TGF‐β Rescues Target‐deprived Preganglionic Sympathetic Neurons in the Spinal Cord
TGF‐β Rescues Target‐deprived Preganglionic Sympathetic Neurons in the Spinal Cord
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TGF-β 拯救脊髓中目标缺失的节前交感神经元
DOI：
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发表时间：
1996
影响因子：
3.4
通讯作者：
K. Unsicker
中科院分区：
文献类型：
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作者：
D. Blottner;N. Wolf;A. Lachmund;K. Flanders;K. Unsicker
转化生长因子β（Transforming growth factors β，TGF-β）是一个多效性细胞因子家族，广泛分布于发育和成人神经系统。为了进一步确定TGF-β的神经功能，我们在成年大鼠肾上腺髓质中定位了TGF-β亚型1、2和3，并研究了一种代表性家族成员TGF-β2对那些支配肾上腺嗜铬细胞并在肾上腺髓质破坏后死亡的脊髓神经元的神经保护能力。肾上腺髓质的单侧延髓性破坏导致25%的交感节前神经元消失，交感节前神经元位于胸脊髓第7-10节段的中间外侧（IML）柱，可以通过NADPH-黄递酶选择性标记。肾上腺髓质切除后消失的神经元构成了支配肾上腺髓质的全套神经元。将浸泡有0.5 μg TGF-β2的明胶海绵植入肾上腺创伤腔内，可挽救损伤侧同侧IML中的所有脊髓神经元。细胞色素C无效。将[125 I]TGF-β2注射到肾上腺髓质中不会导致脊髓神经元的逆行转运和随后的标记，这表明TGF-β可能通过间接机制发挥其神经保护作用。应用于培养的肾上腺皮质细胞的TGF-β并未明显增加成纤维细胞生长因子-2的mRNA量，成纤维细胞生长因子-2是交感神经节前脊髓神经元的一种既定营养分子。因此，TGF-β发挥其神经营养作用的机制尚不清楚。即便如此，我们的数据提供了第一个证据，表明TGF-β可能在体内控制脊髓神经元群体的维持中发挥重要作用。
Transforming growth factors β (TGF‐β), a family of pleiotropic cytokines, are widely distributed in the developing and adult nervous system. In order to further determine the neural functions of TGF‐β, we have localized the TGF‐β isoforms 1, 2 and 3 in the adult rat adrenal medulla and studied the neuroprotective capacity of one representative family member, TGF‐β2, for those spinal cord neurons which innervate adrenal chromaffin cells and which die after destruction of the adrenal medulla. Unilateral electrothermal destruction of the adrenal medulla led to the disappearance of 25% of sympathetic preganglionic neurons, which are located in the intermediolateral (IML) column of thoracic spinal cord segments 7–10 and can be selectively marked by NADPH‐diaphorase. The neurons which disappeared following adrenomedullectomy constitute the full set of neurons that innervate the adrenal medulla. Implantation of gelfoam soaked with 0.5 μg TGF‐β2 into the adrenal wound cavity rescued all spinal cord neurons in the IML ipsilaterally to the lesioned side. Cytochrome c was not effective. Injections of [125l]TGF‐β2 into the adrenal medulla did not result in retrograde transport and subsequent labelling of spinal cord neurons, suggesting that TGF‐β may exert its neuroprotective actions by indirect mechanisms. TGF‐β applied to cultured adrenocortical cells did not overtly increase the amount of mRNA for fibroblast growth factor‐2, an established trophic molecule for sympathetic preganglionic spinal cord neurons. The mechanisms by which TGF‐β exerts its neurotrophic effect are therefore unclear. Even so, our data provide the first evidence that TGF‐β may play an important role in vivo in the control of maintenance of a population of spinal cord neurons.
DOI：
10.1073/pnas.88.17.7797
发表时间：
1991-09-01
影响因子：
11.1
作者：
DAWSON, TM;BREDT, DS;SNYDER, SH
通讯作者：
SNYDER, SH