Galectin-1 in injured rat spinal cord: implications for macrophage phagocytosis and neural repair.
Galectin-1 in injured rat spinal cord: implications for macrophage phagocytosis and neural repair.
复制标题
DOI：
10.1016/j.mcn.2014.12.006
复制
发表时间：
2015-01
期刊：
影响因子：
--
通讯作者：
Popovich PG
中科院分区：
文献类型：
--
作者：
Gaudet AD;Sweet DR;Polinski NK;Guan Z;Popovich PG
半乳糖凝集素(Gal)-1是一种小的碳水化合物结合蛋白和免疫调节细胞因子，在周围神经损伤部位局部合成。在这种环境下，Gal1可以促进受损外周轴突的再生，部分原因是通过改变招募到损伤部位的巨噬细胞的功能。与受损的周围神经不同，巨噬细胞不能促进受损中枢神经系统（CNS）的轴突再生，这可能是因为Gal1水平没有得到适当的调节。由于内源性Gal1在中枢神经系统损伤后的动态和细胞定位尚未得到严格的表征，我们研究了标准化挫伤大鼠脊髓中Gal1的时空分布。尽管Gal1在未损伤的脊髓中不表达，但在脊髓损伤后，Gal1明显上调，尤其是在病变核心。损伤后3-28天，约40%的病变局部巨噬细胞表达Gal1, 7-28天，约45%的病变边缘星形胶质细胞表达Gal1。大多数病变定位的Gal1+巨噬细胞不表达吞噬标志物ED1， Gal1+细胞含有较少的被吞噬脂质。这些数据表明，巨噬细胞（和星形胶质细胞）对Gal1的时间和位置依赖性调节可能对脊髓损伤后吞噬、炎症/胶质形成和轴突生长的调节很重要。
Galectin (Gal)-1 is a small carbohydrate-binding protein and immune modulatory cytokine that is synthesized locally at the site of peripheral nerve injury. In this environment, Gal1 can promote regeneration of injured peripheral axons, in part by modifying the function of macrophages recruited to the site of injury. Unlike in injured peripheral nerves, macrophages do not promote axon regeneration in the injured central nervous system (CNS), perhaps because Gal1 levels are not regulated appropriately. Because the dynamics and cellular localization of endogenous Gal1 have not been rigorously characterized after CNS injury, we examined the spatio-temporal distribution of Gal1 in rat spinal cords subjected to a standardized contusion injury. Whereas Gal1 was not expressed in uninjured spinal cord, it was significantly upregulated after SCI, especially within the lesion core. Gal1 was expressed in ~40% of lesion-localized macrophages at 3–28 days post-injury (dpi), and in ~45% of astrocytes in the lesion border at 7–28 dpi. Most lesion-localized Gal1+ macrophages did not express the phagocytosis marker ED1, and Gal1+ cells contained less phagocytosed lipids. These data suggest time- and location-dependent regulation of Gal1 by macrophages (and astrocytes) could be important for modulating phagocytosis, inflammation/gliosis, and axon growth after SCI.
登录
查看更多内容
影响因子：
4.2
作者：
Carrico, Kimberly M.;Vaishnav, Radhika;Hall, Edward D.
通讯作者：
Hall, Edward D.
DOI：
10.1046/j.1432-1327.2000.01311.x
发表时间：
2000-05-01
期刊：
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子：
--
作者：
Inagaki, Y;Sohma, Y;Kadoya, T
通讯作者：
Kadoya, T
影响因子：
5.3
作者：
Greenhalgh, Andrew D.;David, Samuel
通讯作者：
David, Samuel
影响因子：
5.3
作者：
McGraw, J;Gaudet, AD;Ramer, MS
通讯作者：
Ramer, MS
DOI：
10.1523/jneurosci.3257-09.2009
发表时间：
2009-10-28
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Kigerl KA;Gensel JC;Ankeny DP;Alexander JK;Donnelly DJ;Popovich PG
通讯作者：
Popovich PG