Key result
G-CSF had no effect in a rabbit model of atherosclerosis, but had dose-dependent effects in a porcine heart model, worsening arterial disease at low or high doses and improving it at a medium dose.
Why the study?
Previous studies suggest G-CSF can promote progenitor cells to mediate cardiovascular repair, potentially reversing mechanical dysfunction in chronic ischaemic heart disease and post myocardial infarction.
Does G-CSF improve arterial remodeling and endothelial function in rabbit and porcine models of chronic obliterative arterial disease?
Does G-CSF improve arterial remodeling and endothelial function in rabbit and porcine models of chronic obliterative arterial disease?
G-CSF exerts dose-dependent effects on intimal hyperplasia in a porcine model of chronic ischemic heart disease, worsening it at low and high doses but improving it at a medium dose, while showing no effect in a rabbit atherosclerosis model.
Answers are grounded in this paper and cite their sources.
Inconsistent G-CSF effects on arterial disease across animal models are hypothesis-generating; should not yet inform clinical practice.
Previous studies suggest that granulocyte colony‑stimulating factor (G‑CSF) can promote bone marrow derived progenitor cells to mediate cardiovascular repair, potentially reversing mechanical dysfunction in chronic ischaemic heart disease and post myocardial infarction. Two models were used in the present study both using a surgical ameroid constrictor to induce arterial stenosis. The first model used the carotid artery of rabbits. They were divided into high fat diet (inducing atherosclerosis) or normal fat diet (control) groups. Each was subdivided into surgical exposure group without constrictor, ameroid constrictor receiving normal saline or receiving G‑CSF 15 µg/kg/day. Endothelial markers of endothelial nitric oxide synthase and endothelin 1 were increased by the use of ameroid constrictor in both atherosclerotic and non‑atherosclerotic mice, however were not further altered by G‑CSF. Scanning electron microscopy indicated that ameroid constrictor application altered endothelial morphology from an oval shape to a round shape and this was more prominent in the atherosclerotic compared with the non‑atherosclerotic group. G‑CSF injection increased the number of endothelial cells in all groups. The second model used the left coronary artery of pigs. They were equally divided into following groups, receiving normal saline (control), G‑CSF 2.5 µg/kg/day (low dose), 5 µg/kg/day (medium dose) and 10 µg/kg/day (high dose) for 5 days. G‑CSF at a low or high dose worsened intimal hyperplasia however at a medium dose improved it. In conclusion, G‑CSF had no effect in a rabbit carotid artery model of atherosclerosis. Its effects on the porcine heart were dose‑dependent; arterial disease worsened at a low or high dose, but improved at a medium dose.
No takes yet. Share an insight, caveat, or question.
Hu et al. (2019) studied Chronic obliterative arterial disease (n=60). Granulocyte colony-stimulating factor (G-CSF) vs. Normal saline was evaluated on Endothelial function and intimal hyperplasia. G-CSF had no effect in a rabbit model of atherosclerosis, but had dose-dependent effects in a porcine heart model, worsening arterial disease at low or high doses and improving it at a medium dose.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: