Search

Objectives: To reveal the expression level of cystathionine β-synthase (CBS) in adenocarcinoma of esophagogastric junction (AEG) and discuss the relationship between CBS expression level and tumor microvascular density (MVD), clinical features and prognosis., Methods: Paraffin samples from 214 patients with AEG were selected to make pathological microchips. Immunohistochemistry was performed based on the microchips to detect the expression level of CBS and microvascular density (MVD) in cancer tissues and adjacent control tissues. Relationships between expression level of CBS and MVD, clinical characteristics and prognosis were analyzed., Results: In total, 214 AEG cases were classified into three groups: CBS negative staining ( n =26), low staining ( n =44), and high staining ( n =144). Quantitative alterations in CBS and CD31 expression were explored using immunohistochemistry. The 5-year recurrence rate of enrolled patients was followed up and found that CBS expression was significantly increased in tumor tissue compared with adjacent non-tumor tissue ( P <0.0001). There were significant differences in microvascular density between the groups with negative and high CBS staining ( P <0.0001), and between the groups with low and high CBS staining ( P <0.0001). Univariate analysis revealed significant differences in tumor stage ( P <0.0001), T stage ( P =0.008), N stage ( P =0.028), differentiation degree ( P =0.037), and 5-year survival ( P =0.0034) among the three groups. Multivariate logic regression analysis showed that increased CBS scores were associated with an increased probability of 5-year recurrence ( P =0.018). Finally, different CBS expression levels were associated with disease-free survival in AEG patients., Conclusions: CBS expression level is closely related to microvascular density and tumor stage in AEG. High level of CBS not only accelerates tumor angiogenesis but also affects patient's survival and prognosis., Competing Interests: None., (AJTR Copyright © 2022.)

Massive neuron loss is the key reason for poor prognoses in patients with traumatic brain injury (TBI), and astrocytes function as nutrition-providing neurons. Therefore, researchers must determine the potential role of astrocytes in neural regeneration after TBI. Our previous studies established that upregulating CD24 in the hippocampus might improve cognitive functions after TBI. However, whether CD24 in hippocampal astrocytes is involved in neural regeneration after TBI remains unknown. Therefore, we detected the CD24 expression in the ipsilateral hippocampus via western blot and quantitative real-time PCR. We further investigated the CD24 expression patterns in hippocampal astrocytes via immunofluorescence staining. We then injected adeno-associated virus-Gfa2-siRNA-CD24 (AAV-CD24) into the astrocytes to downregulate CD24 and analyzed the related cellular signals. Golgi-Cox staining and the growth associated protein-43 (GAP43) level were used to observe neuronal morphology and neural regeneration around the astrocytes in the ipsilateral hippocampus, and the Morris water maze test was used to assess neural functional recovery. The CD24 protein and mRNA levels in the cornu ammonis and dentate gyrus regions of the ipsilateral hippocampus were elevated after TBI, and high CD24 expression was widespread in the hippocampal astrocytes after TBI. Specific inhibition of CD24 in the hippocampal astrocytes interfered with the activation of Src homology region 2 containing protein tyrosine phosphatase 2 (SHP2) and extracellular signal regulated kinase (ERK), shortened the neuronal dendritic spines, decreased the GAP43 level and impaired the cognitive functions of the TBI-model mice. These results revealed that elevated hippocampal CD24 in astrocytes participated in neural regeneration in mice after TBI, possibly by activating the SHP2/ERK pathway., Competing Interests: None., (AJTR Copyright © 2020.)