PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Yi-Lin Tang - Top 30 Publications

A homozygous missense variant in HSD17B4 identified in a consanguineous Chinese Han family with type II Perrault syndrome.

Perrault syndrome is a rare multisystem disorder that manifests with sensorineural hearing loss in both sexes, primary ovarian insufficiency in females and neurological features. The syndrome is heterogeneous both genetically and phenotypically.

Fasudil, a Rho kinase inhibitor, promotes the autophagic degradation of A53T α-synuclein by activating the JNK 1/Bcl-2/beclin 1 pathway.

Accumulation of α-synuclein (α-syn) is pivotally implicated in the pathogenesis of Parkinson׳s disease (PD), and enhancing its clearance might be a promising strategy in PD treatment. It has recently been shown that Rho kinase (ROCK) activation is involved in many neurodegenerative diseases, and some ROCK inhibitors might promote the degradation of abnormal protein aggregates. However, it is not known if fasudil, the only ROCK inhibitor available in clinical setting, could promote the degradation of α-syn, and ameliorate the α-syn induced neurotoxicity. In this regard, we investigated the effect of fasudil on neurite injury caused by A53T α-syn overexpression and the implicated pathway it might mediate. In the current study, we found that under the condition of A53T α-syn overexpression, the neurite outgrowth decreased significantly with the increasing expression of ROCK2. Fasudil, the ROCK inhibitor, ameliorated such neurotoxicity and promoted the clearance of A53T α-syn. Its underlying mechanism was supported by that fasudil could increase the macroautophagy activation via JNK 1 and Bcl-2 phosphorylation and beclin 1/Vps34 complex formation. Taken together, fasudil might be able to provide a novel and promising strategy for PD treatment by enhancing α-syn clearance and activating the JNK 1/Bcl-2/beclin 1 pathway.

Trehalose alleviates PC12 neuronal death mediated by lipopolysaccharide-stimulated BV-2 cells via inhibiting nuclear transcription factor NF-κB and AP-1 activation.

Inflammation is implicated in the pathogenesis of Parkinson's disease (PD). Trehalose is a disaccharide which exhibits a variety of effects like anti-aggregation, autophagy enhancement in PD. It has also been known to suppress inflammation in many experimental models, involving endotoxin shock, murine dry eye and subarachnoid hemorrhage. However, whether trehalose has an anti-inflammation effect on PD is largely unknown. In the present study, we found trehalose inhibited generation of interleukin-1β, interleukin-6, tumor necrosis factor-α, and nitric oxide in the conditioned medium released from lipopolysaccharide (LPS)-stimulated BV-2 cells. LPS-induced nuclear transcription factors of NF-κB and AP-1 activation were also inhibited by trehalose. Then the conditioned medium of BV-2 cells was applied to PC12 neurons. As a result, both MTT and LDH indicated that trehalose decreased PC12 neuronal death. TUNEL assay showed that trehalose suppressed apoptosis of PC12 neurons. These results implied that trehalose exerted a protective effect on PC12 neurons against the neurotoxic effect triggered by BV-2 microglial activation through inhibiting NF-κB and AP-1 activation and inflammatory mediators and cytokines production in BV-2 cells.