School of Biomedical Sciences cordially invites you to join the following Post-doctoral Fellow (PDF) Seminar:

Date: 22 January 2025 (Wednesday)
Time: 4:00 pm – 5:00 pm
Venue: Seminar Room 1, G/F, Laboratory Block, 21 Sassoon Road
Host: Dr. Haifeng Fu

Light refreshments will be served. Please register via the below link by 20 January 2025 (Monday):
Registration: https://hku.au1.qualtrics.com/jfe/form/SV_1ziRBJRiLDb8hwy
 

Induction of proinflammatory cytokine release in macrophages by extracellular vesicle-delivered SARS-CoV-2 accessory protein ORF3a
Dr. Sin Yee Fung (Post-doctoral Fellow)
[Supervisor: Professor Dong-Yan Jin]

Although the COVID-19 pandemic has ended, many important questions about SARS-CoV-2 pathogenesis remain to be elucidated. In severe COVID-19, exacerbated proinflammatory cytokine release is often related to acute respiratory distress syndrome and associated with poor prognosis.  Macrophages are thought to be major producers of proinflammatory cytokines. However, the relevance of proinflammatory cytokine release from macrophages to the life cycle of SARS-CoV-2 remains to be established. We hypothesized that certain secretory viral factors might be responsible for hyperinflammatory response in macrophages. Here, we identified viral ORF3a protein as a key player in proinflammatory cytokine release from macrophages. The existence of ORF3a in extracellular vesicles (EVs) was detected by Western blotting and immuno-electron microscopy. Its transfer to neighboring cells was confirmed. Feeding phorbol-12-myristate-13-acetate-differentiated THP-1 cells with ORF3a EVs triggers proinflammatory cytokine release. Our findings highlighted ORF3a as a biomarker for novel diagnostic and therapeutic strategies to mitigate cytokine storm in severe COVID-19.

Investigation of the therapeutic values of Flavopiridol in Alzheimer’s disease
Dr. Ruijun Chen (Post-doctoral Fellow)
[Supervisor: Dr. You-qiang Song]

Alzheimer’s disease (AD), a chronic neurodegenerative disorder, is characterized by cognitive dysfunction and memory loss. There are two pathological hallmarks of Alzheimer’s disease: amyloid-β plaques and neurofibrillary tangles. The molecular link between amyloid-β plaques and neurofibrillary tangles was rarely reported. However, our previous work showed that Pax 6 was a key gene to link both amyloid-β plaques and neurofibrillary tangles. Amyloid-β could upregulate the hyperphosphorylation of tau protein through pax6 pathway. And Flavopiridol, a potent CDK inhibitor, protected cortical neurons against amyloid-β-induced death and significantly blocked amyloid-β-induced upregulation of Pax6 and c-Myb. Based on it, we further investigated Flavopiridol in AD models and found that Flavopiridol could protect against AD. Furthermore, we are developing a nasal drug delivery system by using a microfluidics liposomes approach. By combined targeting the Pax6 pathway and nasal delivery system, we will develop an approach for the treatment of Alzheimer's disease.

All are welcome.