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首页> 外文期刊>Endocrinology >Fibroblast growth factor-2 autofeedback regulation in pituitary folliculostellate TtT/GF cells.
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Fibroblast growth factor-2 autofeedback regulation in pituitary folliculostellate TtT/GF cells.

机译：垂体滤泡状TtT / GF细胞中成纤维细胞生长因子2的自动反馈调节。

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To investigate paracrine regulation of pituitary cell growth, we tested fibroblast growth factor (FGF) regulation of TtT/GF folliculostellate (FS) cells. FGF-2, and FGF-4 markedly induced cell proliferation, evidenced by induction of pituitary tumor transforming gene-1 (Pttg1) mRNA expression and percentage of cells in S phase. Signaling for FGF-2-induced FS cell proliferation was explored by specific pharmacological inhibition. A potent inhibitory effect on FGF-2 action was observed by blocking of Src tyrosine kinase with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine (>or=0.1 microm), followed by protein kinase C (PKC) inhibition with GF109203X. Treatment with FGF-2 (30 ng/ml; 10 min) activated phosphorylation of signal transducer and activator of transcription-3, ERK, stress-activated protein kinase/c-Jun N-terminal kinase, Akt, and focal adhesion kinase. Src inhibition with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine suppressed FGF-2-induced Akt and focal adhesion kinase, indicating effects downstream of FGF-2-induced Src activation. FGF-2 also markedly induced its own mRNA expression, peaking at 2-4 h, and this effect was suppressed by Src tyrosine kinase inhibition. The PKC inhibitor GF109203X abolished FGF-2 autoinduction, indicating PKC as the primary pathway involved in FGF-2 autoregulation in these cells. In addition to pituitary FGF-2 paracrine activity on hormonally active cells, these results show an autofeedback mechanism for FGF-2 in non-hormone-secreting pituitary FS cells, inducing cell growth and its own gene expression, and mediated by Src/PKC signaling.
机译：为了研究垂体旁分泌对垂体细胞生长的调节，我们测试了TtT / GF卵泡星状细胞（FS）细胞的成纤维细胞生长因子（FGF）调节。 FGF-2和FGF-4可以显着诱导细胞增殖，这通过诱导垂体肿瘤转化基因1（Pttg1）mRNA表达和S期细胞百分比来证明。通过特定的药理学抑制作用探索了FGF-2诱导的FS细胞增殖的信号。通过用4-氨基-5-（4-氯苯基）-7-（叔丁基）吡唑并[3,4-d]嘧啶阻断Src酪氨酸激酶，观察到了对FGF-2作用的强抑制作用（>或= 0.1微米），然后用GF109203X抑制蛋白激酶C（PKC）。用FGF-2（30 ng / ml; 10分钟）处理可激活信号转导和转录激活子3的磷酸化，ERK，应激激活的蛋白激酶/ c-Jun N末端激酶，Akt和粘着斑激酶。用4-氨基-5-（4-氯苯基）-7-（叔丁基）吡唑并[3,4-d]嘧啶对Src的抑制作用抑制了FGF-2诱导的Akt和粘着斑激酶，表明了FGF-2的下游作用-诱导的Src激活。 FGF-2还显着诱导其自身的mRNA表达，在2-4 h达到峰值，这种作用被Src酪氨酸激酶抑制所抑制。 PKC抑制剂GF109203X废除了FGF-2自诱导，表明PKC是这些细胞中FGF-2自调控的主要途径。除了对激素活性细胞的垂体FGF-2旁分泌活性外，这些结果还显示了非分泌激素的垂体FS细胞中FGF-2的自动反馈机制，诱导细胞生长及其自身基因表达，并由Src / PKC信号传导介导。 。

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