Early adventitial activation characterized by NADPH oxidase expression and neovascularization in an aortic transplantation model

Sun, Mengyao; Ji, Jian; Guo, Xiaoxiao; Liu, Wenjun; Wang, Yanyan; Ma, Siqin; Hu, Weicheng; Wang, JianLi; Jiang, Fan

doi:10.1016/j.yexmp.2015.12.001

Cited by 7 publications

(18 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This paracrine process may represent a novel alternative mechanism underlying the pathogenic actions of macrophages in arterial remodeling. Previously we found that macrophage accumulation in the tunica adventitia was an early pathological change preceding the development of neointima in transplanted rat aorta [14]. In the present study, we showed that macrophage depletion suppressed neointimal hyperplasia and reduced transplantation-induced vascular inflammation, supporting that macrophages had a pivotal role in the pathogenesis of transplant vasculopathy.…”

Section: Discussionsupporting

confidence: 82%

“…Male F344 and Lewis inbred rats (weighing 220–270 g) were purchased from Charles River Laboratories (Beijing, China). Allograft aortic transplantation was performed as described previously using a cuff-based technique [14, 15]. Briefly, thoracic aortas from F344 rats were removed and inserted into the abdominal region of recipient Lewis rats between the levels of renal artery and iliac bifurcation.…”

Section: Methodsmentioning

confidence: 99%

“…Paraffin-embedded tissue sections were cut and stained with hematoxylin and eosin. Morphometric measurements of the average thickness of the intimal, medial and adventitial layers were carried out as described in our previous studies [14, 15]. …”

Section: Methodsmentioning

confidence: 99%

“…Using a rat model of aortic allograft transplantation [9–13], we have discovered that activation of the adventitial layer is the initial pathological event which occurs prior to the appearance of neointima [14], suggesting that the adventitia may have important roles in the pathogenesis of neointimal hyperplasia in response to transplantation. This early adventitial activation is characterized by cellularization and thickening of the layer, increased proliferation and trans-differentiation of fibroblasts, expression of multiple pro-inflammatory molecules, and increased expression of NADPH oxidase [14, 15].…”

Section: Introductionmentioning

confidence: 99%

“…This early adventitial activation is characterized by cellularization and thickening of the layer, increased proliferation and trans-differentiation of fibroblasts, expression of multiple pro-inflammatory molecules, and increased expression of NADPH oxidase [14, 15]. Interestingly, we have identified that CD68 + macrophages, but not CD3 + T lymphocytes, are the predominant type of leukocytes infiltrating the activated adventitia [14]. …”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

et al. 2017

Self Cite

View full text Add to dashboard Cite

In this study, we tested the possibility that macrophages might contribute to neointima formation by stimulating microRNA expressions in mural cells. Thoracic aortas from F344 rats were transplanted into recipient Lewis rats. Clodronate liposome was used for in vivo macrophage depletion. Using miR-21 as a prototypic example of vascular enriched microRNA, we showed that macrophage depletion reduced the expression level of miR-21, which was upregulated in the allograft. This effect of macrophage depletion was accompanied by attenuations in neointimal hyperplasia and transplantation-induced vascular inflammation. Using in vitro assays, we identified that macrophages might stimulate miR-21 expression in smooth muscle cells and adventitial fibroblasts via the release of tumor necrosis factor-α. We also showed that silencing of miR-21 suppressed tumor necrosis factor-induced proliferation, migration, and inflammatory responses in mural cells. Our results suggest that macrophage may promote transplantation-induced neointima formation by stimulating miR-21 expression in vascular mural cells, which promotes mural cell proliferation, migration and/or inflammation. Moreover, we have established that tumor necrosis factor-α has a major role in mediating this paracrine process.

show abstract

Section: Discussionsupporting

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

et al. 2017

Self Cite

View full text Add to dashboard Cite

show abstract

Adventitial Activation in the Pathogenesis of Injury-Induced Arterial Remodeling

Wang

et al. 2018

The American Journal of Pathology

Self Cite

View full text Add to dashboard Cite

Transplant vasculopathy is one of the major causes of chronic rejection after solid organ transplantation. The pathogenic mechanisms of transplant vasculopathy are still poorly understood. Herein, we summarize current evidence suggesting that activation of the tunica adventitia may be involved in the pathogenesis of transplant vasculopathy. Adventitia is an early responder to various vascular injuries and plays an integral role in eliciting vascular inflammation and remodeling. Accumulation of macrophages in the adventitia promotes the development of vascular remodeling by releasing a variety of paracrine factors that have profound impacts on vascular mural cells. Targeting adventitial macrophages has been shown to be effective for repressing transplantation-induced arterial remodeling in animal models. Adventitia also fosters angiogenesis, and neovascularization of the adventitial layer may facilitate the transport of inflammatory cells through the arterial wall. Further investigations are warranted to clarify whether inhibiting adventitial oxidative stress and/or adventitial neovascularization are better strategies for preventing transplant vasculopathy.

show abstract

CX-5461 is a potent immunosuppressant which inhibits T cell-mediated alloimmunity via p53-DUSP5

Pan

Zhang

Han

et al. 2022

Pharmacological Research

View full text Add to dashboard Cite

Early adventitial activation characterized by NADPH oxidase expression and neovascularization in an aortic transplantation model

Cited by 7 publications

References 40 publications

Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

Macrophage-stimulated microRNA expression in mural cells promotes transplantation-induced neointima formation

Adventitial Activation in the Pathogenesis of Injury-Induced Arterial Remodeling

CX-5461 is a potent immunosuppressant which inhibits T cell-mediated alloimmunity via p53-DUSP5

Contact Info

Product

Resources

About