Data on the expression and role of TREM-1 in the development of in-stent restenosis

The data presented in this article are related to the research article entitled “Increased serum TREM-1 level is associated with in-stent restenosis, and activation of TREM-1 promotes inflammation, proliferation and migration in vascular smooth muscle cells” (Wang et al., 2017) [1], which demonstrated that TREM-1 is expressed on vascular smooth cells (VSMCs) and promotes inflammation, proliferation and migration in cultured VSMCs. In this dataset, the expression of TREM-1 in leukocytes and endothelial cells of carotid artery after ligation was evaluated. The effect of TREM-1 on stenosis was analyzed in cultured human saphenous veins (HSVs) that spontaneously undergo remodeling which involves VSMC proliferation and migration.

The data presented in this article are related to the research article entitled "Increased serum TREM-1 level is associated with in-stent restenosis, and activation of TREM-1 promotes inflammation, proliferation and migration in vascular smooth muscle cells" (Wang et al., 2017) [1], which demonstrated that TREM-1 is expressed on vascular smooth cells (VSMCs) and promotes inflammation, proliferation and migration in cultured VSMCs. In this dataset, the expression of TREM-1 in leukocytes and endothelial cells of carotid artery after ligation was evaluated. The effect of TREM-1 on stenosis was analyzed in cultured human saphenous veins (HSVs) that spontaneously undergo remodeling which involves VSMC proliferation and migration.
& Both the expression and molecular function of TREM-1 in the model of vascular stenosis was analyzed Data accessibility The data are available with this article

Value of the data
The data analyze changes in the expression of TREM-1 during the development of vascular stenosis.
The data delineate the cellular source of TREM-1 in the vascular wall under basal conditions and after stenosis.
The data provide evidence for the participation of TREM-1 signaling in the stenotic process.

Data
Dual immunofluorescence investigated whether TREM-1 was co-localized with endothelial cells (CD31 þ ) or infiltrated leukocytes (CD45 þ ) besides smooth muscle cells [1] within the vessel wall of the ligated carotid arteries (Fig. 1). Thickness of the intimal, medial and adventitial layers of the HSVs was measured after cultured ex vivo for 7 days with or without LP17 or TREM-1-activating antibody (Fig. 2).

Animals and carotid ligation
All animal experiments were conducted in accordance with experimental protocols approved by the Committee on Animal Resources of Shanghai Jiaotong University. Wild type C57BL/6 mice were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd (Beijing, China). Complete carotid ligation was performed on C57BL/6 mice anesthetized using 2.0% isoflurane, placed on a heated surgical board. A midline cervical incision was made and the left common carotid was isolated and ligated.

Immunofluorescence
Immunofluorescence was performed as previously described [2]. Paraffin-embedded sections of the carotid artery were deparaffinized and incubated with primary goat anti-TREM-1 antibody (#sc- Fluor 546 and 488, respectively; Invitrogen, Carlsbad, CA, USA), images were acquired using an inverted epi-fluorescence microscope (Olympus BX61) equipped with a DP72 camera.

Human saphenous veins culture ex vivo
HSVs, not required for surgery, were collected from discards after coronary artery bypass graft surgery and were cultured as previously described [3]. Briefly, the vein segments were opened longitudinally and cultured individually with luminal surface facing up in 12-well plates in RPMI 1640 medium supplemented with 30% FBS, 2 mmol/l L-glutamine, 100 IU/ml penicillin and 100 μg/ml streptomycin for 7 days with or without LP17 or TREM-1-activating antibody. The vein segments were then fixed and embedded in paraffin. Cross-sections were cut and stained with α-smooth muscle actin. Thickness of intima, media, and adventitia was measured by Image-Pro Plus 6.0.

Statistics
Data are expressed as mean 7SD or SEM from 4 to 7 independent experiments. Differences between two groups were analyzed by two-tailed Student's t-test. Probability values less than 0.05 were considered statistically significant. All statistical analysis was performed with SPSS 19.0 for Windows (SPSS, Inc., Chicago, IL, USA).