Department of Physiology and Pharmacology, University of Toledo College of Medicine, Toledo, OH 43614, USA.
Prostaglandins Other Lipid Mediat. 2012 Jan;97(1-2):1-16. doi: 10.1016/j.prostaglandins.2011.10.002. Epub 2011 Nov 15.
MSCs are considered to be the natural precursors to adipocyte development through the process of adipogenesis. A link has been established between decreased protective effects of EETs or HO-1 and their interaction in metabolic syndrome. Decreases in HO-1 or EET were associated with an increase in adipocyte stem cell differentiation and increased levels of inflammatory cytokines. EET agonist (AKR-I-27-28) inhibited MSC-derived adipocytes and decreased the levels of inflammatory cytokines. We further describe the role of CYP-epoxygenase expression, HO expression, and circulating cytokine levels in an obese mouse, ob/ob(-/-) mouse model. Ex vivo measurements of EET expression within MSCs derived from ob/ob(-/-) showed decreased levels of EETs that were increased by HO induction. This review demonstrates that suppression of HO and EET systems exist in MSCs prior to the development of adipocyte dysfunction. Further, adipocyte dysfunction can be ameliorated by induction of HO-1 and CYP-epoxygenase, i.e. EET.
间充质干细胞（MSCs）被认为是通过脂肪生成过程向脂肪细胞发育的天然前体细胞。已经建立了 EET 或 HO-1 保护作用降低及其在代谢综合征中的相互作用之间的联系。HO-1 或 EET 的减少与脂肪干细胞分化增加和炎症细胞因子水平升高有关。EET 激动剂（AKR-I-27-28）抑制 MSC 来源的脂肪细胞，并降低炎症细胞因子水平。我们进一步描述了 CYP-环氧合酶表达、HO 表达和循环细胞因子水平在肥胖小鼠（ob/ob(-/-) 模型）中的作用。来自 ob/ob(-/-) 的 MSC 中 EET 表达的体外测量显示 EET 水平降低，HO 诱导后增加。本综述表明，在脂肪细胞功能障碍发生之前，HO 和 EET 系统在 MSCs 中受到抑制。此外，通过诱导 HO-1 和 CYP-环氧合酶（即 EET）可以改善脂肪细胞功能障碍。
