Background: Cell adhesion molecules (CAMs) have been implicated in cardiac allograft rejection. However, previous studies have used qualitative analysis of immunohistochemical data and did not exclude patients with infection or malignancy.
Methods And Results: We analyzed 40 endomyocardial biopsy specimens from 25 cardiac transplant patients and 8 specimens from patients undergoing cardiac surgery. Patients with evidence of infection or malignancy were excluded. Specimens were stained with monoclonal antibodies against ICAM-1, E-selectin, VCAM-1, and PECAM-1 (which labels all vessels). ICAM-1 expression was assessed by counting ICAM-1-positive vessels and dividing by the total number of vessels (measured by PECAM staining). Specimens were scored as positive or negative for VCAM-1 and E-selectin. We also determined whether serum-soluble ICAM-1 levels (sICAM) correlated with rejection by evaluating 145 serum specimens from 48 cardiac transplant patients and 8 specimens from patients undergoing diagnostic cardiac catheterization. ICAM-1 was present on 50% to 60% of vessels in normal and nonrejecting specimens. Specimens with histologically significant rejection (focal moderate, moderate, or severe) had an increased percentage of ICAM-1-positive vessels: focal moderate, 77%; moderate/severe, 92% (P < .01). E-selectin expression did not differ between groups. VCAM-1 frequently was not present on rejecting specimens. No correlation was noted between sICAM levels and the presence or absence of rejection.
Conclusions: (1) ICAM-1 expression is strongly correlated with histologically significant cardiac allograft rejection. (2) The use of PECAM-1 staining as a vascular marker permits quantitative analysis of ICAM-1 expression. (3) VCAM-1 and E-selectin are not consistently increased during cardiac allograft rejection. (4) sICAM levels do not accurately reflect endomyocardial biopsy results.
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http://dx.doi.org/10.1161/01.cir.89.4.1760 | DOI Listing |
Mol Biol Rep
January 2025
Department of Biology, Adelphi University, One South Avenue, P.O. Box 701, Garden City, NY, 11530-0701, USA.
Background: von Hippel-Lindau (VHL) hereditary cancer syndrome is caused by mutations in the VHL tumor suppressor gene and is characterized by a predisposition to form various types of tumors, including renal cell carcinomas, hemangioblastomas, and pheochromocytomas. The protein products of the VHL gene, pVHL, are part of an ubiquitin ligase complex that tags hypoxia inducible factor alpha (HIF-α) for proteosomal degradation. pVHL has also been reported to bind to atypical protein kinase C (aPKC).
View Article and Find Full Text PDFArch Gynecol Obstet
January 2025
Division of Minimally Invasive Surgery and Gynecological Laparoendoscopy, Department of Obstetrics and Gynecology, Gangneung Asan Hospital, University of Ulsan College of Medicine, 38, Bangdong-gil, Sacheon-Myeon, Gangneung-Si, 25440, Gangwon-do, Korea.
Purpose: The emergence of minimally invasive surgery has led to the development of laparoscopic surgery to reduce the number of ports. Although the incision for the umbilical port is sufficiently large, thus reducing the number of ports used during laparoscopic surgery, postoperative complications involving incisions at port sites have been reported. Thus, we analyzed postoperative intraperitoneal outcomes after laparoscopy by reviewing operation records and photographs of consecutive surgeries.
View Article and Find Full Text PDFBackground: Although invasiveness is one of the major determinants of the poor glioblastoma (GBM) outcome, the mechanisms of GBM invasion are only partially understood. Among the intrinsic and environmental processes promoting cell-to-cell interaction processes, eventually driving GBM invasion, we focused on the pro-invasive role played by Extracellular Vesicles (EVs), a heterogeneous group of cell-released membranous structures containing various bioactive cargoes, which can be transferred from donor to recipient cells.
Methods: EVs isolated from patient-derived GBM cell lines and surgical aspirates were assessed for their pro-migratory competence by spheroid migration assays, calcium imaging, and PYK-2/FAK phosphorylation.
Biol Open
February 2025
Department of Biology, University of North Carolina at Chapel Hill, CB#3280, Chapel Hill, NC 27599-3280, USA.
The network of proteins at the interface between cell-cell adherens junctions and the actomyosin cytoskeleton provides robust yet dynamic connections that facilitate cell shape change and motility. While this was initially thought to be a simple linear connection via classic cadherins and their associated catenins, we now have come to appreciate that many more proteins are involved, providing robustness and mechanosensitivity. Defining the full set of proteins in this network remains a key objective in our field.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
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