Rahm M, Hultgårdh-Nilsson A
Department of Medical Cell Genetics, Medical Nobel Institute, Karolinska Institutet, Stockholm, Sweden.
Biochem Biophys Res Commun. 1990 Dec 31;173(3):1322-30. doi: 10.1016/s0006-291x(05)80932-5.
Neurokinin A (NKA), a neuropeptide belonging to the tachykinin family, induced c-fos proto-oncogene mRNA expression in serum-deprived L6J1 rat skeletal myoblasts in vitro. The marked increase reached maximal levels after 15 to 30 min. In contrast to this, c-jun and c-myc proto-oncogene expression were only slightly induced, with peak levels after 30 min. NKA did not stimulate DNA synthesis or cell proliferation in serum-deprived L6J1 myoblasts. We demonstrate a relationship between NKA treatment and induction of c-fos, c-jun and c-myc mRNA expression in serum-deprived L6J1 rat myoblasts. The results on DNA synthesis and cell proliferation indicate that the induced proto-oncogene expression alone is not enough to induce a cellular response to NKA. Possible mechanisms of action are discussed.
神经激肽A（NKA）是一种属于速激肽家族的神经肽，它在体外可诱导血清饥饿的L6J1大鼠骨骼肌成肌细胞中c-fos原癌基因mRNA的表达。显著的增加在15至30分钟后达到最高水平。与此相反，c-jun和c-myc原癌基因的表达仅受到轻微诱导，在30分钟后达到峰值水平。NKA不会刺激血清饥饿的L6J1成肌细胞中的DNA合成或细胞增殖。我们证明了在血清饥饿的L6J1大鼠成肌细胞中，NKA处理与c-fos、c-jun和c-myc mRNA表达的诱导之间存在关联。关于DNA合成和细胞增殖的结果表明，单独诱导原癌基因表达不足以诱导细胞对NKA产生反应。文中讨论了可能的作用机制。
