Email Service Notes (Tony)

Your Original Email

Q: Tell us about your current project.
A: My current project is to disclose the role of sorting nexins 10 (SNX10) in atherosclerosis (AS). First, a quick word on the research background. AS is a complex chronic inflammatory disease with passive accumulation of lipids in the vessel wall. LAL is a PH-sensitive lipase that helps to decompose lipids and therefore suppress the atherosclerosis progression. In addition, LAL can promote the polarization of M2-type macrophages by regulating fatty acid oxidation.
The major purpose of my research is to study whether LAL is involved in SNX10 mediated-macrophage polarization and whether SNX10 plays an important role in AS. We found that SNX10 deficiency arrested intracellular V-ATPases, resulting in increased endosomal/lysosomal acidification, and enhanced LAL-mediated lipolysis, therefore promoted M2-polarization of macrophages. Consist with our expectation, SNX10 deficiency could lower lipids deposition of aorta intima and inhibit the formation of atherosclerotic plaque.
For me, the most intriguing part in this study is to construct SNX10 and APOE double knockout mice. With SNX10-/- mice under FVB background and APOE-/- mice under C57 background on hand, I first need to acquire SNX10-/+ mice on C57 background, which requires two generations of crossbreeding with WT C57 mice. Then I need to perform crossbreeding between the acquired mice and APOE-/- mice for two generations before, with a small probability, getting eligible mice. This was a pretty interesting and challenging process which I immensely enjoyed.

Your Edited Email

Q: Tell us about your current project.
A: My current project is to disclose the role of sorting nexins 10 (SNX10) in atherosclerosis (AS). First, a quick word on the research background. AS is a complex chronic inflammatory disease with passive accumulation of lipids in the vessel wall. LAL is a PH-sensitive lipase that helps to decompose lipids and therefore suppress the atherosclerosis progression. In addition, LAL can promote the polarization of M2-type macrophages by regulating fatty acid oxidation.
The major purpose of my research is to study whether LAL is involved in SNX10 mediated-macrophage polarization and whether SNX10 plays an important role in AS. We found that a deficiency of SNX10 arrested intracellular V-ATPases, resulting in increased endosomal/lysosomal acidification, and enhanced LAL-mediated lipolysis, therefore it promoted M2-polarization of macrophages. Consistent with our expectations, a SNX10 deficiency could lower the depositing of lipids in the aorta intima and inhibit the formation of atherosclerotic plaque.
For me, the most intriguing part in this study is to construct SNX10 and APOE double knockout mice. With SNX10-/- mice under FVB background and APOE-/- mice under C57 background on hand, I first need to acquire SNX10-/+ mice on C57 background, which requires two generations of crossbreeding with WT C57 mice. Then I need to perform crossbreeding between the acquired mice and APOE-/- mice from two generations before, with a small probability of obtaining eligible mice. This was a pretty interesting and challenging process which I immensely enjoyed.