Allogenic immune response promotes the accumulation of host-derived smooth muscle cells in transplant arteriosclerosis

Religa, Piotr; Bojakowski, Krzysztof; Bojakowska, Maria; Gaciong, Zbigniew; Thyberg, Johan; Hedin, Ulf

doi:10.1016/j.cardiores.2004.10.011

Cited by 22 publications

(26 citation statements)

References 27 publications

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“…Alloimmune activation is a prerequisite for the development of OAD. [13][14][15] This study supports the central role of IL-2-dependent T-cell-mediated alloimmune injury in the development of OAD. First, although mild inflammation is seen in syngeneic grafts due to graft ischemia during the first post-operative days, these grafts recover completely with normal histology 30 days after transplantation.…”

Section: Discussionsupporting

confidence: 78%

Tacrolimus Treatment Effectively Inhibits Progression of Obliterative Airway Disease Even at Later Stages of Disease Development

Hollmén

Tikkanen

Nykänen

et al. 2008

The Journal of Heart and Lung Transplantation

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Section: Discussionsupporting

confidence: 78%

Tacrolimus Treatment Effectively Inhibits Progression of Obliterative Airway Disease Even at Later Stages of Disease Development

Hollmén

Tikkanen

Nykänen

et al. 2008

The Journal of Heart and Lung Transplantation

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“…Traditionally, it was believed that neointimal smooth muscle cells in transplant arteriosclerosis were derived from the excessive proliferation and migration of donor-derived medial smooth muscle cells [6,7] . Recently, several studies reported that the origin of neointimal smooth muscle cells were derived from recipient cells rather than the donor medial smooth muscle cells [8] . Our previous study suggested that recipient cells were the main source of neointimal cells [5] .…”

Section: Discussionmentioning

confidence: 99%

The origin of neointimal smooth muscle cells in transplant arteriosclerosis from recipient bone-marrow cells in rat aortic allograft

Song

Zheng

et al. 2007

J. Huazhong Univ. Sc. Technol.

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In order to investigate the origin of neointimal smooth muscle cells in transplant arteriosclerosis in rat aortic allograft, sex-mismatched bone marrow transplantation was performed from male Wistar rats to female Wistar rats. Four weeks after transplantation, the aortic transplant model was established by means of micro-surgery in rats. The recipients were divided into 4 groups: female Wistar-female Wistar aortic isografts, female SD female Wistar aortic allografts, male SD-male Wistar aortic allografts, female SD-chimera Wistar aortic allografts. Eight weeks after transplantation, aortic grafts were removed at autopsy and processed for histological evaluation and immunohistochemistry. The results indicated that excessive accumulation of alpha-SMA-positive smooth muscle cells resulted in significant neointima formation and vascular lumen stricture in rat aortic allografts. Neointima assay revealed that the neointimal area and NIA/MA ratio of transplanted artery were significantly increased in all of aortic allograft groups as compared with those in aortic isograft group (P<0.01). Neointimal smooth muscle cells were harvested from cryostat sections of aortic allograft by microdissection method. The Sry gene-specific PCR was performed, and the result showed that a distinct DNA band of 225 bp emerged in the male-male aortic allograft group and chimera aortic allograft group respectively, but not in the female-female aortic allograft group. It was suggested that recipient bone-marrow cells, as the origin of neointimal smooth muscle cells, contributed to the pathological neointimal hyperplasia of aortic allograft and transplant arteriosclerosis.

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“…2,59 In analogy to wire injury-induced vascular remodeling, restraint of caspase 3-mediated apoptosis abates neointima formation in transplant arteriosclerosis. 60 Although direct evidence for apoptosis-induced SDF-1␣ expression in graft vasculopathy is lacking, SDF-1␣ is upregulated in the adventitia and subsequently in the media and neointima of aortic allografts and provokes mobilization and neointimal recruitment of SPCs.…”

Section: Vascular Remodeling By Sdf-1␣-mediated Recruitment Of Progenmentioning

confidence: 99%

Chemokines in Vascular Dysfunction and Remodeling

Schober¹

2008

ATVB

259

213

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Abstract-Vascular remodeling stands for structural changes of the vessel wall in response to various noxious stimuli, which results in reorganization of the vessel wall architecture. Luminal narrowing because of neointima formation and constrictive remodeling leading to hypoperfusion is the most relevant clinical effect. Smooth muscle cell (SMC) accumulation, inflammatory cell recruitment, and endothelial regeneration are the critical parts in obstructive vascular remodeling. Chemokines and chemokine receptors have a great impact on initiating and progressing neointimal formation by controlling each step of the remodeling process. SDF-1␣ regulates vascular repair by CXCR4-dependent smooth muscle progenitor cell recruitment, which contributes to the maladaptive response to injury. The three distinct chemokine-chemokine receptor pairs MCP-1/CCR2, RANTES/CCR5, and Fractalkine/CX 3 CR1 direct lesional leukocyte infiltration. In addition MCP-1/CCR2 and Fractalkine/CX 3 CR1 increase neointimal SMC expansion. In contrast, KC/Gro-␣ supports endothelial recovery through CXCR2, which attenuates neointima formation. These findings highlight the importance to characterize specific functions of the chemokine network to enable therapeutic intervention. V ascular remodeling denotes morphological changes of the vessel wall in response to various noxious stimuli inducing reorganization of the vessel wall structure. This impacts the cross-sectional vessel diameter and the thickness of the arterial wall in every direction; however, luminal narrowing and resulting hypoperfusion are the most detrimental sequelae of vascular remodeling. Hemodynamic stress, mechanical injury, inflammation, or hypoxia are only some of the clinically met triggers for adaptive remodeling of the vessel wall, for instance after percutaneous interventions, heart transplantation, or vein grafting. 1 Morphologically, all three layers of the arterial wall are concurrently affected by neointimal hyperplasia, medial thickening, and adventitial fibrosis attributable to the interaction of leukocyte recruitment, smooth muscle cell (SMC) accumulation, and endothelial recovery. 2,3 Molecularly, chemokines play an everemerging role in vascular repair through guidance of circulating mononuclear cells to the injury site and activation of resident vascular cells. 4,5 Considering the cell-type specific expression of chemokine receptors and the substantial overlap in ligand-receptor specificity, an interactive network of chemokines and chemokine receptors emerges with enormous plasticity in different types of vascular injury. However, a growing number of chemokine-chemokine receptor pairs with confined effects in vascular diseases have been described. 6,7 To modulate the maladaptive response in arterial remodeling, it is essential to identify specific therapeutic targets in the chemokine network. The contribution of the chemokine system to arteriosclerotic diseases has been previously reviewed in-depth. 8 -10 This review focuses on most recent findings in regulation and f...

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Allogenic immune response promotes the accumulation of host-derived smooth muscle cells in transplant arteriosclerosis

Abstract: Development of intimal thickenings during transplant vasculopathy involves an allogenic immune response, which promotes accumulation of host-derived SMCs and apoptosis of resident graft SMCs.

Cited by 22 publications

References 27 publications

Tacrolimus Treatment Effectively Inhibits Progression of Obliterative Airway Disease Even at Later Stages of Disease Development

Tacrolimus Treatment Effectively Inhibits Progression of Obliterative Airway Disease Even at Later Stages of Disease Development

The origin of neointimal smooth muscle cells in transplant arteriosclerosis from recipient bone-marrow cells in rat aortic allograft

Chemokines in Vascular Dysfunction and Remodeling

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