Induction of innervation by encapsulated adipocytes with engineered vitamin A metabolism

Shen, Qiwen; Yasmeen, Rumana; Marbourg, Jessica; Xu, Lu; Yu, Lianbo; Fadda, Paolo; Flechtner, Alan D.; Lee, L. James; Popovich, Phillip G.; Ziouzenkova, Ouliana

doi:10.1016/j.trsl.2017.10.005

Cited by 9 publications

(10 citation statements)

References 51 publications

(76 reference statements)

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“…The mechanism by which EREG could contribute to energy expenditure state remains unknown, since EREG was not able to induce direct thermogenic responses in preadipocytes (Kir, White, Kleiner, Kazak, Cohen, Baracos & Spiegelman 2014). However, thermogenic modifications in adipocytes deficient in aldehyde dehydrogenase a1 were accompanied by Ereg expression (Shen, Yasmeen, Marbourg, Xu, Yu, Fadda, Flechtner, Lee, Popovich & Ziouzenkova 2018). Here we test EREG efficacy in the induction of LEP secretion, in vivo and in vitro, and the relevance of this secretion for the induction of catabolic energy expenditure states.…”

Section: Introductionmentioning

confidence: 99%

Epiregulin induces leptin secretion and energy expenditure in high-fat diet-fed mice

Yasmeen

Shen

Lee

et al. 2018

Journal of Endocrinology

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Adipokine leptin regulates neuroendocrine circuits that control energy expenditure, thermogenesis, and weight loss. However, canonic regulators of leptin secretion, such as insulin and malonyl CoA, do not support these processes. We hypothesize that epiregulin (EREG), a growth factor that is secreted from fibroblasts under thermogenic and cachexia conditions, induces leptin secretion associated with energy dissipation. The effects of EREG on leptin secretion were studied ex vivo, in the intra-abdominal, white adipose tissue (iAb WAT) explants, as well as in vivo, in wild type mice with diet-induced obesity (DIO) and in ob/ob mice. These mice were pair fed a high-fat diet and treated with intraperitoneal injections of EREG. EREG increased leptin production and secretion in a dose-dependent manner in iAb fat explants via the EGFR/MAPK pathway. After 2 weeks, the plasma leptin concentration was increased by 215% in the EREG treated group compared to the control DIO group. EREG treated DIO mice had an increased metabolic rate and core temperature during the active dark cycle, and displayed cold-induced thermogenesis. EREG treatment reduced iAb fat mass, the major site of leptin secretion, but did not reduce the mass of the other fat depots. In the iAb fat, expression of genes supporting mitochondrial oxidation and thermogenesis was increased in EREG-treated mice vs. control DIO mice. All metabolic and gene regulation effects of EREG-treatment were abolished in leptin-deficient ob/ob mice. Our data revealed a new role of EREG in induction of leptin secretion leading to the energy expenditure state. EREG could be a potential target protein to regulate hypo- and hyperleptinemia, underlying metabolic and immune diseases.

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Section: Introductionmentioning

confidence: 99%

Epiregulin induces leptin secretion and energy expenditure in high-fat diet-fed mice

Yasmeen

Shen

Lee

et al. 2018

Journal of Endocrinology

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“…Some research showed that ALDH1A1 could transform precursor retinaldehydes into retinoic acid receptor (RAR) which was a kind of steroid hormone receptor ( Kiefer et al, 2012 ). Interestingly, deficiency of the ALDH1A1 gene also limited the formation of RAR ( Shen et al, 2018 ). Besides, Hammond et al (2001) demonstrated that antagonists of retinoic acid receptors (RARs) effectively inhibited the growth prostate carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

Silybin Prevents Prostate Cancer by Inhibited the ALDH1A1 Expression in the Retinol Metabolism Pathway

Jiang

Song

Jiang

et al. 2020

Front. Cell Dev. Biol.

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Background Silybin was known to exert inhibition in prostate cancer, but the underlying mechanism remained largely unknown. This study was designed to find out the potential target of Silybin on prostate cancer and explore the relative mechanisms. Methods Firstly, we screened the possible targets of Silybin through the PubChem database and Subpathway – GM. Then DU145 cells were transferred to investigate the correction about related targets, magnetic bead sorting and flow cytometry were used to sort and identify the cells. Proliferation, migration and invasion ability of DU145 cells were detected by MTT assay, Transwell assay, plate clonality and sphere formation assay. BALB/c nude mice were constructed models with implanted sarcoma and measured the tumor volume every 5 days as wells tumor weight. The levels of proteins were detected by Western blot and immunocytochemistry. RT-PCR was selected to test the expression of protein’s mRNA. Results It was screened out the ALDH1A1 was highly correlated with subpathways of the Silybin risk metabolic pathway. And ALDH1A1 expression was positively correlated RARα with Ets1 by interfering with the ALDH1A1 gene. Importantly, ALDH1A1(+) cells showed proliferation, migration and invasion ability. In addition, it showed that Silybin exerted the inhibition on prostate cells by suppressed the proliferation, migration and invasion ability of cells in vitro experiment. Silybin also reduced the tumor volume and weight. And Silybin displayed obviously reduced the proteins and mRNA of ALDH1A1, RARα, Ets1 and MMP9 expressions. Conclusion Our results indicated that Silybin showed inhibition of prostate cancer and the mechanism was involving with downregulating ALDH1A1 expression, thereby inhibiting the activation of RARα and preventing the activation of Ets1 to inhibit the growth and invasion of prostate cancer.

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“…These observations suggest that perhaps EphB2 forward signaling is important for the inhibition of adipogenesis by MSC. Moreover, Eph-ephrin communication has been reported in white adipose tissue, where ephrin-A4 and ephrin-A5 were found to be a downstream signaling pathway to aldehyde dehydrogenase, which stimulates the development and innervation of white adipose tissue (Shen et al, 2018 ). Also, ephrin-B1 was identified to be down-regulated in mature adipocytes of obese mice and shown to suppress the adipose inflammatory response (Mori et al, 2013 ).…”

Section: The Role Of Eph-ephrin Signaling Within the Mesenchymal Linementioning

confidence: 99%

Eph-Ephrin Signaling Mediates Cross-Talk Within the Bone Microenvironment

Arthur

Gronthos

2021

Front. Cell Dev. Biol.

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Skeletal integrity is maintained through the tightly regulated bone remodeling process that occurs continuously throughout postnatal life to replace old bone and to repair skeletal damage. This is maintained primarily through complex interactions between bone resorbing osteoclasts and bone forming osteoblasts. Other elements within the bone microenvironment, including stromal, osteogenic, hematopoietic, endothelial and neural cells, also contribute to maintaining skeletal integrity. Disruption of the dynamic interactions between these diverse cellular systems can lead to poor bone health and an increased susceptibility to skeletal diseases including osteopenia, osteoporosis, osteoarthritis, osteomalacia, and major fractures. Recent reports have implicated a direct role for the Eph tyrosine kinase receptors and their ephrin ligands during bone development, homeostasis and skeletal repair. These membrane-bound molecules mediate contact-dependent signaling through both the Eph receptors, termed forward signaling, and through the ephrin ligands, referred to as reverse signaling. This review will focus on Eph/ ephrin cross-talk as mediators of hematopoietic and stromal cell communication, and how these interactions contribute to blood/ bone marrow function and skeletal integrity during normal steady state or pathological conditions.

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Induction of innervation by encapsulated adipocytes with engineered vitamin A metabolism

Cited by 9 publications

References 51 publications

Epiregulin induces leptin secretion and energy expenditure in high-fat diet-fed mice

Epiregulin induces leptin secretion and energy expenditure in high-fat diet-fed mice

Silybin Prevents Prostate Cancer by Inhibited the ALDH1A1 Expression in the Retinol Metabolism Pathway

Eph-Ephrin Signaling Mediates Cross-Talk Within the Bone Microenvironment

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