SEMA3A

Generally, taste sensitivity is known to change with age. However, the molecular mechanisms underlying this phenomenon remain unclear. Mammalian taste buds are classified into type I, II, III, and IV cells; among them, type II and III cells have an important role in the taste detection process. We hypothesized that age-related changes in the proportion of taste cell types would be a factor in changes in taste sensitivity. To test this hypothesis, we compared the expression patterns of type II and III cell markers in taste buds obtained from the circumvallate papillae of young and old mice. Gustducin, SEMA3A, PLCβ2, and CAR4 were used as type II and III cell markers, respectively. When we performed double-fluorescence staining using antibodies for these molecules, Gustducin and SEMA3A immune-positive cells were 22.7 ± 1.2% and 27.6 ± 0.9% in young mice and 22.0 ± 0.7% and 25.9 ± 1.1% in old mice, respectively. PLCβ2 and CAR4 immune-positive cells were 30.3 ± 1.5% and 20.7 ± 1.3% in young mice and 29.1 ± 0.8% and 21.1 ± 1.2% in old mice, respectively. There were no significant differences in the percentage of immunopositive cells for all antibodies tested between young and old mice. These results suggest that the proportion of type II and III cells does not change with aging.

Enhancing axonal regeneration is one of the most important processes in treating nerve injuries. Both magnetic and electrical stimulation have the effect of promoting nerve axon regeneration. But few study has investigated the effects of trans-spinal magnetic stimulation (TsMS) combined with electroacupuncture (EA) on nerve regeneration in rats with sciatic nerve injury. In this study, we compared the improvement of neurological function in rats with sciatic nerve crush injuries after 4 weeks of different interventions (EA, TsMS, or TsMS combined with EA). We further explored the morphological and molecular biological alterations following sciatic nerve injury by HE, Masson, RT-PCR, western blotting, immunofluorescence staining and small RNA transcriptome sequencing. The results showed that TsMS combined with EA treatment significantly promoted axonal regeneration, increased the survival rate of neurons, and suppressed denervation atrophy of the gastrocnemius muscle. Subsequent experiments suggested that the combination treatment may play an active role by mediating the miR-539-5p/Sema3A/PlexinA1 signaling axis.

Breast cancer is a major health concern, and its accurate diagnosis and management depend on identifying its histological type and biological subtype. Semaphorin-3A (SEMA3A) is a membrane protein with diverse roles in cellular processes, including cancer progression and angiogenesis regulation. However, its role in breast cancer remains poorly understood. This study aimed to evaluate SEMA3A expression in breast cancer and investigate its distribution across breast cancer subtypes: luminal A, luminal B, HER2-positive, and triple-negative breast cancer (TNBC). Immunohistochemical evaluation was performed on 98 breast cancer patients' tumor specimens, and SEMA3A expression was assessed in tumor cells and vessels. The study included the analysis of the Ki67 proliferation index, estrogen receptor (ER) expression, progesterone receptor (PR) expression, and HER2 status in conjunction with SEMA3A expression. Analysis indicated positive expression of SEMA3A in breast cancer cells in 60 out of 98 cases. SEMA3A expression correlated positively with Ki67 levels in tumor cells (p = 0.0005, R Spearman 0.338). Notably, a negative correlation was found between SEMA3A expression and ER and PR levels in tumor cells (p = 0.04, Spearman's R = - 0.21 and p = 0.016, Spearman's R = - 0.25 respectively). HER2 status did not significantly influence SEMA3A expression. The study demonstrated positive SEMA3A expression in tumor vessels across all subtypes in 91 out of 98 cases, suggesting its involvement in endothelial cell function. However, no significant differences in SEMA3A expression were observed between breast cancer subtypes either in vessels or tumor cells. These findings suggest that elevated SEMA3A expression may be associated with worse prognosis in breast cancer, especially in ER- and PR-negative tumors. Further investigations are warranted to fully comprehend the role of SEMA3A in breast cancer biology, which may lead to the identification of novel therapeutic targets and personalized treatment strategies for breast cancer patients.