Platelet Deposition Onto Vascular Wall Regulated by Electrical Signal

Platelets deposition at the site of vascular injury is a key event for the arrest of bleeding and for subsequent vascular repair. Therefore, the regulation of platelet deposition onto the injured site during the process of platelet plug formation is an important event. Herein, we showed that electrical signal could regulate the deposition of platelets onto the injured site. On the one hand, the area of platelet deposition was reduced when the cathode of the applied electric field was placed at the injured site beforehand, while it was increased when the anode was at the site. On the other hand, if a cathode was placed at the injured site after the injury, the electrical signal could remove the outer layer of the deposited platelets. Furthermore, an electric field could drive rapid platelet deposition onto the blood vessel wall at the site beneath the anode even in uninjured blood vessels. Platelet deposition could thus be manipulated by externally applied electric field, which might provide a mechanism to drive platelet deposition onto the wall of blood vessels.

The mechanobiological theory: a unifying hypothesis on the pathogenesis of moyamoya disease based on a systematic review

OBJECTIVE Moyamoya angiopathy (MMA) affects the distal internal carotid artery and is designated as moyamoya disease (MMD) when predisposing conditions are absent, or moyamoya syndrome (MMS) when it occurs secondary to other causes. The authors aimed to investigate the reason for this anatomical site predilection of MMA. There is compelling evidence to suggest that MMA is a phenomenon that occurs due to stereotyped mechanobiological processes. Literature regarding MMD and MMS was systematically reviewed to decipher a common pattern relating to the development of MMA. METHODS A systematic review was conducted to understand the pathogenesis of MMA in accordance with PRISMA guidelines. PubMed MEDLINE and Scopus were searched using “moyamoya” and “pathogenesis” as common keywords and specific keywords related to six identified key factors. Additionally, a literature search was performed for MMS using “moyamoya” and “pathogenesis” combined with reported associations. A progressive search of the literature was also performed using the keywords “matrix metalloprotease,” “tissue inhibitor of matrix metalloprotease,” “endothelial cell,” “smooth muscle cell,” “cytokines,” “endothelin,” and “transforming growth factor” to infer the missing links in molecular pathogenesis of MMA. Studies conforming to the inclusion criteria were reviewed. RESULTS The literature search yielded 44 published articles on MMD by using keywords classified under the six key factors, namely arterial tortuosity, vascular angles, wall shear stress, molecular factors, blood rheology/viscosity, and blood vessel wall strength, and 477 published articles on MMS associations. Information obtained from 51 articles that matched the inclusion criteria and additional information derived from the progressive search mentioned above were used to connect the key factors to derive a network pattern of pathogenesis. CONCLUSIONS Based on the available literature, the authors have proposed a unifying theory for the pathogenesis of MMA. The moyamoya phenomenon appears to be the culmination of an interplay of vascular anatomy, hemodynamics, rheology, blood vessel wall strength, and a plethora of intricately linked mechanobiological molecular mediators that ultimately results in the mechanical process of occlusion of the blood vessel, stimulating angiogenesis and collateral blood supply in an attempt to perfuse the compromised brain.

Roles and Mechanisms of Dipeptidyl Peptidase 4 Inhibitors in Vascular Aging

Vascular aging is characterized by alterations in the constitutive properties and biological functions of the blood vessel wall. Endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are indispensability elements in the inner layer and the medial layer of the blood vessel wall, respectively. Dipeptidyl peptidase-4 (DPP4) inhibitors, as a hypoglycemic agent, play a protective role in reversing vascular aging regardless of their effects in meliorating glycemic control in humans and animal models of type 2 diabetes mellitus (T2DM) through complex cellular mechanisms, including improving EC dysfunction, promoting EC proliferation and migration, alleviating EC senescence, obstructing EC apoptosis, suppressing the proliferation and migration of VSMCs, increasing circulating endothelial progenitor cell (EPC) levels, and preventing the infiltration of mononuclear macrophages. All of these showed that DPP4 inhibitors may exert a positive effect against vascular aging, thereby preventing vascular aging-related diseases. In the current review, we will summarize the cellular mechanism of DPP4 inhibitors regulating vascular aging; moreover, we also intend to compile the roles and the promising therapeutic application of DPP4 inhibitors in vascular aging-related diseases.

Examination of Mechanical Properties and Photoelastic Properties of Gel Material for Blood Vesssel Mimics

Catheter surgery is a minimally invasive treatment in which visual information is limited to a two-dimensional image generated by an X-ray camera. This results in the possibility that stress applied by the catheter onto a blood vessel wall damages the vessel. Doctors must therefore be skillful at catheter surgery. We proposed a catheter surgery simulator that visualizes the stress applied to the blood vessel wall using photoelasticity. The manufacture of this simulator requires creating blood vessel mimics that reproduce the physical properties of blood vessel tissue using photoelasticity. This study investigated the mechanical and photoelastic properties of gel materials and selected a gel composition suitable for making blood vessel mimics. We showed that by changing the compositions of polyvinyl alcohol (PVA) hydrogel and double network (DN) gel we could reproduce various blood vessel tissue properties.

R-Ras Deficiency in Pericytes Causes Frequent Microphthalmia and Perturbs Retinal Vascular Development

<b><i>Purpose:</i></b> The retinal vasculature is heavily invested by pericytes. Small GTPase R-Ras is highly expressed in endothelial cells and pericytes, suggesting importance of this Ras homolog for the regulation of the blood vessel wall. We investigated the specific contribution of pericyte-expressed R-Ras to the development of the retinal vasculature. <b><i>Methods:</i></b> The effect of R-Ras deficiency in pericytes was analyzed in pericyte-targeted conditional <i>Rras</i> knockout mice at birth and during the capillary plexus formation in the neonatal retina. <b><i>Results:</i></b> The offspring of these mice frequently exhibited unilateral microphthalmia. Analyses of the developing retinal vasculature in the eyes without microphthalmia revealed excessive endothelial cell proliferation, sprouting, and branching of the capillary plexus in these animals. These vessels were structurally defective with diminished pericyte coverage and basement membrane formation. Furthermore, these vessels showed reduced VE-cadherin staining and significantly elevated plasma leakage indicating the breakdown of the blood-retinal barrier. This defect was associated with considerable macrophage infiltration in the retina. <b><i>Conclusions:</i></b> The normal retinal vascular development is dependent on R-Ras expression in pericytes, and the absence of it leads to unattenuated angiogenesis and significantly weakens the blood-retinal barrier. Our findings underscore the importance of R-Ras for pericyte function during the normal eye development.

A case report: Early findings of distal vessel occlusion pre and post-thrombolysis using three-dimensional black blood vessel wall imaging in acute stroke.

Distal vessel occlusion of an eloquent area in acute stroke may lead to significant disability. Advances in magnetic resonance imaging enable direct visualization of thrombus within the small distal intracranial artery. The evolution of medical devices for mechanical thrombectomy has allowed the smaller distal vessels to be treated. It may change the approach to how we treat distal vessel occlusion in the future. This case highlights the value of three-dimensional black blood vessel wall imaging assessing distal vessel occlusion and respond towards reperfusion therapy.