Yamashita H, Sato N, Kizaki T, Oh-ishi S, Segawa M, Saitoh D, Ohira Y, Ohno H
Department of Hygiene, National Defense Medical College, Tokorozawa, Japan.
Cell Growth Differ. 1995 Nov;6(11):1457-62.
To elucidate the role of norepinephrine (NE) in the hyperplasia of brown adipose tissue (BAT), we investigated the effects of NE on the expression of fibroblast growth factor-2 (FGF-2) in rat brown adipocyte primary culture and on capillary growth in an in vitro angiogenesis model in which microvascular fragments and brown adipocyte precursor cells isolated from rat BAT were grown in coculture. NE significantly increased the number of brown adipocyte precursor cells. The NE effect on cell proliferation was greatly inhibited by anti-FGF-2-specific antibody. Likewise,NE considerably increased the levels of FGF-2 mRNA and the antigen in brown adipocyte primary culture. The ability of NE to stimulate the expression of FGF-2 mRNA was blocked by actinomycin D or was inhibited partly by propranolol. Moreover, NE considerably increased the in vitro capillary growth and the level of FGF-2 antigen in the coculture. These results suggest that NE is a crucial factor to mediate FGF-2 production, in part via the beta-adrenergic receptor, in rat brown adipocytes and to stimulate the cell proliferation and capillary growth in BAT by an autocrine/paracrine mechanism.
为阐明去甲肾上腺素（NE）在棕色脂肪组织（BAT）增生中的作用，我们研究了NE对大鼠棕色脂肪细胞原代培养中成纤维细胞生长因子-2（FGF-2）表达的影响，以及对体外血管生成模型中毛细血管生长的影响，该模型中，从大鼠BAT分离的微血管片段和棕色脂肪细胞前体细胞共培养生长。NE显著增加了棕色脂肪细胞前体细胞的数量。抗FGF-2特异性抗体极大地抑制了NE对细胞增殖的作用。同样，NE显著增加了棕色脂肪细胞原代培养中FGF-2 mRNA和抗原的水平。放线菌素D阻断了NE刺激FGF-2 mRNA表达的能力，普萘洛尔则部分抑制了该能力。此外，NE显著增加了共培养中的体外毛细血管生长和FGF-2抗原水平。这些结果表明，NE是介导大鼠棕色脂肪细胞中FGF-2产生的关键因素，部分通过β-肾上腺素能受体，并通过自分泌/旁分泌机制刺激BAT中的细胞增殖和毛细血管生长。
