Neuro-oncological ventral antigen 1 (Nova1) is a well known brain-specific splicing factor. Several studies have identified Nova1 as a regulatory protein at the top of a hierarchical network. However, the function of Nova1 during hypoxia remains poorly understood. This study aimed to investigate the protective effect of Nova1 against cell hypoxia and to further explore the Bax/Bcl-2/caspase-3 pathway as a potential mechanism. During hypoxia, the survival rate of pheochromocytoma PC12 cells was gradually decreased and the apoptosis rate was gradually increased, peaking at 48 h of hypoxia. At 48 h after transfection of PC12 cells with pCMV-Myc-Nova1, the expression of Nova1 was significantly increased, with wide distribution in the cytoplasm and nucleus. Moreover, the survival rate was significantly increased and the apoptosis rate was significantly decreased. Additionally, the mRNA and protein expression levels of Bax and caspase-3 were significantly increased in the pCMV-Myc group and significantly decreased in the pCMV‑Myc-Nova1 group, whereas that of Bcl-2 was significantly decreased in the pCMV-Myc group and significantly increased in the pCMV-Myc-Nova1 group. This study indicated that Nova1 could be linked to resistance to the hypoxia-induced apoptosis of PC12 cells via the Bax/Bcl-2/caspase-3 pathway, and this finding may be of significance for exploring novel mechanisms of hypoxia and the treatment of hypoxia-associated diseases.

The toxic effects of micro(nano)plastics are long-standing, flourishing and fadeless as a research topic because of its' underlying threats to the ecology and human health. Nevertheless, in most of the existing studies, some model organisms are exposed to micro(nano)plastics at a high concentration unlikely to occur in the real environment, and there is limited data available on the impact of micro(nano)plastics at environmentally relevant concentrations (ERC) on environmental organisms. To gain a better insight into micro(nano)plastic toxicity to the environmental organisms, here we integrate the related publications of micro(nano)plastic research at ERC in the past 10 years using a bibliometric analysis, and focus on the analysis of publication trends, research focuses, collaborations, and research status. In addition, we further analyze the 33 final filtered literature, and elucidate the organismal response to micro(nano)plastics at ERC from the perspective of in vivo toxic effects and mechanisms involved. This paper also puts forward some limitations of the current study and some suggestions for future research. Our study may be of great significance in further understanding the ecotoxicity of micro(nano)plastics.

A bifunctional TPE-based fluorescent sensor (TPE-Q) for both liquid viscosity and amyloid β (Aβ) has been synthesized straightforwardly by the introduction of an ethylene glycol chain and quaternary ammonium to the classical tetraphenyl ethylene core. Due to the rotation of the intramolecular restriction (RIR) effect of TPE-Q, the sensor displayed liquid viscosity sensing capability with a promising linear relationship within 37 to 609 cp. The fluorescence enhancement was around 11.77 folds. On the other hand, TPE-Q showed both in vitro and in vivo Aβ sensing capabilities. By mixing with Aβ₁₋₄₂ solution, TPE-Q showed a maximum fluorescence enhancement of 21.60 folds, with a detection limit of 160 nM. In addition, fluorescence colocalization experiments revealed a good merging of TPE-Q and commercial Th T, proving the in vivo imaging capability of TPE-Q in Aβ₁₋₄₂ over-expressing Caenorhabditis elegans (C. elegans, CL4176). Furthermore, computational docking prediction revealed the binding pattern of TPE-Q towards Aβ aggregates.

Objective: This study investigated how dopaminergic (DAergic) depletion-induced ventral hippocampal neurogenesis triggers hypothalamic–pituitary–adrenal (HPA) axis hyperactivity. Methods: Three-month-old male C57BL/6 mice were subjected to systemic 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or ventral tegmental area (VTA) injections of 1-methyl-4-phenylpyridinium ion (MPP+). We observed tyrosine hydroxylase (TH)-positive cells in the midbrain VTA and hippocampal DA content. We examined BrdU-positive cells in the ventral hippocampal dentate gyrus (vDG) on day 7 (D7) and day 28 (D28) after the BrdU injection. The expression of GAD67 and c-Fos-positive cells reflected the activation of GABAergic neurons. We assessed HPA-axis activity based on the levels of CORT, ACTH, and CRH mRNA. Results: TH immunoreactivity in VTA DAergic neurons and hippocampal DA were markedly reduced on D7 post-MPTP/MPP+ and recovered on D28. The numbers of BrdU-positive cells on D7 and D28 in the vDG were drastically reduced and were remedied by SKF38393 rather than quinpirole. MPTP significantly elevated levels of CORT, ACTH, and CRH mRNA on D28. A SKF38393 injection in the vDG, an AMPA injection in the amBNST, or a muscimol injection in the PVN effectively reversed HPA-axis hyperactivity. Conclusions: These results indicate that VTA DAergic depletion reduces the number of BrdU-labeled newborn cells within the vDG in a D1R-dependent manner. Given our previous work demonstrating unchanged progenitor cell proliferation but impaired survival of vDG newborn neurons under MPTP insult, we propose that disrupted D1R-dependent maintenance of newborn cell populations impairs vHPC-originated glutamatergic input to the amBNST, with associated alterations in the HPA-axis activity.