Vascular damage by unstable hemoglobins: The role of heme-depleted globin

2005 ◽  
Vol 436 (2) ◽  
pp. 307-315 ◽  
Author(s):  
V.A. Tsemakhovich ◽  
V.V. Bamm ◽  
M. Shaklai ◽  
N. Shaklai
Keyword(s):  
Vascular Damage ◽  
Unstable Hemoglobins

scholarly journals AB0026 DECREASE OF ANGIOGENIC T CELLS IN CONNECTIVE TISSUE DISEASE-ASSOCIATED INTERSTITIAL LUNG DISEASE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1046.3-1047
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo Martinez ◽  
F. Genre ◽  
B. Atienza-Mateo ◽  
V. M. Mora-Cuesta ◽  
...  
Keyword(s):  
T Cells ◽  
Interstitial Lung Disease ◽  
Connective Tissue ◽  
Lung Disease ◽  
Cell Subset ◽  
Vascular Damage ◽  
Type I ◽  
Research Support ◽  
Angiogenic T Cells

Background:Interstitial lung disease (ILD) is one of the most significant complications of connective tissue diseases (CTD), leading to an increase of the morbidity and mortality in patients with CTD [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, have been involved in the pathogenesis of CTD [2-4]. However, to the best of our knowledge, no information regarding the role of TAng in CTD-ILD+ is available.Objectives:To study, for the first time, the potential role of TAng related to vascular damage in CTD-ILD+.Methods:Peripheral venous blood was collected from 40 patients with CTD-ILD+ and three comparative groups: 44 CTD-ILD- patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 20 healthy controls (HC). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4.Results:Patients with CTD-ILD+ exhibited a significantly lower TAng frequency than CTD-ILD- patients (p<0.001). Similar results were obtained when patients with CTD-ILD+ were compared with HC (p=0.004) although no difference was observed between CTD-ILD+ and IPF. In addition, a significant increase of TAng frequency was shown in patients with CTD-ILD- in relation to IPF patients (p<0.001), while no difference was observed between CTD-ILD- and HC.Conclusion:Our results reveal a decrease of TAng frequency related to vascular damage in CTD-ILD+. Furthermore, we disclose that the presence of ILD is associated with lower TAng frequency.References:[1]Expert Rev Clin Immunol 2018;14(1):69-82.[2]Circulation 2007;116(15):1671-82.[3]Ann Rheum Dis 2015 74(5):921-7.[4]PLoS One 2017;12(8):e0183102.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

scholarly journals Role of Interleukin-25 in allergic airway inflammation and vascular damage

2011 ◽  
Vol 31 (5) ◽  
pp. 420-424
Author(s):  
Hiroshi Nakajima ◽  
Saki Kawashima ◽  
Tomohiro Tamachi ◽  
Kentaro Takahashi ◽  
Koichi Hirose
Keyword(s):  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Vascular Damage ◽  
Interleukin 25

The Elegant Platelet: Signals Controlling Actin Assembly

1999 ◽  
Vol 82 (08) ◽  
pp. 392-398 ◽  
Author(s):  
Kurt Barkalow ◽  
Anser Azim ◽  
Joe Italiano ◽  
John Hartwig
Keyword(s):  
Actin Filaments ◽  
Active Form ◽  
Blood Platelet ◽  
Vascular Damage ◽  
Structural Basis ◽  
Actin Assembly ◽  
Small Disc ◽  
Specific Proteins

SummaryThe function of the blood platelet is defined by its two physical states. The platelet is born in the first state, in long cytoplasmic extensions from megakaryocytes, as a small disc of reproducible structure having an elegant, actin-based cytoskeleton. At rest, the platelet circulates through the vasculature in this form. In the second state, in response to vascular damage, the platelet rapidly converts into its active form with filopodia and lamellipodia that derive from a remodeled actin skeleton and a massive assembly of new actin filaments. In the last two decades, we have begun to understand the structural basis for these two platelet states, the role of specific proteins that define the architecture of both shapes, and the proteins and signals that drive this conversion of shapes.

Study on clinical and endocrine characteristics of dexamethasone-suppressible hyperaldosteronism compared with those in primary aldosteronism owing to aldosterone-producing adenoma

1989 ◽  
Vol 121 (3) ◽  
pp. 334-344 ◽  
Author(s):  
Noriyoshi Yamakita ◽  
Keigo Yasuda ◽  
Nobuyasu Noritake ◽  
Leilani B. Mercado-Asis ◽  
Hiroshi Murase ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Primary Aldosteronism ◽  
Blood Pressure Response ◽  
Laboratory Data ◽  
Japanese Patients ◽  
Pressure Response ◽  
Plasma Aldosterone ◽  
Vascular Damage ◽  
Aldosterone Producing Adenoma

Abstract. The clinical and endocrine characteristics of 12 Japanese patients with dexamethasone-suppressible hyperaldosteronism were compared with those in 49 Japanese patients with primary aldosteronism due to aldosteronoma. The results were as follows: 1. Most of the laboratory data in the two groups were almost the same. 2. The grade of vascular damage in both uncontrolled (3) and well-controlled (9) patients with dexamethasonesuppressible hyperaldosteronism did not correlate with blood pressure response. 3. The responsiveness of plasma aldosterone to exogenous ACTH in 6 patients with dexamethasone-suppressible hyperaldosteronism was not different from that in 9 patients with aldosteronoma. Even in 3 well-controlled patients in the former group, the plasma aldosterone response was as low as in all the 3 patients with small aldosteronomas. 4. In 4 patients with small aldosteronomas, plasma aldosterone was continuously suppressed with daily dexamethasone to the same degree as in dexamethasone-suppressible hyperaldosteronism. 5. The blood pressure, however, did not improve even in the patients with small aldosteronomas. The possible indistinguishable mechanism in dexamethasone-suppressible hyperaldosteronism and primary aldosteronism with small adenomas and the role of unknown hypertensinogenic steroid(s) other than aldosterone in inducing hypertension in dexamethasone-suppressible hyperaldosteronism are discussed.

scholarly journals Uric Acid and Vascular Damage in Essential Hypertension: Role of Insulin Resistance

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2509
Author(s):  
Velia Cassano ◽  
Daniele Crescibene ◽  
Marta Letizia Hribal ◽  
Corrado Pelaia ◽  
Giuseppe Armentaro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Uric Acid ◽  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Pulse Wave ◽  
Vascular Damage ◽  
Newly Diagnosed ◽  
Hypertensive Patients

Increased levels of uric acid (UA) have been shown to be correlated with many clinical conditions. Uric acid may adversely affect the insulin signalling pathway inducing insulin resistance (IR). Several studies report the association between arterial stiffness (AS), an early indicator of atherosclerosis, and UA. The purpose of the present study was to evaluate the association between UA and AS, considering the potential role of IR. We enrolled 1114 newly diagnosed, never-treated hypertensive patients. Insulin resistance was assessed by the homeostatic model assessment (HOMA) index. Arterial stiffness was evaluated as the measurement of the carotid–femoral pulse wave velocity (PWV). The study cohort was divided into subgroups, according to increasing tertiles of UA. The mean values of UA were 5.2 ± 1.6 mg/dL in the overall population. Pulse wave velocity was linearly correlated with UA (p < 0.0001), HOMA (p < 0.0001), high sensitivity C-reactive protein (p < 0.0001), systolic blood pressure (p < 0.0001) and LDL cholesterol (p = 0.005). Uric acid was the strongest predictor of PWV and was associated with the highest risk for increased AS. The interaction analysis showed that the joint effect of increased UA and HOMA was significantly higher than that expected in the absence of interaction under the additive model, indicating that the two biomarkers synergically interacted for promoting vascular damage. Our data showed that UA interacted with IR to increase AS in a large cohort of newly diagnosed, never-treated hypertensive patients.

Role of selenium in cytoprotection against cholesterol oxide-induced vascular damage in rats

2002 ◽  
Vol 162 (1) ◽  
pp. 137-144 ◽  
Author(s):  
Kaixun Huang ◽  
Hongmei Liu ◽  
Zexian Chen ◽  
Huibi Xu
Keyword(s):  
Vascular Damage ◽  
Cholesterol Oxide

scholarly journals Role of the Receptor for the Globular Domain of C1q Protein in the Pathogenesis of Hepatitis C Virus-Related Cryoglobulin Vascular Damage

2009 ◽  
Vol 183 (9) ◽  
pp. 6013-6020 ◽  
Author(s):  
Domenico Sansonno ◽  
Felicia Anna Tucci ◽  
Berhane Ghebrehiwet ◽  
Gianfranco Lauletta ◽  
Ellinor I. B. Peerschke ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Vascular Damage ◽  
Globular Domain

scholarly journals Role of symmetric dimethylarginine in vascular damage by increasing ROS via store-operated calcium influx in monocytes

2008 ◽  
Vol 24 (5) ◽  
pp. 1429-1435 ◽  
Author(s):  
E. Schepers ◽  
G. Glorieux ◽  
A. Dhondt ◽  
L. Leybaert ◽  
R. Vanholder
Keyword(s):  
Calcium Influx ◽  
Vascular Damage ◽  
Symmetric Dimethylarginine
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