes-act-network were built according to the Kyoto Encyclopedia of Genes and Genomes database. Some differentially expressed genes were subjected to qRT-PCR to verify the microarray data. Results. We detected a total of 3,821 differentially expressed genes, of which 753 were upregulated and 3,068 downregulated. These genes were well represented in a variety of functional categories, including collagen fibril organization, brown fat cell differentiation, cell division, and S phase of mitotic cell cycle. Subsequently, pathway analysis was conducted, and significant pathways (from top 50) were selected for pathway-act-network analysis, which indicated that the mitogen-activated protein kinase (MAPK) pathway and cell cycle were of high degrees (> 10). Gene-act-network analysis showed that insulin-like growth factor 1 receptor (IGF1R), histone deacetylase 1 (HDAC1), HDAC2, MAPK13, MAPK8, phosphoinositide-3-kinase regulatory subunit 1 (PI3KR1), and PI3KR2 also had high degrees (> 18). Conclusions. Collectively, these data provide novel information and could serve as a basis for future study to clarify the mechanisms underlying adipocyte differentiation of hMSCs.

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“…Hence it integrates various nutritional and hormonal signals to promote the expansion of WAT under sustained nutrient excess. Redox states of major intracellular redox pairs (oxidized/reduced glutathione, thioredoxin, and cysteine) (Imhoff and Hansen, 2011) as well as ROS, such as the NOX4-generated H 2 O 2 have been recognized as important modulators of adipogenesis and adipose tissue function in health and disease. Other factors that regulate adipogenesis involve epigenetic mechanisms, as shown by several recent investigations in the epigenetic landscape of differentiating adipocytes.…”

Section: Adipogenesismentioning

confidence: 99%

The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

Castro

Grune

Speckmann

2016

Biological Chemistry

125

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White adipose tissue (WAT) is actively involved in the regulation of whole-body energy homeostasis via storage/release of lipids and adipokine secretion. Current research links WAT dysfunction to the development of metabolic syndrome (MetS) and type 2 diabetes (T2D). The expansion of WAT during oversupply of nutrients prevents ectopic fat accumulation and requires proper preadipocyte-to-adipocyte differentiation. An assumed link between excess levels of reactive oxygen species (ROS), WAT dysfunction and T2D has been discussed controversially. While oxidative stress conditions have conclusively been detected in WAT of T2D patients and related animal models, clinical trials with antioxidants failed to prevent T2D or to improve glucose homeostasis. Furthermore, animal studies yielded inconsistent results regarding the role of oxidative stress in the development of diabetes. Here, we discuss the contribution of ROS to the (patho)physiology of adipocyte function and differentiation, with particular emphasis on sources and nutritional modulators of adipocyte ROS and their functions in signaling mechanisms controlling adipogenesis and functions of mature fat cells. We propose a concept of ROS balance that is required for normal functioning of WAT. We explain how both excessive and diminished levels of ROS, e.g. resulting from over supplementation with antioxidants, contribute to WAT dysfunction and subsequently insulin resistance.

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Differential redox potential profiles during adipogenesis and osteogenesis

Cited by 54 publications

References 23 publications

Nrf2 activation diminishes during adipocyte differentiation of ST2 cells

Nrf2 activation diminishes during adipocyte differentiation of ST2 cells

Gene expression profiling of human bone marrow-derived mesenchymal stem cells during adipogenesis

The two faces of reactive oxygen species (ROS) in adipocyte function and dysfunction

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