Flanking Recipient Vasculature, Not Circulating Progenitor Cells, Contributes to Endothelium and Smooth Muscle in Murine Allograft Vasculopathy

Hagensen, Mette K.; Shim, Jeong; Falk, Erling; Bentzon, Jacob F.

doi:10.1161/atvbaha.110.221184

Cited by 37 publications

(21 citation statements)

References 29 publications

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“…Chen et al 19 found resident progenitor cells near the vasa vasorum and suggested that the vasa vasorum served as a means of transport and as a reservoir of mobilized progenitor cells. Hagensen et al 29 used a double-transplantation technique to exclude the interference of circulating cells and reported that the flanking recipient vasculature contributed to neointima hyperplasia in TA lesions instead of circulating progenitor cells. Our study did not provide direct evidence to identify the source of SMPCs.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-155 Promotes the Directional Migration of Resident Smooth Muscle Progenitor Cells by Regulating Monocyte Chemoattractant Protein 1 in Transplant Arteriosclerosis

Sun

Wang

et al. 2016

ATVB

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Objective— Smooth muscle–like cells are major cell components of transplant arteriosclerosis lesions. This study investigated the origin of the smooth muscle–like cells, the mechanisms responsible for their accumulation in the neointima, and the factors that drive these processes. Approach and Results— A murine aortic transplantation model was established by transplanting miR-155 −/− bone marrow cells into miR-155 +/+ mice. MicroRNA-155 was found to play a functional role in the transplant arteriosclerosis. Moreover, we found that the nonbone marrow–derived progenitor cells with markers of both early differentiated smooth muscles and stem cells in the allograft adventitia were smooth muscle progenitor cells. Purified smooth muscle progenitor cells expressed a mature smooth muscle cell marker when induced by platelet-derived growth factor-BB in vitro. In vivo, these cells could migrate into the intima from the adventitia and could contribute to the neointimal hyperplasia. The loss of microRNA-155 in bone marrow–derived cells decreased the concentration gradient of monocyte chemoattractant protein 1 between the intima and the adventitia of the allografts, which reduced the migration of smooth muscle progenitor cells from the adventitia into the neointima. Conclusions— This study demonstrated that microRNA-155 promoted the directional migration of smooth muscle progenitor cells from the adventitia by regulating the monocyte chemoattractant protein 1 concentration gradient, which aggravated transplant arteriosclerosis.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-155 Promotes the Directional Migration of Resident Smooth Muscle Progenitor Cells by Regulating Monocyte Chemoattractant Protein 1 in Transplant Arteriosclerosis

Sun

Wang

et al. 2016

ATVB

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“…30 One critical regulator of endothelial cell survival and function is the B2R. The prevention of kinin degradation and thus activation of B2R signaling are considered to contribute to beneficial effects of ACE inhibitors on endothelial function and blood pressure.…”

Section: Discussionmentioning

confidence: 99%

Novel Insights Into the Critical Role of Bradykinin and the Kinin B2 Receptor for Vascular Recruitment of Circulating Endothelial Repair–Promoting Mononuclear Cell Subsets

et al. 2013

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hi monocytes, from CAD patients as compared with healthy subjects. B2R stimulation induced CD18 activation in early outgrowth cells of healthy subjects, but not in early outgrowth cells of CAD patients. Adenoviral B2R overexpression enhanced in vivo vascular recruitment and rescued impaired endothelial repair capacity of early outgrowth cells from CAD patients. Conclusions-We newly report that bradykinin/B2R signaling may promote endothelial repair after arterial injury by selective recruitment and functional activation of B2R-expressing circulating mononuclear cell subsets. In CAD patients, B2R downregulation on endothelial repair-promoting circulating mononuclear cells substantially impairs the bradykinindependent endothelial repair, representing a novel mechanism promoting endothelial injury in CAD patients. (Circulation. 2013;127:594-603.)

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“…Indeed, the reduced CX3CL1/CX3CR1 response in femoral arteries is probably a reflection of more complete EC removal. Although the remaining ECs in the injured vessel may be either inflamed or undergoing apoptosis, while still present, it may be assumed that clearly visible CX3CL1 expression, evident in figure 3, is functionally competent to bind its ligand CX3CR1; however, the resolution of injury predominantly involves migration of ECs from the margins of the site of injury [17]. …”

Section: Discussionmentioning

confidence: 99%

Differential Endothelial Coverage, Response to Injury and Neointimal Integration of CX3CR1/Smooth Muscle-Like Cells after Carotid or Femoral Arterial Injury

Martin

Kumar²,

Klinkert³

et al. 2013

J Vasc Res

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Background: Previously, we established the importance of the CX3CL1/CX3CR1 axis in the promotion of myeloid cell differentiation into neointimal smooth muscle-like cells (SMLC). Methods: In this study, acute (24 h) endothelial coverage and CX3CL1 expression as well as chronic (2 weeks) vascular remodeling was examined with respect to whether myeloid CX3CR1⁺ SMLC number in the neointima differed between carotid and femoral artery wire injury. Results and Conclusion: Twenty-four hours after injury, CX3CL1 expression was significantly elevated in injured carotid compared to femoral arteries. In mice with CX3CR1 promoter-driven expression of green fluorescent protein, neointima formation was significantly greater (p < 0.05) 2 weeks after injury in femoral versus carotid arteries as determined by the intima/media ratio. Although the percentage of F4/80/CX3CR1⁺ cell integration was similar in both models, the carotid lesion had greater proportions of cells coexpressing CX3CR1 and both α-smooth muscle actin and calponin (p < 0.05). Wire injury of carotid arteries was associated with greater CX3CL1 expression in the acute phase followed by greater CX3CR1 coexpressing SMLC content in later lesions as well as less neointima formation than in femoral arteries. This may, in part, explain the variability in lesion composition after carotid versus femoral wire injury.

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Flanking Recipient Vasculature, Not Circulating Progenitor Cells, Contributes to Endothelium and Smooth Muscle in Murine Allograft Vasculopathy

Cited by 37 publications

References 29 publications

MicroRNA-155 Promotes the Directional Migration of Resident Smooth Muscle Progenitor Cells by Regulating Monocyte Chemoattractant Protein 1 in Transplant Arteriosclerosis

MicroRNA-155 Promotes the Directional Migration of Resident Smooth Muscle Progenitor Cells by Regulating Monocyte Chemoattractant Protein 1 in Transplant Arteriosclerosis

Novel Insights Into the Critical Role of Bradykinin and the Kinin B2 Receptor for Vascular Recruitment of Circulating Endothelial Repair–Promoting Mononuclear Cell Subsets

Differential Endothelial Coverage, Response to Injury and Neointimal Integration of CX3CR1/Smooth Muscle-Like Cells after Carotid or Femoral Arterial Injury

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