IL-33 Alleviated Brain Damage via Anti-apoptosis, Endoplasmic Reticulum Stress, and Inflammation After Epilepsy.

Interleukin (IL)-33 belongs to a novel chromatin-associated cytokine newly recognized by the IL-1 family, and its specific receptor is the orphan IL-1 receptor (ST2). Cumulative evidence suggests that IL-33 plays a crucial effect on the pathological changes and pathogenesis of central nervous system (CNS) diseases and injuries, such as recurrent neonatal seizures (RNS). However, the specific roles of IL-33 and its related molecular mechanisms in RNS remain confused. In the present study, we investigated the protein expression changes and co-localized cell types of IL-33 or ST2, as well as the effect of IL-33 on RNS-induced neurobehavioral defects, weight loss, and apoptosis. Moreover, an inhibitor of IL-33, anti-IL-33 was performed to further exploited underlying mechanisms. We found that administration of IL-33 up-regulated the expression levels of IL-33 and ST2, and increased the number of its co-localization with Olig-2-positive oligodendrocytes and NeuN-positive neurons at 72 h post-RNS. Noteworthily, RNS-induced neurobehavioral deficits, bodyweight loss, and spatial learning and memory impairment, as well as cell apoptosis, were reversed by IL-33 pretreatment. Additionally, the increase in IL-1ß and TNF-α levels, up-regulation of ER stress, as well as a decrease in anti-apoptotic protein Bcl-2 and an increase in pro-apoptotic protein CC-3 induced by RNS are prevented by administration of IL-33. Moreover, IL-33 in combination with Anti-IL-33 significantly inverted the effects of IL-33 or Anti-IL-33 alone on apoptosis, ER stress, and inflammation. Collectively, these data suggest that IL-33 attenuates RNS-induced neurobehavioral disorders, bodyweight loss, and spatial learning and memory deficits, at least in part through mechanisms involved in inhibition of apoptosis, ER stress, and neuro-inflammation.

The Effects of YAP and Its Related Mechanisms in Central Nervous System Diseases.

Yes-associated protein (YAP) is a key effector downstream of the Hippo signaling pathway and plays an important role in the development of the physiology and pathology of the central nervous system (CNS), especially regulating cell proliferation, differentiation, migration, and apoptosis. However, the roles and underlying mechanisms of YAP in CNS diseases are still puzzling. Here, this review will systematically and comprehensively summarize the biological feature, pathological role, and underlying mechanisms of YAP in normal and pathologic CNS, which aims to provide insights into the potential molecular targets and new therapeutic strategies for CNS diseases.

Overexpression of long non-coding RNA differentiation antagonizing non-protein coding RNA inhibits the proliferation, migration and invasion and promotes apoptosis of renal cell carcinoma.

Renal cell carcinoma (RCC) is the third most common cancer in the urological system; however, the pathogenesis remains unknown. Accumulating evidence has demonstrated that long non­coding RNAs are dysregulated in various tumors and serves an important role in tumorigenesis and development. In the present study, expression of lncRNA differentiation antagonizing non­protein coding RNA (DANCR) in 24 paired RCC and adjacent normal tissues was detected by reverse transcription­quantitative polymerase chain reaction. The results revealed that DANCR is downregulated in RCC tissues compared with adjacent normal tissues. Subsequent study revealed that overexpression of lncRNA DANCR by transfection of pcDNA3.1­DANCR could suppress 786­O and ACHN (RCC cell) proliferation, migration and invasion, and induce apoptosis compared with cells transfected with the pcDNA3.1 vector. The results revealed that DANCR functions as a tumor suppressor in RCC. In conclusion, the present study, to the best of our knowledge, was the first to reveal DANCR as a tumor suppressor. The results implicate DANCR as a potential biomarker of RCC, and further study will be focused on the clinical significance and signaling pathways of DANCR.

Turn on ESPT: novel salicylaldehyde based sensor for biological important fluoride sensing.

A novel and simple salicylaldehyde based anion fluorescent sensor 1 has been designed, which can selectively sense fluoride by 'turn on' excited-state intermolecular proton transfer (ESPT). The binding constant and the stoichiometry were obtained by non-linear least-square analysis of the titration curves.