Conditioned media from (pre)adipocytes stimulate fibrinogen and PAI-1 production by HepG2 hepatoma cells

Faber, Daniel; Kalkhoven, Eric; Westerink, Jan; Bouwman, John; Monajemi, Houshang; Visseren, Frank L.J.

doi:10.1038/nutd.2012.25

Cited by 7 publications

(6 citation statements)

References 42 publications

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“…Adipocyte stimulation of spleen cell production of inflammatory cytokines such as IL-6 was expected and consistent with their own capacity to produce inflammatory mediators such as IL-1, TNF-α and IL-6 [13]. However, the increased production of IL-6 did not come from either CD4 + or CD8 + T-cells.…”

Section: Discussionmentioning

confidence: 60%

“…It has been previously shown that adipocytes can produce immune mediators such as IL-6 and TNF-α [13]. However, our studies suggest that their immune capacity might not be limited to directly producing immune mediators, but may include modulation of other immune cells (diagrammed in Fig.…”

Section: Discussionmentioning

confidence: 82%

“…Similar results are seen in the obese human population, with levels of leptin and adiponectin returning to normal levels following gastric bypass surgery [12]. Adipocytes are not only potent producers of adipokines such as adiponectin, adipsin, leptin, and visfatin, but respond to and produce various cytokines including interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-10 [7,13]. In obesity, levels of IL-6, TNF-α and leptin are increased [14].…”

Section: Introductionmentioning

confidence: 81%

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Adipocytes as immune regulatory cells

Vielma¹,

Klein²,

Levingston³

et al. 2013

International Immunopharmacology

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Obesity is a chronic inflammatory state and adipocytes are capable of contributing to this inflammation by their production of inflammatory mediators. The present study used fibroblast-derived adipocytes and normal spleen cells as a model to determine if adipocytes can also serve as immune regulatory cells by modulating the functions of conventional immune cells. Media conditioned by the adipocytes stimulated release of the Th1-type cytokines IL-2, IFN-γ and GM-CSF from cultures of normal spleen cells. The adipocytes also stimulated spleen cell release of inhibitory cytokines, although to varying degrees. This included IL-10, IL-13 and, to a lesser extent, IL-4. Spleen cell production of the inflammatory cytokines IL-6, TNF-α and IL-9 was stimulated by adipocytes, although production of the Th17-derived cytokine, IL-17, was not stimulated. The adipocyte-conditioned medium did not stimulate production of predominantly monocytes-derived chemokines CXCL9, CCL2, CCL3, CCL4, but stimulated production of the predominantly T-cell-derived chemokine CCL5. In all cases where cytokine/chemokine production from spleen cells was stimulated by adipocytes, it was to a far greater level than was produced by the adipocytes themselves. Studies initiated to determine the identity of the adipocyte-derived mediators showed that the spleen cell modulation could not be attributed to solely adiponectin or leptin. Studies to determine the source of some of the cytokines whose production was stimulated by adipocytes showed that expression of the inflammatory cytokine IL-6 was not increased in either CD4+ or CD8+ T-cell. When the splenic T-cells were examined for IFN-γ, the adipocyte stimulation of IFN-γ was within CD8+ T-cells, not CD4+ T-cells. These studies show that adipocytes may be able to serve as immune regulatory cells to stimulate conventional immune cells to release a spectrum of immune mediators.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 81%

See 1 more Smart Citation

Adipocytes as immune regulatory cells

Vielma¹,

Klein²,

Levingston³

et al. 2013

International Immunopharmacology

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“…While animal models used in diabetes have been very valuable in providing mechanistic insights, the underlying confounding factors of the other organs such as the pancreas and brain can seldom be ruled out in the in vivo studies [6]. Moreover, since functional culture of primary cells such as primary hepatocytes is challenging, the in vitro studies that are conducted using modified immortalized cell lines provide limited value [7][8][9]. An alternative is to use microfluidic organ-on-chips that offer a controlled microenvironment to facilitate the physiological function of the cells.…”

Section: Introductionmentioning

confidence: 99%

Investigation of insulin resistance through a multiorgan microfluidic organ-on-chip

Tanataweethum¹,

Trang²,

Lee³

et al. 2022

Biomed. Mater.

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The development of hepatic insulin resistance (IR) is a critical factor in developing type 2 diabetes (T2D), where insulin fails to inhibit hepatic glucose production but retains its capacity to promote hepatic lipogenesis. Improving insulin sensitivity can be effective in preventing and treating T2D. However, selective control of glucose and lipid synthesis has been difficult. It is known that excess white adipose tissue is detrimental to insulin sensitivity, whereas brown adipose tissue transplantation can restore it in diabetic mice. However, challenges remain in our understanding of liver-adipose communication because the confounding effects of hypothalamic regulation of metabolic function cannot be ruled out in previous studies. There is a lack of in vitro models that use primary cells to study cellular-crosstalk under insulin resistant conditions. Building upon our previous work on the microfluidic primary liver and adipose organ-on-chips, we report for the first time the development of integrated insulin resistant liver-adipose (white and brown) organ-on-chip. The design of the microfluidic device was carried out using computational fluid dynamics; the experimental studies were conducted by carrying out detailed biochemical analysis RNA-seq analysis on both cell types. Further, we tested the hypothesis that brown adipocytes regulated both hepatic insulin sensitivity and lipogenesis. Our results show effective co-modulation of hepatic glucose and lipid synthesis through a platform for identifying potential therapeutics for IR and diabetes.

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“…Related to the mechanism in which the conditioned medium had beneficial effects, some considerations are needed to choose the cells to produce conditioned medium because different types of cells will secrete different proteins or growth factors. There are many sources of the cells to produce or harvest conditioned medium, such as mesenchymal stem cells, neural stem cells, or adipocyte-derived stem cells [ 9 10 11 12 ].…”

Section: Introductionmentioning

confidence: 99%

Conditioned medium of E17 rat brain cells induced differentiation of primary colony of mice blastocyst into neuron-like cells

et al. 2021

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Background Conditioned medium is the medium obtained from certain cultured cells and contained secretome from the cells. The secretome, which can be in the form of growth factors, cytokines, exosomes, or other proteins secreted by the cells, can induce the differentiation of cells that still have pluripotent or multipotent properties. Objectives This study examined the effects of conditioned medium derived from E17 rat brain cells on cells with pluripotent properties. Methods The conditioned medium used in this study originated from E17 rat brain cells. The CM was used to induce the differentiation of primary colonies of mice blastocysts. Primary colonies were stained with alkaline phosphatase to analyze the pluripotency. The morphological changes in the colonies were examined, and the colonies were stained with GFAP and Neu-N markers on days two and seven after adding the conditioned medium. Results The conditioned medium could differentiate the primary colony, beginning with the formation of embryoid-body-like structure; round GFAP positive cells were identified. Finally, neuron-like cells testing positive for Neu-N were observed on the seventh day after adding the conditioned medium. Conclusions Conditioned medium from different species, in this case, E17 rat brain cells, induced and promoted the differentiation of the primary colony from mice blastocysts into neuron-like cells. The addition of CM mediated neurite growth in the differentiation process.

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Conditioned media from (pre)adipocytes stimulate fibrinogen and PAI-1 production by HepG2 hepatoma cells

Cited by 7 publications

References 42 publications

Adipocytes as immune regulatory cells

Adipocytes as immune regulatory cells

Investigation of insulin resistance through a multiorgan microfluidic organ-on-chip

Conditioned medium of E17 rat brain cells induced differentiation of primary colony of mice blastocyst into neuron-like cells

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