Donor heart selection during the COVID-19 pandemic: A case study
JOURNAL OF HEART AND LUNG TRANSPLANTATION
2020; 39 (5): 497?98
Donor heart selection during the COVID-19 pandemic: A case study.
The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
2020; 39 (5): 497?98
Donor-specific anti-HLA antibody production following pediatric ABO-incompatible heart transplantation
2019; 23 (2)
Blood flow reprograms lymphatic vessels to blood vessels
JOURNAL OF CLINICAL INVESTIGATION
2012; 122 (6): 2006?17
Platelets regulate lymphatic vascular development through CLEC-2-SLP-76 signaling
2010; 116 (4): 661?70
Human vascular malformations cause disease as a result of changes in blood flow and vascular hemodynamic forces. Although the genetic mutations that underlie the formation of many human vascular malformations are known, the extent to which abnormal blood flow can subsequently influence the vascular genetic program and natural history is not. Loss of the SH2 domain-containing leukocyte protein of 76 kDa (SLP76) resulted in a vascular malformation that directed blood flow through mesenteric lymphatic vessels after birth in mice. Mesenteric vessels in the position of the congenital lymphatic in mature Slp76-null mice lacked lymphatic identity and expressed a marker of blood vessel identity. Genetic lineage tracing demonstrated that this change in vessel identity was the result of lymphatic endothelial cell reprogramming rather than replacement by blood endothelial cells. Exposure of lymphatic vessels to blood in the absence of significant flow did not alter vessel identity in vivo, but lymphatic endothelial cells exposed to similar levels of shear stress ex vivo rapidly lost expression of PROX1, a lymphatic fate-specifying transcription factor. These findings reveal that blood flow can convert lymphatic vessels to blood vessels, demonstrating that hemodynamic forces may reprogram endothelial and vessel identity in cardiovascular diseases associated with abnormal flow.
View details for DOI 10.1172/JCI57513
View details for Web of Science ID 000304736300011
View details for PubMedID 22622036
View details for PubMedCentralID PMC3366395
Engineering of fiber-reinforced tissues with anisotropic biodegradable nanofibrous scaffolds.
Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
2006; 1: 787?90
Although platelets appear by embryonic day 10.5 in the developing mouse, an embryonic role for these cells has not been identified. The SYK-SLP-76 signaling pathway is required in blood cells to regulate embryonic blood-lymphatic vascular separation, but the cell type and molecular mechanism underlying this regulatory pathway are not known. In the present study we demonstrate that platelets regulate lymphatic vascular development by directly interacting with lymphatic endothelial cells through C-type lectin-like receptor 2 (CLEC-2) receptors. PODOPLANIN (PDPN), a transmembrane protein expressed on the surface of lymphatic endothelial cells, is required in nonhematopoietic cells for blood-lymphatic separation. Genetic loss of the PDPN receptor CLEC-2 ablates PDPN binding by platelets and confers embryonic lymphatic vascular defects like those seen in animals lacking PDPN or SLP-76. Platelet factor 4-Cre-mediated deletion of Slp-76 is sufficient to confer lymphatic vascular defects, identifying platelets as the cell type in which SLP-76 signaling is required to regulate lymphatic vascular development. Consistent with these genetic findings, we observe SLP-76-dependent platelet aggregate formation on the surface of lymphatic endothelial cells in vivo and ex vivo. These studies identify a nonhemostatic pathway in which platelet CLEC-2 receptors bind lymphatic endothelial PDPN and activate SLP-76 signaling to regulate embryonic vascular development.
View details for DOI 10.1182/blood-2010-02-270876
View details for Web of Science ID 000280502800025
View details for PubMedID 20363774
View details for PubMedCentralID PMC3324297
The repair of dense fiber-reinforced tissues poses a significant challenge for the tissue engineering community. The function of these structures is largely dependent on their architectural form, and as such, scaffold organization is an important design parameter in generating tissue analogues. To address this issue, we have recently utilized electrospinning to instill controllable fiber anisotropy in nanofibrous scaffolds. This abstract details the mechanical characterization of the bulk and local properties of these scaffolds, and points to their potential application in the repair and/or generation of fiber-reinforced tissues that recapitulate the native form.
View details for PubMedID 17946860