Is the Efficacy of LDL Apheresis in Ischemic Optic Neuropathy Linked to a Reduction in Endothelial Activation Markers?

2006 ◽  
Vol 24 (4) ◽  
pp. 405-412 ◽  
Author(s):  
A. Ramunni ◽  
G. Ranieri ◽  
G. Giancipoli ◽  
S. Guerriero ◽  
R. Ria ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Endothelial Activation ◽  
Ischemic Optic Neuropathy ◽  
Ldl Apheresis ◽  
Activation Markers

LDL-Apheresis Accelerates the Recovery of Nonarteritic Acute Anterior Ischemic Optic Neuropathy

2005 ◽  
Vol 9 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Alfonso Ramunni ◽  
Giovanni Giancipoli ◽  
Silvana Guerriero ◽  
Lucia Lapenna ◽  
Angelo Saracino ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Ldl Apheresis

LDL-apheresis in Acute Anterior Ischemic Optic Neuropathy

2004 ◽  
Vol 27 (4) ◽  
pp. 337-341 ◽  
Author(s):  
A. Ramunni ◽  
G. Giancipoli ◽  
A. Saracino ◽  
S. Guerriero ◽  
M.T. Saliani ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Ldl Apheresis

Blood rheology in acute anterior ischemic optic neuropathy

1991 ◽  
Vol 11 (6) ◽  
pp. 623-634 ◽  
Author(s):  
B. Bertram ◽  
A. Hoberg ◽  
O. Arend ◽  
S. Wolf ◽  
F. Jung ◽  
...  
Keyword(s):  
Optic Neuropathy ◽  
Blood Rheology ◽  
Anterior Ischemic Optic Neuropathy ◽  
Ischemic Optic Neuropathy

Posterior Ischemic Optic Neuropathy Related to Profound Shock After Penetrating Thoracoabdominal Trauma

2002 ◽  
Vol 95 (9) ◽  
pp. 1053-1057 ◽  
Author(s):  
JUAN A. ASENSIO ◽  
WALTER FORNO ◽  
GUSTAVO A. ROLDÁN CASTILLO ◽  
ESTEBAN GAMBARO ◽  
PATRIZIO PETRONE
Keyword(s):  
Optic Neuropathy ◽  
Ischemic Optic Neuropathy ◽  
Posterior Ischemic Optic Neuropathy

scholarly journals Protective Effects of Oroxylin A on Retinal Ganglion Cells in Experimental Model of Anterior Ischemic Optic Neuropathy

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 902
Author(s):  
Jia-Ying Chien ◽  
Shu-Fang Lin ◽  
Yu-Yau Chou ◽  
Chi-Ying F. Huang ◽  
Shun-Ping Huang
Keyword(s):  
Retinal Ganglion Cells ◽  
Optic Neuropathy ◽  
Ganglion Cells ◽  
Ischemic Injury ◽  
Anterior Ischemic Optic Neuropathy ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Ischemic Optic Neuropathy ◽  
Retinal Ganglion ◽  
Oroxylin A

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute vision loss in older people, and there is no effective therapy. The effect of the systemic or local application of steroids for NAION patients remains controversial. Oroxylin A (OA) (5,7-dihydroxy-6-methoxyflavone) is a bioactive flavonoid extracted from Scutellariae baicalensis Georgi. with various beneficial effects, including anti-inflammatory and neuroprotective effects. A previous study showed that OA promotes retinal ganglion cell (RGC) survival after optic nerve (ON) crush injury. The purpose of this research was to further explore the potential actions of OA in ischemic injury in an experimental anterior ischemic optic neuropathy (rAION) rat model induced by photothrombosis. Our results show that OA efficiently attenuated ischemic injury in rats by reducing optic disc edema, the apoptotic death of retinal ganglion cells, and the infiltration of inflammatory cells. Moreover, OA significantly ameliorated the pathologic changes of demyelination, modulated microglial polarization, and preserved visual function after rAION induction. OA activated nuclear factor E2 related factor (Nrf2) signaling and its downstream antioxidant enzymes NAD(P)H:quinone oxidoreductase (NQO-1) and heme oxygenase 1 (HO-1) in the retina. We demonstrated that OA activates Nrf2 signaling, protecting retinal ganglion cells from ischemic injury, in the rAION model and could potentially be used as a therapeutic approach in ischemic optic neuropathy.

scholarly journals Structural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthma

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Renata Calciolari Rossi ◽  
Raquel Anonni ◽  
Diogenes Seraphim Ferreira ◽  
Luiz Fernando Ferraz da Silva ◽  
Thais Mauad
Keyword(s):  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Pulmonary Arteries ◽  
Endothelial Activation ◽  
Bronchial Arteries ◽  
Activation Markers ◽  
Asthma Attack ◽  
Collagen Iii ◽  
Asthma Patients ◽  
Fatal Asthma

Abstract Background There is interest in better understanding vessel pathology in asthma, given the findings of loss of peripheral vasculature associated with disease severity by imaging and altered markers of endothelial activation. To date, vascular changes in asthma have been described mainly at the submucosal capillary level of the bronchial microcirculation, with sparse information available on the pathology of bronchial and pulmonary arteries. The aim of this study was to describe structural and endothelial activation markers in bronchial arteries (BAs) and pulmonary arteries (PAs) of asthma patients who died during a fatal asthma attack. Methods Autopsy lung tissue was obtained from 21 smoking and non-smoking patients who died of an asthma attack and nine non-smoking control patients. Verhoeff–Masson trichrome staining was used to analyse the structure of arteries. Using immuno-histochemistry and image analyses, we quantified extracellular matrix (ECM) components (collagen I, collagen III, versican, tenascin, fibronectin, elastic fibres), adhesion molecules [vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1)] and markers of vascular tone/dysfunction [endothelin-1 (ET-1) and angiotensin II type 2 receptor (AT2)] in PAs and BAs. Results There were no significant differences in ECM components, ICAM-1, ET-1 or AT2 between asthma patients and controls. Smoking asthma patients presented with decreased content of collagen III in both BA (p = 0.046) and PA (p = 0.010) walls compared to non-smoking asthma patients. Asthma patients had increased VCAM-1 content in the BA wall (p = 0.026) but not in the PA wall. Conclusion Our data suggest that the mechanisms linking asthma and arterial functional abnormalities might involve systemic rather than local mediators. Loss of collagen III in the PA was observed in smoking asthma patients, and this was compatible with the degradative environment induced by cigarette smoking. Our data also reinforce the idea that the mechanisms of leukocyte efflux via adhesion molecules differ between bronchial and pulmonary circulation, which might be relevant to understanding and treating the distal lung in asthma.

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