On Sunday, April 20th 2025, starting 8:30am GMT, there will be maintenance work that will involve the website being unavailable during parts of the day. We apologize for any inconvenience this may cause and appreciate your understanding.
We noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Regression: from bad to better?
- Mouse model of regression (1)
- Absence of macrophages after regression
- Mouse model of regression (2)
- Rapid exit of monocyte-derived cells
- First hint of macrophage heterogeneity
- Heterogeneity of cell types in arterial lesions
- Example of LCM of macrophage foam cells
- Blocking the CCR7 pathway blocks regression
- Summary of part 1
- Lipoprotein changes from apoE-/- to WT mice
- HDL and vascular protection
- Model to test selective normalization of HDL-C
- Normalization of HDL-C promotes regression
- Regression is impaired
- HDL modulates CCR7 levels
- Molecular mechanism for CCR7 regulation
- Evidence for SRE-activation in vivo
- Summary of part 2
- Part 3: changes in macrophage polarization
- Classification of macrophages in tissues
- HDL regulates the inflammatory state (1)
- HDL regulates the inflammatory state (2)
- HDL enriches CD68+ cells in M2 markers (1)
- HDL enriches CD68+ cells in M2 markers (2)
- Are the changes model dependent?
- MiR-33 negatively regulates ABCA1 expression
- Predicted effects of blocking miR-33
- miR-33 in LDLr-/- mice regulates HDL Levels
- Less inflammation in plaque macrophages
- Some models of macrophage "plasticity"
- Summary of part 3
- Overall summary (1)
- Overall summary (2)
- Acknowledgements
Topics Covered
- Novel research tools
- Developing mouse models to study atherosclerosis regression
- Developing the tools to analyze macrophage trafficking and molecular phenotypes in vivo
- The regression of atherosclerosis by HDL due to its effects on the quantity and phenotype of macrophages in plaques
- Macrophage polarization
- Plasticity during atherosclerosis regression
- Models for the enrichment in cells in the M2 state
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Fisher, E. (2012, June 11). Macrophage heterogeneity in atherosclerosis regression [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 15, 2025, from https://doi.org/10.69645/IODW9558.Export Citation (RIS)
Publication History
- Published on June 11, 2012
Financial Disclosures
- Prof. Edward Fisher, Consultant: Merck; Speaker’s Bureau: Merck; Grant/Research Support (Principal Investigator): Merck