Endothelial Regeneration of Large Vessels Is a Biphasic Process Driven by Local Cells with Distinct Proliferative Capacities

McDonald, Austin I.; Shirali, Aditya S.; Aragón, Raquel; Ma, Feiyang; Hernandez, Gloria; Vaughn, Don A.; Mack, Julia J.; Lim, Tiffany Y.; Sunshine, Hannah; Zhao, Peng; Kalinichenko, Vladimir V.; Hai, Tsonwin; Pelegrini, Matteo; Ardehali, Reza; Iruela‐Arispe, M. Luisa

doi:10.1016/j.stem.2018.07.011

Cited by 159 publications

(189 citation statements)

References 34 publications

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“…This is consistent with the observation that the transplant vasculature in humans undergoes alloimmune injury along the length of the arterial tree, from artery to the microvasculature (4). Recent work identifies reparative endothelial progenitor cells embedded in the mouse aortic endothelium, but repair from mechanical injury involved EC dedifferentiation and proliferation (34). We confirmed that apelin expression in human heart explant coronary artery endothelium was induced versus unutilized donor arteries, but these specimens had advanced disease with heterogeneous expression of the biomarkers, and may not all reflect evolving lesions.…”

Section: Discussionsupporting

confidence: 62%

Apelin directs endothelial cell differentiation and vascular repair following immune-mediated injury

Masoud¹,

Lin²,

Azad³

et al. 2019

Journal of Clinical Investigation

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Section: Discussionsupporting

confidence: 62%

Apelin directs endothelial cell differentiation and vascular repair following immune-mediated injury

Masoud¹,

Lin²,

Azad³

et al. 2019

Journal of Clinical Investigation

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“…15,16 Beside the risk for thrombus development, which was the focus of a previous study, 11 the further process and changes of the intimal lesion itself is consistently topic of research. [17][18][19][20][21] Most remarkable observation during our study was the determination of a clear trend in reduction of defect sizes 7 days after defect creation. Mean shrinkage was calculated 42.8%, absolute decrease in size was 0.75 mm 2 on average.…”

Section: Discussionsupporting

confidence: 53%

Alterations in Surgically Created Intimal Lesions: An Observation Study in the Aortic Rat Model

Wolff

Ritschl

Düring

et al. 2020

J Reconstr Microsurg

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Background Intimal injury in microvessels due to common risk factors such as atherosclerosis or inadequate manipulation are known to have a major impact on developing thrombosis and eventually vascular obstruction. Understanding of these injuries is therefore of great significance to prevent far-reaching consequences such as flap loss in free tissue transfer. It was the aim of this study to evaluate artificially induced intimal lesions with focus on alteration in size and configuration. Methods Intimal defects were created surgically in the abdominal aorta of 30 male Wistar rats. After planimetric measurement of the defect sizes, configuration of defects were classified as round, horizontal, or vertical. Seven days postoperatively, the rats underwent a second-look surgery. Finally, the abdominal aorta was harvested, and the endothelial defects were reevaluated concerning size and configuration using a defined pattern. Results The mean defect size created intraoperatively was 1.68 ± 0.6 mm2. The classification of the defects configurations resulted in 43.3% round, 20% horizontal, and 36.7% vertical defects. Reevaluation at 7 days after surgery showed defect shrinkage in 96.7% in total and 42.8% averaging due to reendothelialization. A shift in defect configuration was detected in 56.7%, the strongest being in vertical defect configurations (100%). Vascular occlusion did not occur in any of the specimen. Conclusion Intimal injuries undergo a fast repair process in terms of size reduction and configuration modification due to reendothelialization. Especially vertical defects, representing a great risk for thrombus formation, convert into lower risk horizontal defect configurations. In high-flow vessels such as the rat aortas, small endothelial damage seems to have no significant impact to produce complete vascular occlusion. Still, all efforts should be made to avoid any kind of intimal injury.

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“…However, based on the literature that reendothelialization of arteries, endothelial proliferation (39), and reduced atherosclerosis (21) is linked to CXCR4 expression and function, we argue that CXCR4 itself has a protective role. Additional recent RNA sequencing data analysis of locally regenerating ECs to recover from endothelial injury in vivo shows enhancement of CXCR4 expression (45). Endothelial CXCR4 is also reported to be athero-protective through attenuating vascular permeability by enhancing VE-cadherin expression and stabilizing VE-cadherin complexes (21).…”

Section: Discussionmentioning

confidence: 99%

CXCR4-binding PET tracers link monocyte recruitment and endothelial injury in murine atherosclerosis

Randolph¹,

Elvington²,

Baba

et al. 2020

Preprint

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Viral macrophage inflammatory protein 2 (vMIP-II/vCCL2) binds to multiple chemokine receptors, and vMIP-II based PET tracer ( 64 Cu-DOTA-vMIP-II: vMIP-II tracer) accumulates at atherosclerotic lesions in mice. The magnitude of 64 Cu-DOTA-vMIP-II accumulation correlated with monocyte recruitment, as Apoe -/mice treated with AAV-mApoE showed PET signal declining as monocyte recruitment subsided. Unexpectedly, monocytes themselves were not the major target of the 64 Cu-DOTA-vMIP-II tracer.Using fluorescence-tagged vMIP-II tracer, competitive receptor blocking with CXCR4 antagonists, CXCR4-specific tracer 64 Cu-DOTA-FC131, or CXCR4 staining during disease progression and regression, endothelial cell expression of CXCR4 proved to be the main target of 64 Cu-DOTA-vMIP-II imaging. Expression of CXCR4 was low in nonplaque areas, but strongly detected on endothelium at the edges of progressing plaques, corresponding to a population of proliferating endothelium and to the location in plaques where monocyte recruitment occurred. Thus, endothelial injury status of plaques is marked by CXCR4 expression and that this injury correlates with the tendency of such plaques to recruit monocytes. Furthermore, our findings suggest PET tracers that, through binding CXCR4, may be useful to monitor plaque injury status.

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Endothelial Regeneration of Large Vessels Is a Biphasic Process Driven by Local Cells with Distinct Proliferative Capacities

Cited by 159 publications

References 34 publications

Apelin directs endothelial cell differentiation and vascular repair following immune-mediated injury

Apelin directs endothelial cell differentiation and vascular repair following immune-mediated injury

Alterations in Surgically Created Intimal Lesions: An Observation Study in the Aortic Rat Model

CXCR4-binding PET tracers link monocyte recruitment and endothelial injury in murine atherosclerosis

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