Background: KLOTHO is a regulator of endothelial cells activity and integrity. It has been described for the first time because of its anti-aging properties. KLOTHO encoding gene is present in many functional variants in humans, including "KL-VS" variant that has been connected with longevity and cardiovascular disease development. Few mechanisms have been proposed to explain these associations, but none of them focused on cells from CD34+ population. The aim of our study was to investigate influence of KLOTHO KL-VS polymorphism on populations of CD34+ and CD34+VEGFR2+ cells.
Methods And Results: We examined 167 Polish subjects from Pomeranian region. The analysis concerned KL-VS polymorphism, flow cytometry evaluation of whole blood cells and determination of endothelium-associated serum/plasma factors. Our results indicate that individuals possessing at least one KL-VS allele are characterized by greater number of CD34+ and CD34+VEGFR2+ and their various subpopulations (CD34+CD133+, CD34+c-Kit+, CD34+CXCR4+ and CD34+VEGFR2+c-Kit+) than wild-type volunteers. This group also exhibited more favorable lipid profile and statistically insignificant decrease of vWF and angiotensin II in their blood, whereas VEGF levels were elevated.
Conclusion: One of the mechanisms that are responsible for previously described KL-VS heterozygote advantage may be connected with maintaining greater size of hematopoietic and endothelial progenitor cells population.
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http://dx.doi.org/10.1016/j.mvr.2018.03.014 | DOI Listing |
Metab Brain Dis
December 2024
Department of Neurology, Shanghai YangZhi Rehabilitation Hospital (Shanghai Sunshine Rehabilitation Center), School of Medicine, Tongji University, 201613, Shanghai, China.
We used spontaneously hypertensive rats (SHR) as a hypertensive cerebral small vessel disease (CSVD) model to quantify blood-brain barrier (BBB) disruption by 11.7TMR T1mapping and to investigate white matter lesions and microangiopathy in CSVD. Male SHR were used as a hypertensive CSVD animal model and normotensive Wistar-Kyoto rats (WKY) were used as a control model.
View Article and Find Full Text PDFInt Endod J
December 2024
Sir John Walsh Research Institute, Faculty of Dentistry, University of Otago, Dunedin, New Zealand.
Aim: To investigate the influence of type 2 diabetes (T2D) and hyperglycaemia on blood vessels and angiogenic markers in the dental pulp.
Methodology: Extracted non-carious permanent molar teeth were collected from patients with well-controlled T2D (n = 10) and non-T2D (controls) (n = 10). The pulp was examined qualitatively using haematoxylin and eosin and Van Gieson stains.
Am J Prev Cardiol
December 2024
Department of Cardiology, Rabin Medical Center, Petah Tikva, Israel.
Background: The role of circulating endothelial progenitor cells (cEPCs) in vascular repair and their association to cardiovascular protection is well established.
Objectives: We examined the effect of proprotein convertase subtilisin kexin type 9 monoclonal antibodies (PCSK9 mAb) on cEPCs in adults with hypercholesterolemia and cardiovascular disease, aiming to establish a pleotropic class effect.
Methods: Non-interventional prospective study in patients with cardiovascular disease treated with either evolocumab or alirocumab.
Circ Res
November 2024
Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA (Z.H., I.C., F.L., J.L., H.G., E.I.P., M.S.-G., Y.S.E.N., P.A.D.).
Background: EMCN (endomucin), an endothelial-specific glycocalyx component, was found to be highly expressed by the endothelium of the renal glomerulus. We reported an anti-inflammatory role of EMCN and its involvement in the regulation of VEGF (vascular endothelial growth factor) activity through modulating VEGFR2 (VEGF receptor 2) endocytosis. The goal of this study is to investigate the phenotypic and functional effects of EMCN deficiency using the first global EMCN knockout mouse model.
View Article and Find Full Text PDFJ Stroke Cerebrovasc Dis
November 2024
Shineway Pharmaceutical Group Co. Ltd. Shijiahzuang 51430, China.
Background: Angiogenesis of brain microvascular endothelial cells (BMECs) after cerebral ischemia was conducive to improving the blood supply of ischemia tissues, which was upregulated by glycolysis. Hydroxysafflor Yellow A (HSYA) mends damaged tissues through increasing angiogenesis.
Methods: HSYA treated proliferation, migration and angiogenesis of BMECs in vitro in vitro during OGD/R.
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