Dr. Shyue, Song-Kun ’s Lab徐松錕 博士 實驗室

RESEARCH

Caveolin-1 (Cav-1) is the major structure protein of caveolae and involved in protein and cholesterol trafficking, signaling transduction and protein degradation. My laboratory has been working on the roles of prostaglandins/eicosanoids in cardiovascular diseases and the role of Cav-1 in bacteria- and LPS-associated immune response and cyclooxygenase (COX)-2 degradation. Previously, we showed that deletion of Cav-1 reduces brain injury in intracerebral hemorrhage (ICH) mouse model. We therefore investigated the role Cav-1 Ab in inflammatory response in ICH.

1. Role of caveolin (Cav-1) antibody (Ab) in immune regulation and therapy for inflammatory diseases.  Our results show that Cav-1 Ab treatment alleviated brain damage via reducing brain inflammatory response in intracerebral hemorrhage (ICH) mouse model.  Cav-1 Ab treatment reduced microglial activation and modulated microglial M1/M2 polarization toward the M2 phenotype.  A patent application for this finding has been filed.  We are working on the underline mechanism of how Cav-1 Ab modulate monocyte/macrophage polarization and its therapeutic efficacy in inflammatory diseases such as atherosclerosis, psoriasis and inflammatory brain diseases with the monoclonal Cav-1 Abs we developed.

2. Searching for novel genes involved in proteasome- and autophagy-mediated COX-2 degradation.  Using CRISPR/Cas9 techniques, we have identified several genes which may mediate COX-2 degradation. Two novel genes are under investigation: one may mediate the retrotranslocation of COX-2 from endoplasmic reticulum (ER) to cytosol, and the other may regulate both ER-associated degradation and autophagy. Several novel genes which may be involved in autophagy have been identified for future study.

3. Novel role of a prostaglandin (PGX) in cardiovascular disease.  High dose of non-specific non-steroid anti-inflammatory drugs (NSAIDs) and COX-2 specific inhibitors are associated with increased risk of myocardial infarction (MI), suggesting cardiovascular protective roles of unidentified prostaglandins.  We have identified PGX which may play protective roles in cardiovascular diseases.  Deletion of PGX increased atherosclerosis in apoE KO mice.  Moreover, deletion of PGX increased cardiac fibrosis and deteriorate cardiac function in MI mouse model.  Ongoing projects are involved in the function of PGX in lipid homeostasis, endothelial function and cardiac fibrosis.

4. Role of Cav-1 in erythrocytes homeostasis.  An ongoing study focus on the molecular mechanism of Cav-1 in red blood cell counts in Cav-1-deleted mice. 

5. Adenovirus vector construction and modification.  We are in charge for the core facility of recombinant adenovirus vector and have develop an efficient system for adenovirus vector construction and amplification. 

研究介紹

Caveoliin-1為細胞內小窩器的主要蛋白,調控蛋白質的傳遞、活性與降解。前列腺素為脂質的代謝物,調控血管平衡、痛覺感受與發炎等生理功能。研究發現caveolin-1可以調控環氧酶(COX)-2降解。臨床上高劑量的COX的抑制藥物如NSAID或COX-2抑制劑,會提升病人的心肌梗塞的風險,前列腺素在心血管的保護功能仍不清楚。

研究方向

1. 找尋與proteasome 暨 autophagy 有關,調控蛋白質降解的相關基因。

2. 研究caveolin-1 抗體在免疫系統上的調節功能。

2. 研究caveolin-1在紅血球恆定上的角色。

3. 研究caveolin-1抑制心臟肥大的原理。

4. 探索非類固醇止痛藥對心血管疾病傷害的原理。我們已經找到有保護效果的eicosanoid。 一般的止痛藥會抑制至它的產生。

Dr. Shyue, Song-Kun
徐松錕 博士

Associate Research Fellow
長聘副研究員



Ph.D. Univ. of Texas-Houston, Health Science Center
Specialty:
  • Caveolin-1
  • Protein Degradation
  • PGs & Cardiovascular Diseases
  • Adenovirus vector gene therapy
     

HIGHLIGHT 重要成果

Atypical antipsychotics and CD36 pathway
Metabolism: clinical and experimental, Aug 06, 2021
Deletion of caveolin‐1 attenuates LPS/GalN‐induced acute liver injury in mice
Journal of Cellular and Molecular Medicine, Aug 22, 2018
Linear correlation between average fluorescence intensity of green fluorescent protein and the multiplicity of infection of recombinant adenovirus
Journal of Biomedical Science, May 14, 2015

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