Regeneration of vascular endothelium with early proatherogenic changes induced by bacterial components in the presence of high fat substances

Krupa, A., et al. “Regeneration of vascular endothelium with early proatherogenic changes induced by bacterial components in the presence of high fat substances.” Atherosclerosis 355 (2022): 2. https://doi.org/10.1016/j.atherosclerosis.2022.06.235

Abstract

Background and Aims : Endothelial dysfunction induced mostly by oxidized sterols and microbial components is one of the main causes of atherosclerotic lesion formation. Understanding the mechanisms involved in the process of development and progression of proatherogenic changes may help to find different ways to modulate the course of coronary heart disease (CHD). Our study aimed on analyzing the role of various sterols in the process of vessels regeneration, also in the environment of bacterial components. Also, we tried to explain the possible mechanism that is run during endothelial regeneration and differentiate it between cell migration and cell proliferation.

Methods: We employed cell line of vascular endothelial cells (HMEC-1) and performed a tube formation assay using Matrigel, wound repair test “scratch assay” and cell proliferation, as well as measured collagen production. Cells were treated with various sterols alone (involving oxidized) or together with bacterial components of Helicobacter pylori (HP).

Results: Based on results we can suggest that cholesterol has a proangiogenic potential, in the contrary components of the oxidized LDL fraction, such as 7 ketocholesterol and calcitriol, do not have any significant impact on the formation of vascular structure by endothelial cells. Based on our observation we can also suggest that bacterial components of HP may modulate the activity of endothelial cells and have proregenerative effect on the vascular endothelium. The study was supported by Foundation for Polish Science (POIR.04.04.00-00-16D7/18) carried out within the TEAM-NET (European Union under the European Regional Development Fund).

Conclusions: Cholesterol promotes endothelial cell migration which is not based on collagen release.