A new En face method is useful to quantitate endothelial damage in vivo

Azuma, Kosuke; Watada, Hirotaka; Niihashi, Mari; Otsuka, Aiko; Sato, Fumihiko; Kawasumi, Masahiko; Shimada, Satoshi; Tanaka, Yasushi; Kawamori, Ryuzo; Mitsumata, Masako

doi:10.1016/j.bbrc.2003.08.013

Cited by 28 publications

(26 citation statements)

References 22 publications

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“…Specimens were viewed under a microscope (E800; Nikon, Tokyo, Japan) connected to an XYZ controller and a digital camera (Media Cybernetics, Silver Spring, MD, USA). Images were captured at various focal lengths with an automatically regulated Z-stepper and the clearest images were selected automatically to produce a composite image of the whole thoracic aorta using Image-Pro 4.5J (Planetron, Tokyo, Japan) [12].…”

Section: Methodsmentioning

confidence: 99%

“…We defined the area bound by this rectangle as the area around the branching site and the area outside the rectangle was defined as the non-branching area [12]. The total numbers of CD68-immunopositive cells around the branching site and in the non-branching areas were counted separately in each aorta.…”

Section: Methodsmentioning

confidence: 99%

“…This method [12] facilitates observation of the entire endothelial surface with a clear focused image, thus enabling quantitation of the precise number of monocytes adhering to a specific region of the rat thoracic aorta after immunostaining for the monocyte/macrophage-specific protein, CD68.…”

Section: Introductionmentioning

confidence: 99%

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Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta

et al. 2005

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Aims/hypothesis: Several epidemiological data suggest that patients with postprandial hyperglycaemia are at high risk of cardiovascular disease. The aim of this study was to elucidate the effect of a glucose 'spike' on monocyte adhesion to rat aortic endothelial cells. Materials and methods: Monocyte adhesion to endothelial cells in vivo was quantitated using an en face method for observation of endothelial surface after immunohistochemical staining for CD68 in the thoracic aortas of Sprague-Dawley rats after several kinds of blood glucose rises. Results: The number of monocytes adhering to endothelial cells increased at 30 min after injection of glucose in 8-week-old Sprague-Dawley rats. The increased adhesion returned to the basal level at 120 min after glucose injection, concomitantly with the return of blood glucose levels to normal. The infusion of octreotide to inhibit endogenous insulin secretion did not prevent the glucose-induced increase in monocyte adhesion to endothelial cells. On the other hand, the number of monocytes adhering to endothelial cells did not increase in rats with streptozotocin-induced diabetes and sustained hyperglycaemia. Conclusions/interpretation: Our data demonstrate that a temporary rise in blood glucose levels can in itself promote a reversible increase in monocyte adhesion to arterial endothelial cells.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta

et al. 2005

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“…At the end of the treatment, monocyte adhesion to the thoracic aorta was quantified by NEMOes, as described previously [17][18][19][20][21]. Briefly, rats were sacrificed under anesthesia induced by intraperitoneal injection of sodium pentobarbital (50 mg/kg; Nembutal, Abbott Laboratories, Abbott Park, IL).…”

Section: Nemoesmentioning

confidence: 99%

“…This method provides a clear focused image of the entire endothelial surface, enabling quantitation of monocytes that adhere to a specific region of rat thoracic aorta after immunostaining for the monocyte/macrophage-specific protein, CD68 [17][18][19][20][21]. Here, we used this method to investigate the effect of ARB on monocyte adhesion to endothelial cells in spontaneously hypertensive rats (SHR).…”

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confidence: 99%

Angiotensin II Type 1 Receptor Blocker Reduces Monocyte Adhesion to Endothelial Cells in Spontaneously Hypertensive Rats

et al. 2007

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Abstract. Monocyte adhesion to arterial endothelial cells is the initial step in atherosclerosis. Whereas angiotensin II is known to elicit leukocyte adhesion, it is not clear whether blockade of the angiotensin II receptor signaling reduces monocyte adhesion to endothelial cells beyond its antihypertensive action. This study compared the effect of two different antihypertensive drugs on monocyte adhesion to thoracic aorta endothelium in spontaneously hypertensive rats (SHR): the angiotensin II receptor blocker, valsartan (20 mg · kg -1 · day -1 ) and the vasodilator, hydralazine (0.75 mg · kg -1 · day -1 ). The effects were quantitated in vivo using an enface method that optimizes the observation of endothelial surfaces after immunohistochemical staining for CD68. Both agents significantly and comparably reduced blood pressure over 4-week treatment course. Both valsartan and hydralazine profoundly reduced monocyte adhesion compared with nontreated controls, with valsartan having a modestly more reductive effect. Both agents also reduced the intima and medial thickening with valsartan reducing the mean thickness modestly more than hydralazine. Our data confirms that the reduction of blood pressure is effective method to reduce monocyte adhesion. Also, our date demonstrates that valsartan has a modest beneficial effect on monocyte adhesion to endothelial cells and arterial intima-medial vessel thickening beyond its action as an antihypertensive agent.

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Thioredoxin-Interacting Protein (TXNIP) in Cerebrovascular and Neurodegenerative Diseases: Regulation and Implication

2018

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Neurological diseases, including acute attacks (e.g., ischemic stroke) and chronic neurodegenerative diseases (e.g., Alzheimer's disease), have always been one of the leading cause of morbidity and mortality worldwide. These debilitating diseases represent an enormous disease burden, not only in terms of health suffering but also in economic costs. Although the clinical presentations differ for these diseases, a growing body of evidence suggests that oxidative stress and inflammatory responses in brain tissue significantly contribute to their pathology. However, therapies attempting to prevent oxidative damage or inhibiting inflammation have shown little success. Identification and targeting endogenous "upstream" mediators that normalize such processes will lead to improve therapeutic strategy of these diseases. Thioredoxin-interacting protein (TXNIP) is an endogenous inhibitor of the thioredoxin (TRX) system, a major cellular thiol-reducing and antioxidant system. TXNIP regulating redox/glucose-induced stress and inflammation, now is known to get upregulated in stroke and other brain diseases, and represents a promising therapeutic target. In particular, there is growing evidence that glucose strongly induces TXNIP in multiple cell types, suggesting possible physiological roles of TXNIP in glucose metabolism. Recently, a significant body of literature has supported an essential role of TXNIP in the activation of the NOD-like receptor protein (NLRP3)-inflammasome, a well-established multi-molecular protein complex and a pivotal mediator of sterile inflammation. Accordingly, TXNIP has been postulated to reside centrally in detecting cellular damage and mediating inflammatory responses to tissue injury. The majority of recent studies have shown that pharmacological inhibition or genetic deletion of TXNIP is neuroprotective and able to reduce detrimental aspects of pathology following cerebrovascular and neurodegenerative diseases. Conspicuously, the mainstream of the emerging evidences is highlighting TXNIP link to damaging signals in endothelial cells. Thereby, here, we keep the trend to present the accumulative data on CNS diseases dealing with vascular integrity. This review aims to summarize evidence supporting the significant contribution of regulatory mechanisms of TXNIP with the development of brain diseases, explore pharmacological strategies of targeting TXNIP, and outline obstacles to be considered for efficient clinical translation.

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A new En face method is useful to quantitate endothelial damage in vivo

Cited by 28 publications

References 22 publications

Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta

Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta

Angiotensin II Type 1 Receptor Blocker Reduces Monocyte Adhesion to Endothelial Cells in Spontaneously Hypertensive Rats

Thioredoxin-Interacting Protein (TXNIP) in Cerebrovascular and Neurodegenerative Diseases: Regulation and Implication

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