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Updated: Dec 12, 2025
Patch Angioplasty in the Rat Aorta or Inferior Vena Cava
Published on: February 27, 2017
Inhibition of programmed death-1 decreases neointimal hyperplasia after patch angioplasty
Hualong Bai1,2, Zhiwei Wang1, Mingxing Li1
1Department of Vascular and Endovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Abstract:
Neointimal hyperplasia remains an obstacle after vascular interventions. Programmed death-1 (PD-1) antibody treatment decreases tumor cell proliferation and secretion of inflammatory factors, and several antineoplastic drugs show efficacy against neointimal hyperplasia. We hypothesized that inhibition of PD-1 inhibits neointimal hyperplasia in a rat patch angioplasty model. In a rat aorta patch angioplasty model, four groups were compared: the control group without treatment, a single dose of humanized PD-1 antibody (4 mg/kg) injected immediately after patch angioplasty, PD-1 antibody-coated patches, and BMS-1 (PD-1 inhibitor)-coated patches. Patches were harvested (Day 14) and analyzed. After patch angioplasty, PD-1-positive cells were present. Inhibition of PD-1 using both intraperitoneal injection of humanized PD1 antibody as well as using patches coated with humanized PD1 antibody significantly decreased neointimal thickness (p = 0.0199). There were significantly fewer PD-1 (p = 0.0148), CD3 (p = 0.0072), CD68 (p = 0.0001), CD45 (p = 0.001), and PCNA (p < 0.0001)-positive cells, and PCNA/α-actin dual positive cells (p = 0.0005), in the treated groups. Patches coated with BMS-1 showed similarly decreased neointimal thickness and accumulation of inflammatory cells. Inhibition of PD-1 using PD-1 antibody or its inhibitor BMS-1 can significantly decrease neointimal thickness in vascular patches. Inhibition of the PD-1 pathway may be a promising therapeutic strategy to inhibit neointimal hyperplasia.
Insights
Inhibiting programmed death-1 (PD-1) with antibodies or inhibitors significantly reduced neointimal hyperplasia after vascular surgery in rats. This suggests PD-1 pathway inhibition is a promising therapeutic strategy for vascular healing.
Area of Science:
- Vascular Biology
- Immunology
- Regenerative Medicine
Background:
- Neointimal hyperplasia is a significant challenge following vascular interventions.
- Programmed death-1 (PD-1) antibody treatment is known to reduce tumor cell proliferation and inflammatory factors.
- Antineoplastic drugs have demonstrated efficacy in managing neointimal hyperplasia.
Purpose of the Study:
- To investigate the efficacy of programmed death-1 (PD-1) inhibition in mitigating neointimal hyperplasia.
- To evaluate the effects of PD-1 antibody and inhibitor treatments in a rat patch angioplasty model.
Main Methods:
- A rat aorta patch angioplasty model was utilized with four experimental groups: control, PD-1 antibody injection, PD-1 antibody-coated patches, and PD-1 inhibitor (BMS-1)-coated patches.
- Vascular patches were analyzed on Day 14 post-angioplasty.
- Immunohistochemical analysis was performed to quantify PD-1, CD3, CD68, CD45, and PCNA positive cells.
Main Results:
- PD-1 inhibition, via systemic injection or coated patches, significantly reduced neointimal thickness (p = 0.0199).
- Treated groups exhibited significantly fewer PD-1, CD3, CD68, CD45, and PCNA positive cells compared to controls (p < 0.0001 for PCNA).
- BMS-1 coated patches demonstrated comparable reductions in neointimal thickness and inflammatory cell accumulation.
Conclusions:
- Inhibition of the PD-1 pathway, using either PD-1 antibody or its inhibitor BMS-1, effectively decreases neointimal thickness in vascular patches.
- Targeting the PD-1 pathway represents a potentially effective therapeutic strategy for inhibiting neointimal hyperplasia.
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