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. 2018 May 1;11(5):2479-2487.
eCollection 2018.

Heme oxygenase-1 (HO-1) alleviates vascular restenosis after balloon injury in a rabbit carotid artery model

Danan Liu  1   2 , Xiangang Mo  3 , Hongming Zhang  4 , Lirong Wu  1 , Juan Tan  1 , Jincui Xiao  1 , Zheng Qin  1
Affiliations

Heme oxygenase-1 (HO-1) alleviates vascular restenosis after balloon injury in a rabbit carotid artery model

Danan Liu et al. Int J Clin Exp Pathol. .

Abstract

Percutaneous coronary intervention (PCI) is used commonly for coronary artery disease (CAD); however, restenosis is a proliferative response and frequent sequela to this treatment. Although the introduction of drug-eluting stents has convincingly reduced the incidence of vascular restenosis, restenosis remains a problem. The present study was designed to investigate the effects of the heme oxygenase-1 (HO-1) on restenosis formation after balloon injury in a rabbit carotid artery model. We found that involvement of the HO-1 in defensive restenosis formation was independent of the levels of blood lipid. Activation of HO-1 induced by chlorhematin treatment alleviated vascular restenosis after balloon injury in a rabbit carotid artery model, whereas inhibition of HO-1 by zinc protoporphyrin treatment exacerbated restenosis formation. Furthermore, overexpression of HO-1 inhibited nuclear factor kappa B subunit 1 (NF-кB) activity and decreased tumor necrosis factor-alpha (TNF-α) and endothelin 1 (ET-1) expression. In conclusion, our study provides preliminary data suggesting that HO-1 alleviates vascular restenosis after balloon injury in a rabbit carotid artery model by inhibiting NF-кB, TNF-α and ET-1 expression, indicating induction of HO-1 activation may be a feasible therapeutic target for treating vessels resistant to restenosis.

Keywords: HO-1; activation; balloon injury; restenosis.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
Chlorhematin treatment induced HO-1 overexpression. RT-PCR analysis of HO-1 mRNA levels in the carotid artery of S, O, OC and OZ groups. HO-1: heme oxygenase-1; RT-PCR: reverse transcription-PCR; S: sham group; O: operation group; OC: operation + chlorhematin treated group; OZ: operation + zinc protoporphyrin treated group. **P<0.01 vs S or O group.
Figure 2
Figure 2
HO-1 expression was upregulated in the carotid artery after treatment with chlorhematin. A. Immunohistochemical (IHC) analysis of HO-1 proteins levels in the carotid artery of S, O, OC and OZ groups. B. Western blotting was performed to detect HO-1 expression in the four groups. Relative quantitative analysis of HO-1 expression is shown. **P<0.01 vs S or O group.
Figure 3
Figure 3
HO-1 overexpression alleviated restenosis formation after balloon injury in a rabbit carotid artery model. HE staining of the carotid artery in the S, O, OC and OZ groups.
Figure 4
Figure 4
HO-1 overexpression suppressed ET-1 expression. RT-PCR analysis of ET-1 mRNA levels in the carotid artery of S, O, OC and OZ groups. Relative quantitative analysis of ET-1 expression is shown. ET-1: endothelin 1. **P<0.01 vs S or O group.
Figure 5
Figure 5
ET-1 expression was down-regulated in the carotid artery after treatment with chlorhematin. A. Immunohistochemical (IHC) analysis of ET-1 proteins levels in the carotid artery of S, O, OC and OZ groups. B. Western blotting was performed to detect ET-1 expression in the four groups. Relative quantitative analysis of ET-1 expression was showed. **P<0.01 vs S or O group.
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