Swimming reduces the severity of atherosclerosis in apolipoprotein E deficient mice by antioxidant effects

Okabe, Taka-aki; Shimada, Keisuke; Hattori, Miki; Murayama, Toshinori; Yokode, Masayuki; Kita, Toru; Kishimoto, Chiharu

doi:10.1016/j.cardiores.2007.02.019

Cited by 51 publications

(61 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Previous studies have shown that exercise training, such as on a treadmill and swimming, reduced atherosclerotic lesion formation and neointimal growth after carotid injury in mice models [11][12][13][14][15][16][17][18] ; however, such unpleasant exercise may be forced under stressful conditions with disruption of the normal diurnal rhythm [6][7][8][9] . In contrast, voluntary running exercise can be performed to assess the underlying mechanisms by which Levels of aortic mRNA expression of CD68, CD4, and CD11c were measured using real-time PCR in the STD (n 5), HFD (n 5), and HFD Ex (n 5) groups at 18 weeks of age.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Voluntary Exercise Ameliorates the Progression of Atherosclerotic Lesion Formation via Anti-Inflammatory Effects in Apolipoprotein E-Deficient Mice

Fujita

Shimada

Naito

et al. 2010

JAT

View full text Add to dashboard Cite

Aim: A sedentary lifestyle with insufficient exercise is associated with cardiovascular disease. Previous studies have demonstrated that endurance exercise benefits atherosclerosis and cardiovascular disorders; however, the mechanisms by which physical activity, such as voluntary exercise (Ex), produces these effects are not fully understood. Methods and Results: Eight-week-old male apolipoprotein (ApoE)-deficient mice were fed a standard diet (STD) or high fat diet (HFD) for 10 weeks. The HFD Ex group mice performed Ex on a running wheel for 10 weeks. No significant differences in lipid profiles were observed between the HFD and HFD Ex groups. Although changes in body and brown adipose tissue weights were comparable between the HFD and HFD Ex groups, white adipose tissue weight was significantly lower in the HFD Ex group than in the HFD group. The areas of atherosclerotic lesions in the aortic sinus and thoracoabdominal aorta were significantly reduced in the HFD Ex group than in the HFD group (p 0.001). There was a strong negative correlation between atherosclerotic areas and the mean running distance per day in the HFD Ex group (r 0.90, p 0.01). Endothelial function was significantly preserved in the HFD Ex group (p 0.05). Serum interleukin-6 and macrophage chemoattractant protein-1 levels were significantly lower and those of adiponectin were significantly higher in the HFD Ex group than in the HFD group (p 0.05). Conclusions: These results suggest that Ex ameliorates the progression of endothelial dysfunction and atherosclerotic lesion formation through anti-inflammatory effects, despite continued consumption of HFD.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Kishimoto et al reported that NO and antioxidants may play an important role in the effects of exercise 13,18) . In addition, the vascular response to acetylcholine is related to an increase in NO bioavailability as a result of the upregulation of the antioxidant defense system 31) .…”

Section: Discussionmentioning

confidence: 99%

Voluntary Exercise Ameliorates the Progression of Atherosclerotic Lesion Formation via Anti-Inflammatory Effects in Apolipoprotein E-Deficient Mice

Fujita

Shimada

Naito

et al. 2010

JAT

View full text Add to dashboard Cite

show abstract

“…87 ApoE-deficient mice undergoing exercise training were recently found to exhibit a decreased susceptibility to atherosclerotic disease. 88 Interestingly, the protective effects were attributed to a reduction in ROS. 88 In another study, physical activity was shown to increase the production and circulating numbers of EPCs in mice.…”

Section: Physical Activitymentioning

confidence: 99%

“…88 Interestingly, the protective effects were attributed to a reduction in ROS. 88 In another study, physical activity was shown to increase the production and circulating numbers of EPCs in mice. 89 As described previously, EPCs are being investigated as an important component of endothelial regeneration and compensatory angiogenesis, functioning to counteract and protect the vascular wall from inflammatory cytokines.…”

Section: Physical Activitymentioning

confidence: 99%

Inflammation at the Molecular Interface of Atherogenesis

Lamon

Hajjar

2008

The American Journal of Pathology

112

View full text Add to dashboard Cite

Despite the multifactorial nature of atherosclerosis, substantial evidence has established inflammation as an often surreptitious, yet critical and unifying driving force which promotes disease progression. To this end, research has defined molecular networks initiated by cytokines, growth factors and other proinflammatory molecules which promote hallmarks of atherosclerosis such as endothelial dysfunction, macrophage infiltration, LDL oxidation, cell proliferation and thrombosis. Although commonly associated with risk factors such as dyslipidemia, diabetes and hypertension, the global etiology of atherosclerosis may be alternatively attributed to underlying anthropological pressures. The agricultural, industrial and technological revolutions produced alterations in dietary, social and economic factors which have collectively exaggerated the exposure of the human genome to environmental stimuli. Furthermore, advances in sanitation, nutrition, and medicine have increased the lifespan of humans, effectively prolonging blood vessel exposure to these factors. As a result, the vasculature has become conditioned to respond to injury with what is arguably an overzealous immunological response; thus setting the stage for the prevalence of cardiovascular disease, including atherosclerotic plaque development in Western populations. Evidence suggests that each of these alterations can be linked to specific mediators in the inflammatory process. Integration of these factors with an inflammationbased hypothesis of atherosclerosis has yet to be extrapolated to observations in the realms of basic and clinical sciences and is the focus of this review. (Am J Pathol

show abstract

“…To this end, long-term exercise intervention has been shown to reduce the severity of atherosclerosis (31), to stabilize vascular lesion (36), and to lessen post-injury neointima growth (38). The mechanism underlying these adaptive changes is believed to be governed by high wall shear rates occurring during exercise.…”

mentioning

confidence: 99%

Shear stress-induced mitochondrial biogenesis decreases the release of microparticles from endothelial cells

Kim

Lee

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Park J-Y. Shear stress-induced mitochondrial biogenesis decreases the release of microparticles from endothelial cells. Am J Physiol Heart Circ Physiol 309: H425-H433, 2015. First published May 29, 2015 doi:10.1152/ajpheart.00438.2014.-The concept of enhancing structural integrity of mitochondria has emerged as a novel therapeutic option for cardiovascular disease. Flow-induced increase in laminar shear stress is a potent physiological stimulant associated with exercise, which exerts atheroprotective effects in the vasculature. However, the effect of laminar shear stress on mitochondrial remodeling within the vascular endothelium and its related functional consequences remain largely unknown. Using in vitro and in vivo complementary studies, here, we report that aerobic exercise alleviates the release of endothelial microparticles in prehypertensive individuals and that these salutary effects are, in part, mediated by shear stress-induced mitochondrial biogenesis. Circulating levels of total (CD31 ϩ /CD42a Ϫ ) and activated (CD62E ϩ ) microparticles released by endothelial cells were significantly decreased (ϳ40% for both) after a 6-mo supervised aerobic exercise training program in individuals with prehypertension. In cultured human endothelial cells, laminar shear stress reduced the release of endothelial microparticles, which was accompanied by an increase in mitochondrial biogenesis through a sirtuin 1 (SIRT1)-dependent mechanism. Resveratrol, a SIRT1 activator, treatment showed similar effects. SIRT1 knockdown using small-interfering RNA completely abolished the protective effect of shear stress. Disruption of mitochondrial integrity by either antimycin A or peroxisome proliferator-activated receptor-␥ coactivator-1␣ small-interfering RNA significantly increased the number of total, and activated, released endothelial microparticles, and shear stress restored these back to basal levels. Collectively, these data demonstrate a critical role of endothelial mitochondrial integrity in preserving endothelial homeostasis. Moreover, prolonged laminar shear stress, which is systemically elevated during aerobic exercise in the vessel wall, mitigates endothelial dysfunction by promoting mitochondrial biogenesis. shear stress; exercise; mitochondrial biogenesis; endothelial microparticle NEW & NOTEWORTHYThis study assesses effects of aerobic exercise training on the release of microparticles from endothelial cells and corroborates these findings using an in vitro experimental exercise stimulant, laminar shear stress. Furthermore, this study demonstrated that shear stress-induced mitochondrial biogenesis mediates these effects against endothelial cell activation and injury.IN ENDOTHELIAL CELLS (ECs), mitochondria occupy a relatively small compartment of cytoplasmic volume (ϳ2-6%) than other energy demanding cell-types such as cardiomyocytes (32). The endothelial mitochondria are, however, thought to play a key regulatory role in cell signaling (39), calcium handling (44), and cell survival (49). Indeed, an impaired mit...

show abstract

Swimming reduces the severity of atherosclerosis in apolipoprotein E deficient mice by antioxidant effects

Abstract: Exercise training, in which the load did not affect energy metabolism efficacy of the heart, suppressed atherosclerosis by antioxidant effects via the vascular NO system.

Cited by 51 publications

References 47 publications

Voluntary Exercise Ameliorates the Progression of Atherosclerotic Lesion Formation via Anti-Inflammatory Effects in Apolipoprotein E-Deficient Mice

Voluntary Exercise Ameliorates the Progression of Atherosclerotic Lesion Formation via Anti-Inflammatory Effects in Apolipoprotein E-Deficient Mice

Inflammation at the Molecular Interface of Atherogenesis

Shear stress-induced mitochondrial biogenesis decreases the release of microparticles from endothelial cells

Contact Info

Product

Resources

About