Upregulation of the p75 low-affinity neurotrophin receptor by phagocytically active perivascular active cells in the rat neural lobe.
Upregulation of the p75 low-affinity neurotrophin receptor by phagocytically active perivascular active cells in the rat neural lobe.
复制标题
大鼠神经叶中具有吞噬活性的血管周围活性细胞对 p75 低亲和力神经营养素受体的上调。
DOI：
10.1007/s004410000295
复制
发表时间：
2001
影响因子：
3.6
通讯作者：
Paden,CM
中科院分区：
文献类型：
--
作者：
Watt,JA;Paden,CM
在大鼠神经叶 (NL) 部分去神经和全身施用脂多糖 (LPS) 后的轴突变性过程中，通过免疫细胞化学方法在光和超微结构水平上研究了 p75 低亲和力神经营养蛋白受体 (p75NTR) 的表达。与年龄匹配的假手术对照相比，部分去神经动物的 NL 中 p75NTR 免疫反应性的强度和程度显着增加，在去神经后 5-10 天观察到，免疫反应性在 35 天时恢复到对照值。 p75NTR 定位与 C3bi 补体受体（一种小胶质细胞标记物）和 S100（一种星形胶质细胞特异性 Ca2+ 结合蛋白）的双标记共聚焦比较显示没有共定位。免疫电子显微镜检查表明，p75NTR 免疫反应性存在于位于 NL 广泛血管周围空间内的细胞亚群中。在光或超微结构水平上没有观察到 p75NTR 免疫反应性垂体细胞或内皮细胞的例子。在吞噬细胞外碎片的质膜以及血管周围细胞的细胞质内的内衬液泡的内吞欧米伽轮廓周围经常观察到密集的p75NTR免疫反应性。 p75NTR与吞噬作用的关联通过共聚焦显微镜得到证实，显示p75NTR存在于所有表达ED-1抗原的细胞中，其仅限于吞噬细胞的溶酶体膜（Damoiseaux等人，1994）。同样，在全身施用 LPS 后，在 NL 中观察到 p75NTR 和 ED-1 免疫反应性显着增加。这些结果表明 p75NTR 免疫反应性的调节与诱导大鼠 NL 血管周围细胞高水平吞噬活性的条件之间存在很强的相关性。讨论了理解吞噬细胞支持对神经元损伤的代偿反应的机制的意义。
Expression of the p75 low-affinity neurotrophin receptor (p75NTR) was investigated immunocytochemically at the light and ultrastructural level during the axonal degeneration that follows partial denervation of the rat neural lobe (NL) and following systemic administration of lipopolysaccharide (LPS). A significant increase in the intensity and extent of p75NTRimmunoreactivity in the NL of partially denervated animals compared with age-matched, sham-operated controls was observed at 5–10 days postdenervation, with immunoreactivity returning to control values by 35 days. Dual-label confocal comparison of p75NTRlocalization with that of the C3bi complement receptor, a microglial marker, and S100, an astrocyte-specific Ca2+-binding protein, revealed no colocalization. Immunoelectron-microscopic examination demonstrated that the p75NTRimmunoreactivity is present in a subpopulation of cells located within the extensive perivascular space of the NL. No examples of p75NTR-immunoreactive pituicytes or endothelia were observed at the light or ultrastructural level. Dense p75NTRimmunoreactivity was frequently observed surrounding endocytotic omega profiles of plasmalemma engulfing extracellular debris as well as lining vacuoles within the cytoplasm of perivascular cells. The association of p75NTRwith phagocytosis was confirmed by confocal microscopy, showing the presence of p75NTRin all cells expressing the ED-1 antigen, which is restricted to the lysosomal membrane of phagocytes (Damoiseaux et al. 1994). Likewise, a marked increase in p75NTRand ED-1 immunoreactivity was observed in the NL following systemic administration of LPS. These results suggest a strong correlation between modulation of p75NTRimmunoreactivity and conditions that induce high levels of phagocytic activity by perivascular cells in the NL of the rat. Implications for understanding the mechanisms by which phagocytes may support compensatory responses to neuronal injury are discussed.