Backround: The treatment of rotator cuff tears is still challenging. Tendon tissue engineering (TTE) might be an alternative in future. Tenocytes seem to be the most suitable cell type as they are easy to obtain and no differentiation in vitro is necessary. The aim of this study was to examine, if the long head of the biceps tendon (LHB) can deliver viable tenocytes for TTE. In this context, different isolation methods, such as enzymatic digestion (ED) and cell migration (CM), are investigated on differences in gene expression and cell morphology. Methods: Samples of the LHB were obtained from patients, who underwent surgery for primary shoulder arthroplasty. Using ED as isolation method, 0.2% collagenase I solution was used. Using CM as isolation method, small pieces of minced tendon were put into petri-dishes. After cell cultivation, RT-PCR was performed for collagen type I, collagen type III, decorin, tenascin-C, fibronectin, Scleraxis, tenomodulin, osteopontin and agreccan. Results: The total number of isolated cells, in relation to 1 g of native tissue, was 14 times higher using ED. The time interval for cell isolation was about 17 hours using ED and approximately 50 days using CM. Cell morphology in vitro was similar for both isolation techniques. Higher expression of collagen type I could be observed in tenocyte-like cell cultures (TLCC) using ED as isolation method (p < 0.05), however decorin expression was higher in TLCC using CM as isolation method (p < 0.05). Dedifferentiation potential seemed to be similar for both isolation techniques. Conclusion: In summary tenocyte-like cells can be obtained with both isolation methods (ED and CM) from the LHB. As no obvious disadvantage could be seen using ED, this method is more suitable for clinical use, as time for cell isolation is shorter and a remarkably higher number of cells can be obtained. However, both isolation methods can further be improved.

Introduction: Tendon tissue engineering (TTE) tries to produce tendinous tissue of high quality to replace dysfunctional tissue. One possible application of TTE might be the replacement of ruptured tissue of the rotator cuff. Autologous tenocytes seem to be most suitable as no differentiation...

BACKGROUND: Red blood cells (RBCs) contribute to hemostasis and thrombosis by interacting with platelets via the FasL–FasR pathway to induce procoagulant activity and thrombin formation. Here, we identified a novel mechanism of platelet–RBC interaction via the CD36–TSP-1 (thrombospondin-1) signaling pathway that plays a prominent role in arterial thrombosis and abdominal aortic aneurysm (AAA) formation and progression. AAA is a life-threatening atherosclerotic-related disease, characterized by the progressive dilation of the abdominal aorta, due to chronic inflammation and extracellular matrix remodeling/degradation within the vessel wall. The objective of the present study was to elucidate a new mechanism of platelet–RBC interaction via the TSP1–CD36 axis and its significance for arterial thrombosis and the pathology of AAA. METHODS: TSP-1-deficient and CD36 cell-type-specific (RBCs and platelets) knock-out mice were analyzed in experimental mouse models of arterial thrombosis and AAA. Blood samples from patients with AAA from peripheral sites (laminar flow) and from inside the aneurysm segment (turbulent flow) were analyzed by flow cytometry and compared with age-matched controls. RESULTS: After platelet activation, platelet-released TSP-1 binds to CD36 at the RBC and platelet membrane to enhance procoagulant activity of both cells, leading to platelet aggregation and thrombosis. Patients with AAA exhibit enhanced procoagulant activity, elevated TSP-1 and CD36 plasma levels, as well as increased exposure of TSP-1 and CD36 at the RBC and platelet surface. In addition, biomechanically stress in the aneurysmal segment reinforces CD36 externalization on RBCs and platelets as well as the formation of platelet–RBC aggregates. In line, genetic deletion of either CD36 (RBC restricted) or TSP-1 protected mice against experimentally induced AAA formation. CONCLUSIONS: Our findings imply that CD36 on RBCs and platelets, as well as platelet-released TSP-1, contribute to procoagulant activity, playing a crucial role in arterial thrombosis and AAA progression.

Introduction. This study analyzed the patient outcomes following endovascular aortic aneurysm repair (EVAR) for infrarenal aortic pathologies with very narrow aortic bifurcations using the AFX stent graft. Methods. The data was retrieved from the archived medical records of 35 patients treated for abdominal aortic aneurysm (AAA) (48.6%) or penetrating aortic ulcer (PAU) (51.4%) with very narrow aortic bifurcation between January 2013 and May 2020. Patient survival, freedom from endoleak (EL), and limb occlusion were estimated applying the Kaplan–Meier method. Results. The mean follow-up time was months. The mean aortic bifurcation diameter was . Technical success was 100%, and no procedure-related deaths occurred. Two type II ELs occurred within 30-day follow-up. We observed one common iliac artery stenosis at four months and one type III EL at 54 months in the same patient, both of which required re-intervention. Overall patient survival was (AAA: 100%; PAU: ), freedom from limb occlusion was (AAA: ; PAU: 100%), freedom from type II EL was (AAA: ; PAU: 100%), and freedom from EL type III was (AAA: ; PAU: 100%) at the end of the follow-up period. Conclusions. Very narrow aortic bifurcations may predispose patients to procedure-related complications following EVAR. Our results suggest a safe use of the AFX stent graft in such scenarios. The overall short- and long-term procedure-related patient outcomes are satisfying albeit they may seem superior for PAU when compared to AAA.

BACKGROUND: Abdominal aortic aneurysms (AAAs) are characterized by ECM (extracellular matrix) degradation and chronic vascular inflammation, with macrophages playing a key role. The mechanisms regulating macrophage activation in AAA remain incompletely understood. Vascular macrophages express Olfr2 (olfactory receptor 2), a GPCR (G-protein–coupled receptor) implicated in inflammation, but its role in AAA development is unknown. METHODS: We investigated the role of Olfr2 in AAA using PPE (porcine pancreatic elastase) infusion in Olfr2-deficient ( Olfr2 ^−/− ), Ang II (angiotensin II) infusion in Apoe ^−/− Olfr2 ^−/− mice, bone marrow transplantation, and pharmacological modulation experiments. Echocardiography and histology were complemented by spectral flow cytometry, transcriptional profiling, and functional in vivo and ex vivo assays. RESULTS: Microarray analysis revealed increased expression of the human Olfr2 orthologue OR6A2 (olfactory receptor family 6 subfamily A member 2) in AAA tissue. Flow cytometry showed OR6A2 upregulation in monocytes from patients with large versus small AAAs. In both human and murine tissues, up to 30% of vascular macrophages expressed OR6A2/Olfr2, which peaked in MHCII ^high CCR2 ^low monocytes/macrophages on day 7 of experimental AAA. Both whole-body and hematopoietic Olfr2 deficiency protected mice from AAA formation, with reduced ECM degradation, decreased macrophage infiltration, and preserved smooth muscle cell content. Treatment with the Olfr2 agonist octanal exacerbated, while the antagonist citral reduced AAA and inflammation. In Olfr2 ^−/− mice, inflammatory gene expression and aortic leukocyte accumulation were diminished. Despite a similar total leukocyte count, Ly6C ^high monocytes displayed reduced CX3CR1 (CX3C motif chemokine receptor 1) expression and impaired migration toward CX3CL1 in vitro. Competitive transfer confirmed reduced migratory capacity of Olfr2 ^−/− monocytes, while pharmacological CX3CR1 inhibition mitigated the proinflammatory effects of octanal in AAA. CONCLUSIONS: Olfr2 regulates monocyte recruitment and macrophage-driven inflammation during AAA. Its genetic deletion or pharmacological inhibition protects against AAA, whereas receptor activation worsens the disease. Olfr2 represents a critical modulator of vascular inflammation and a potential therapeutic target in AAA.