AI Article Synopsis

  • Optimized biocompatibility is essential for the longevity of cardiovascular implants, with a study focusing on the effects of specific coatings on decellularized rat aortic grafts.
  • Coating the inside (luminal surface) of the grafts with stromal cell-derived factor 1α (SDF1α) led to faster cellular integration and reduced abnormal tissue growth (neo-intimal hyperplasia) compared to uncoated grafts.
  • Additionally, SDF1α coating significantly decreased calcification in the grafts over an eight-week period, highlighting its potential to enhance the performance of vascular implants.

Article Abstract

Optimized biocompatibility is crucial for the durability of cardiovascular implants. Previously, a combined coating with fibronectin (FN) and stromal cell-derived factor 1α (SDF1α) has been shown to accelerate the in vivo cellularization of synthetic vascular grafts and to reduce the calcification of biological pulmonary root grafts. In this study, we evaluate the effect of side-specific luminal SDF1α coating and adventitial FN coating on the in vivo cellularization and degeneration of decellularized rat aortic implants. Aortic arch vascular donor grafts were detergent-decellularized. The luminal graft surface was coated with SDF1α, while the adventitial surface was coated with FN. SDF1α-coated and uncoated grafts were infrarenally implanted (n = 20) in rats and followed up for up to eight weeks. Cellular intima population was accelerated by luminal SDF1α coating at two weeks (92.4 ± 2.95% versus 61.1 ± 6.51% in controls, p < 0.001). SDF1α coating inhibited neo-intimal hyperplasia, resulting in a significantly decreased intima-to-media ratio after eight weeks (0.62 ± 0.15 versus 1.35 ± 0.26 in controls, p < 0.05). Furthermore, at eight weeks, media calcification was significantly decreased in the SDF1α group as compared to the control group (area of calcification in proximal arch region 1092 ± 517 μm versus 11 814 ± 1883 μm, p < 0.01). Luminal coating with SDF1α promotes early autologous intima recellularization in vivo and attenuates neo-intima hyperplasia as well as calcification of decellularized vascular grafts.

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Source
http://dx.doi.org/10.1088/1748-605X/ab54e3DOI Listing

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