Immuno-Magnetic Isolation and Thermogenic Differentiation of White Adipose Tissue Progenitor Cells

Babaeikelishomi, Rohollah; Bayindir‐Buchhalter, Irem; Meln, Irina; Vegiopoulos, Alexandros

doi:10.1007/978-1-4939-6820-6_5

Cited by 6 publications

(8 citation statements)

References 17 publications

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“…However, this system and its regulation appear to underlie an unanticipated complexity. In fact, previous studies demonstrated the ω6 eicosanoid prostacyclin (PGI2, which is derived from ARA via COX-dependent metabolization) as a positive modulator of UCP1 expression and brite adipogenesis in human and murine cellular model systems (42,(45)(46)(47). In line with these findings, transgenic mice with constitutive overexpression of COX-2 (the inducible isoform of COX) show enhanced browning of WAT and resistance to diet-induced obesity (46).…”

Section: Discussionmentioning

confidence: 78%

Impact of dietary ω3 polyunsaturated fatty acid supplementation on brown and brite adipocyte function

Ghandour

Colson

Giroud

et al. 2018

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 78%

Impact of dietary ω3 polyunsaturated fatty acid supplementation on brown and brite adipocyte function

Ghandour

Colson

Giroud

et al. 2018

Journal of Lipid Research

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“…To isolate progenitor cells for seeding or sorting [25], gWAT was dissected and digested as described previously [29], [30]. The Lin-Sca1+ fraction cells were counted using a hemocytometer and seeded on laminin-coated 24-well plates.…”

Section: Methodsmentioning

confidence: 99%

Diet-dependent function of the extracellular matrix proteoglycan Lumican in obesity and glucose homeostasis

Wolff

Taranko

Meln

et al. 2019

Molecular Metabolism

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ObjectiveExtracellular matrix remodeling is required for adipose expansion under increased caloric intake. In turn, inhibited expandability due to aberrant collagen deposition promotes insulin resistance and progression towards the metabolic syndrome. An emerging role for the small leucine-rich proteoglycan Lumican in metabolically driven nonalcoholic fatty liver disease sparks an interest in further understanding its role in diet-induced obesity and metabolic complications.MethodsWhole body ablation of Lumican (Lum−/−) gene and adeno-associated virus-mediated over-expression were used in combination with control or high fat diet to assess energy balance, glucose homeostasis as well as adipose tissue health and remodeling.ResultsLumican was found to be particularly enriched in the stromal cells isolated from murine gonadal white adipose tissue. Likewise murine and human visceral fat showed a robust increase in Lumican as compared to fat from the subcutaneous depot. Lumican null female mice exhibited moderately increased fat mass, decreased insulin sensitivity and increased liver triglycerides in a diet-dependent manner. These changes coincided with inflammation in adipose tissue and no overt effects in adipose expandability, i.e. adipocyte formation and hypertrophy. Lumican over-expression in visceral fat and liver resulted in improved insulin sensitivity and glucose clearance.ConclusionsThese data indicate that Lumican may represent a functional link between the extracellular matrix, glucose homeostasis, and features of the metabolic syndrome.

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“…Adipose progenitors were isolated by magnetic-activated cell sorting (MACS) approach, as previously described (17,18). Briefly, the SVF …”

Section: Progenitor Isolation By Macsmentioning

confidence: 99%

Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

et al. 2018

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The transient activation of inflammatory networks is required for adipose tissue remodeling including the "browning" of white fat in response to stimuli such as 3-adrenergic receptor activation. In this process, white adipose tissue acquires thermogenic characteristics through the recruitment of so-called beige adipocytes. We investigated the downstream signaling pathways impinging on adipocyte progenitors that promote de novo formation of adipocytes. We showed that the Jak family of kinases controlled TGF signaling in the adipose tissue microenvironment through Stat3 and thereby adipogenic commitment, a function that was required for beige adipocyte differentiation of murine and human progenitors. Jak/Stat3 inhibited TGF signaling to the transcription factors Srf and Smad3 by repressing local Tgfb3 and Tgfb1 expression before the core transcriptional adipogenic cascade was activated. This pathway cross-talk was triggered in stromal cells by ATGL-dependent adipocyte lipolysis and a transient wave of IL-6 family cytokines at the onset of adipose tissue remodeling induced by 3-adrenergic receptor stimulation. Our results provide insight into the activation of adipocyte progenitors and are relevant for the therapeutic targeting of adipose tissue inflammatory pathways.

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Immuno-Magnetic Isolation and Thermogenic Differentiation of White Adipose Tissue Progenitor Cells

Cited by 6 publications

References 17 publications

Impact of dietary ω3 polyunsaturated fatty acid supplementation on brown and brite adipocyte function

Impact of dietary ω3 polyunsaturated fatty acid supplementation on brown and brite adipocyte function

Diet-dependent function of the extracellular matrix proteoglycan Lumican in obesity and glucose homeostasis

Jak-TGFβ cross-talk links transient adipose tissue inflammation to beige adipogenesis

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