Acridine orange leukocyte fluorography in mice

Cahoon, Judd; Olson, Paul R.; Nielson, Spencer; Miya, Tadashi R.; Bankhead, Peter; McGeown, J. Graham; Curtis, Tim M.; Ambati, Balamurali K.

doi:10.1016/j.exer.2013.12.002

Cited by 11 publications

(6 citation statements)

References 7 publications

(12 reference statements)

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“…On Acridine orange leukocyte fluorography ( 39 ), leukocyte rolling was significantly elevated in Ins2Akita control (9.8 cells/min) versus WT retinas (3 cells/min, P < 0.01) (quantitative image Fig. 3 C and representative image Fig.…”

Section: Resultsmentioning

confidence: 99%

Intravitreal AAV2.COMP-Ang1 Prevents Neurovascular Degeneration in a Murine Model of Diabetic Retinopathy

et al. 2015

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Diabetic retinopathy (DR) is the leading cause of blindness in the working-age population in the U.S. The vision-threatening processes of neuroglial and vascular dysfunction in DR occur in concert, driven by hyperglycemia and propelled by a pathway of inflammation, ischemia, vasodegeneration, and breakdown of the blood retinal barrier. Currently, no therapies exist for normalizing the vasculature in DR. Here, we show that a single intravitreal dose of adeno-associated virus serotype 2 encoding a more stable, soluble, and potent form of angiopoietin 1 (AAV2.COMP-Ang1) can ameliorate the structural and functional hallmarks of DR in Ins2Akita mice, with sustained effects observed through six months. In early DR, AAV2.COMP-Ang1 restored leukocyte-endothelial interaction, retinal oxygenation, vascular density, vascular marker expression, vessel permeability, retinal thickness, inner retinal cellularity, and retinal neurophysiological response to levels comparable with nondiabetic controls. In late DR, AAV2.COMP-Ang1 enhanced the therapeutic benefit of intravitreally delivered endothelial colony-forming cells by promoting their integration into the vasculature and thereby stemming further visual decline. AAV2.COMP-Ang1 single-dose gene therapy can prevent neurovascular pathology, support vascular regeneration, and stabilize vision in DR.

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Section: Resultsmentioning

confidence: 99%

Intravitreal AAV2.COMP-Ang1 Prevents Neurovascular Degeneration in a Murine Model of Diabetic Retinopathy

et al. 2015

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“…Ten to 15 microvessels of 6–8 μm diameter were measured per animal. To evaluate the leukocyte adhesion, 0.05 ml of the acridine orange (1 mg/ml) was administrated via the left femoral vein for selective staining of leukocytes in vivo (Cahoon et al, 2014 ). The renal microvessels were observed under irradiation at a wavelength of 488 and 647 nm by Leica TCS-SP8 confocal microscope.…”

Section: Methodsmentioning

confidence: 99%

QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function

et al. 2017

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Nephrotoxicity is a serious adverse effect of cisplatin chemotherapy that limits its clinical application, to deal with which no effective management is available so far. The present study was to investigate the potential protective effect of QiShenYiQi Pills (QSYQ), a compound Chinese medicine, against cisplatin induced nephrotoxicity in mice. Pretreatment with QSYQ significantly attenuated the cisplatin induced increase in plasma urea and creatinine, along with the histological damage, such as tubular necrosis, protein cast, and desquamation of epithelial cells, improved the renal microcirculation disturbance as indicated by renal blood flow, microvascular flow velocity, and the number of adherent leukocytes. Additionally, QSYQ prevented mitochondrial dysfunction by preventing the cisplatin induced downregulation of mitochondrial complex activity and the expression of NDUFA10, ATP5D, and Sirt3. Meanwhile, the cisplatin-increased renal thiobarbituric acid-reactive substances, caspase9, cleaved-caspase9, and cleaved-caspase3 were all diminished by QSYQ pretreatment. In summary, the pretreatment with QSYQ remarkably ameliorated the cisplatin induced nephrotoxicity in mice, possibly via the regulation of mitochondrial function, oxidative stress, and apoptosis.

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“…Leukocyte adhesion to the retinal vessels was determined using acridine orange fluorography. 25 A scanning laser ophthalmoscope (Rodenstock Instruments, Munich, Germany) was used to obtain interlaced video frames of the fundus stained using metachromatic fluorochrome acridine orange (Wako Pure Chemicals, Osaka, Japan). The dye emits green fluorescence when interacting with DNA.…”

Section: Methodsmentioning

confidence: 99%

A high-salt diet enhances leukocyte adhesion in association with kidney injury in young dahl salt-sensitive rats

Takahashi

Nakagawa

et al. 2017

Hypertens Res

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Salt-sensitive hypertension is associated with severe organ damage. Generating oxygen radicals is an integral component of salt-induced kidney damage, and activated leukocytes are important in oxygen radical biosynthesis. We hypothesized that a high-salt diet causes the upregulation of immune-related mechanisms, thereby contributing to the susceptibility of Dahl salt-sensitive rats to hypertensive kidney damage. For verifying the hypothesis, we investigated leukocytes adhering to retinal vessels when Dahl salt-sensitive rats were challenged with a high-salt (8% NaCl) diet using acridine orange fluoroscopy and a scanning laser ophthalmoscope. The high-salt diet increased leukocyte adhesion after 3 days and was associated with a significant increase in mRNA biosynthesis of monocyte chemotactic protein-1 and intercellular adhesion molecule-1 (ICAM-1) -related molecules in the kidney. Losartan treatment did not affect increased leukocyte adhesion during the early, pre-hypertensive phase of high salt loading; however, losartan attenuated the adhesion of leukocytes during the hypertensive stage. Moreover, the inhibition of leukocyte adhesion in the pre-hypertensive stage by anti-CD18 antibodies decreased tethering of leukocytes and was associated with the attenuation of functional and morphological kidney damage without affecting blood pressure elevation. In conclusion, a high-salt challenge rapidly increased leukocyte adhesion through the over-expression of ICAM-1. Increased leukocyte adhesion in the pre-hypertensive stage is responsible for subsequent kidney damage in Dahl salt-sensitive rats. Immune system involvement may be a key component that initiates kidney damage in a genetic model of salt-induced hypertension.

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Acridine orange leukocyte fluorography in mice

Cited by 11 publications

References 7 publications

Intravitreal AAV2.COMP-Ang1 Prevents Neurovascular Degeneration in a Murine Model of Diabetic Retinopathy

Intravitreal AAV2.COMP-Ang1 Prevents Neurovascular Degeneration in a Murine Model of Diabetic Retinopathy

QiShenYiQi Pills, a Compound Chinese Medicine, Prevented Cisplatin Induced Acute Kidney Injury via Regulating Mitochondrial Function

A high-salt diet enhances leukocyte adhesion in association with kidney injury in young dahl salt-sensitive rats

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