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    • In the adult normal spinal cord the resident

    2021-12-06

    In the adult normal spinal cord, the resident cells mainly include neurons, astrocytes, oligodendroglia and microglia (Lecca et al., 2012, Miyagi et al., 2012). After SCI, the lesion microenvironment is complex, which includes the functional changes of CNS resident cells and the infiltration of leukocytes (David et al., 2015, Gordh et al., 2006, Karimi-Abdolrezaee and Billakanti, 2012, Popovich et al., 1997, Wang et al., 2009). To detect the cellular localization of HK3 in sham-opened and injured spinal cords, we used β-tubulin III, GFAP, CNPase, IBA-1, CD68 and CD45 to label neurons (von Bohlen Und Halbach, 2007), astrocytes (Eng et al., 2000), oligodendroglia (Rajkowska et al., 2015), microglia (Babcock et al., 2003), activated microglia/macrophages (Holness and Simmons, 1993) and infiltrated total leukocytes (Harvath et al., 1991), respectively. The immunofluorescence staining results indicated that HK3 is mainly expressed in astrocytes, neurons and microglia in the normal spinal cords. This is consistent with the recent report which demonstrated that HK3 is expressed in astrocytes and neurons in the cortex of mouse and human (Lundgaard et al., 2015). However, for the first time to our knowledge, we report that HK3 is expressed in microglia in spinal cord. In contrast, HK3 was almost not detected in oligodendroglia. This is also consistent with two previous reports which demonstrated that oligodendroglia contain relatively low levels of HK compared with whole p 00 or with isolated other neural structures (Kao-Jen and Wilson, 1980, Snyder and Wilson, 1983). After SCI, from complete sections, we can find that different cell populations are distributed in different regions (Fig. 3, Fig. 4, Fig. 5, Fig. 6). The reactive astrocytes were located in injury penumbra (Fig. 3). In the damage area of injury center, the cells are mainly infiltrated leukocytes (Fig. 5) and activated microglia/macrophages (Fig. 6). In the injury center, the gray matter is damaged, and a large number of neurons are lost. The distribution of different cell populations in difference regions is consistent with pathological changes of SCI. For example, the reactive astrocytes in injury penumbra are the main cellular origin of glial scar (Yuan and He, 2013). The infiltrated leukocytes and activated microglia/macrophages are involved in the inflammatory processes and cystic cavitation formation (Fitch et al., 1999). These are very useful in studying the cellular and molecular mechanisms of SCI. However, it has negative effect on the observation of cellular co-localization of HK3. To solve this problem, we used the sections 5 mm distance from the injury center where the gray matter is still preserved to co-localize HK3 with neurons (Fig. 4). Our results determined that HK3 is mainly expressed in astrocytes, neurons, infiltrated leukocytes and activated microglia/macrophages in the injured spinal cords. It still cannot be detected in oligodendroglia. CD45 is the leukocyte common antigen (Harvath et al., 1991). Under normal conditions, CD68 is highly expressed by peripheral monocytes and local tissue macrophages, and is expressed very low by microglia (Holness and Simmons, 1993). Under CNS pathological conditions, CD68 is highly expressed not only by infiltrated circulating macrophages but also by local activated microglia (Ebneter et al., 2017, Papageorgiou et al., 2016). In this study, we demonstrated that after SCI, HK3 is highly enriched in infiltrated leukocytes, and rapidly increase in activated microglia/macrophages and astrocytes. The results of qRT-PCR and WB showed that in subacute phase of SCI (7 dpi), the level of HK3 expression is the highest. These results are consistent with the changes of cell types, quantity and function in the lesion microenvironment, the peaks of leukocyte infiltration and glial activation both occurred in the subacute phase of SCI (Chen et al., 2015, Gadani et al., 2015, Tian et al., 2007, Wu et al., 2016). These data suggest the carbohydrate metabolism is most active in the subacute phase of SCI, which may be related to the large amount of energy requirement of infiltrated leukocytes, activated microglia and astrocytes in the lesion microenvironment (Carlson et al., 2009, Gorgey and Gater, 2011).