Repetitive Fluctuations in Blood Glucose Enhance Monocyte Adhesion to the Endothelium of Rat Thoracic Aorta

Azuma, Kosuke; Kawamori, Ryuzo; Toyofuku, Yukiko; Kitahara, Yoshiro; Sato, Fumihiko; Shimizu, Tomoaki; Miura, Kyoko; Mine, Tomoyuki; Tanaka, Yasushi; Mitsumata, Masako; Watada, Hirotaka

doi:10.1161/01.atv.0000239488.05069.03

Cited by 140 publications

(121 citation statements)

References 21 publications

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“…Monocyte adhesion to the thoracic aorta was quantified by en face immunohistochemistry, as described previously [14][15][16][17][18]. Briefly, rats (n=6 from each group) were killed under anaesthesia induced by i.p.…”

Section: En Face Immunohistochemistry Of Endothelial Surfacementioning

confidence: 99%

“…The segments were then cut open longitudinally along the ventral side with the intimal side up and covered with a coverslip by surface tension. Specimens were viewed under a microscope (E800; Nikon, Tokyo, Japan) as described previously [14]. The density of CD68-immunopositive cells in the thoracic aorta was calculated by examiners blinded to the treatment regimen, as described previously [14,15].…”

Section: En Face Immunohistochemistry Of Endothelial Surfacementioning

confidence: 99%

“…Specimens were viewed under a microscope (E800; Nikon, Tokyo, Japan) as described previously [14]. The density of CD68-immunopositive cells in the thoracic aorta was calculated by examiners blinded to the treatment regimen, as described previously [14,15]. ICAM-1 and VCAM-1 abundance was also evaluated by enface immunostaining using the thoracic aorta of each group (ICAM-1, n=6 each; VCAM-1, n=6 each).…”

Section: En Face Immunohistochemistry Of Endothelial Surfacementioning

confidence: 99%

“…The cross-sectional intimal areas of a lesion in a given photomicrograph were measured with image analysis software (Image-Pro4.5J; Planetron, Tokyo, Japan). The average intimal area was determined as described previously [14].…”

Section: Quantification Of Intimal Thickeningmentioning

confidence: 99%

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Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

et al. 2011

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Aims/hypothesis Severe hypoglycaemia associated with diabetes management is a potential risk for cardiovascular diseases. However, the effect and mechanism of hypoglycaemia on the progression of atherosclerosis remains largely unknown. As a first step towards elucidating the above, we investigated the effect of hypoglycaemia on monocyte-endothelial interaction. Methods Insulin was injected intraperitoneally once every 3 days for 5 weeks in Goto-Kakizaki rats, a non-obese rat model of type 2 diabetes. We counted the number of monocytes adherent to the endothelium of thoracic aorta as an index of early atherosclerogenesis. Cultured HUVEC were used to investigate the mechanism of action. Results Insulin treatment increased the number of monocytes adherent to the vascular endothelium. This increase was abrogated by injection of glucose with insulin. Amosulalol, an α-1 and β-adrenoreceptor antagonist, suppressed monocyte adhesion to endothelium and levels of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in the endothelial surface, which had been enhanced by insulin-induced hypoglycaemia. In HUVEC, adrenaline (epinephrine) significantly increased nuclear translocation of nuclear factor-κB (NF-κB) p65 and levels of adhesion molecules, effects that were abrogated following addition of SQ22536, a specific adenyl cyclase inhibitor. Conclusions/interpretation Our data indicate that repetitive hypoglycaemia induced by insulin enhanced monocyte adhesion to endothelial cells in Goto-Kakizaki rat aorta through enhanced adrenaline activity and that the latter stimulated intracellular cAMP, leading to nuclear translocation of NF-κB with subsequent production of adhesion molecules in endothelial cells.

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Section: En Face Immunohistochemistry Of Endothelial Surfacementioning

confidence: 99%

Section: En Face Immunohistochemistry Of Endothelial Surfacementioning

confidence: 99%

Section: En Face Immunohistochemistry Of Endothelial Surfacementioning

confidence: 99%

Section: Quantification Of Intimal Thickeningmentioning

confidence: 99%

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Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

et al. 2011

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“…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).…”

mentioning

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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Therapeutic Potential of Ginsenosides in Management of Atherosclerosis

Zhang

Wang

et al. 2015

Phytotherapies

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Repetitive Fluctuations in Blood Glucose Enhance Monocyte Adhesion to the Endothelium of Rat Thoracic Aorta

Cited by 140 publications

References 21 publications

Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

Repetitive hypoglycaemia increases serum adrenaline and induces monocyte adhesion to the endothelium in rat thoracic aorta

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

Therapeutic Potential of Ginsenosides in Management of Atherosclerosis

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