BACKGROUND : Research on neural stem cells (NSCs) using rodents to represent NSC protein markers and their anatomical distribution in comparison to humans is still limited. To address this gap, this review aimed to identify the protein markers expressed by NSCs and compare their anatomical locations in rodents and humans. METHODS : A systematic review was performed in accordance with preferred reporting items for systematic reviews and meta-analysis guidelines. Comprehensive searches were performed in PubMed, ScienceDirect, and Nature databases for studies published between March 2023 and March 2024. Eligible studies, data extraction and synthesis focused on the type of NSC markers and the sites of detection. RESULTS : A total of 47 studies were analyzed. Frequently reported NSC markers included Nestin, glial fibrillary acidic protein (GFAP), sex determining region Y (SRY)-box transcription factor 2, SRY-box transcription factor 9, doublecortin, oligodendrocyte transcription factor 2 (Olig2), Ki-67, β-tubulin III, and S100β. In rodent, NSCs were consistently positive detected in the lateral ventricle, hippocampus, peri-infarct area, and cerebral cortex. In humans, similar patterns were observed with additional reports of NSC markers such as Ki-67, GFAP, Olig2, and Nestin may detected in peri-infarct, blood serum, and cerebrospinal fluid. CONCLUSIONS NSC markers and anatomical distribution are similar between rodents and humans, emphasizing the validity of rodent models in neurogenesis research.
biomarkers ; brain ; humans ; neural stem cells ; rodents

Background: An imbalance between pro- and anti-angiogenic factors contributes to impaired trophoblast invasion during pregnancy, leading to failure of uterine spiral artery remodeling, blood vessel ischemia, and pre-eclampsia (PE). Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are expressed in both the placenta and maternal blood. The present study investigated correlations between serum and placental SEMA3B as well as CUL1 levels in late-onset PE. Methods: This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a P < 0.05 considered statistically significant. Results: While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (R = 0.620, P = 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1. Conclusion: Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.