Nitric oxide synthase in aging rat skeletal muscle

Richmonds, Chelliah R.; Boonyapisit, Kanokwan; Kusner, Linda L.; Kaminski, Henry J.

doi:10.1016/s0047-6374(99)00035-4

Cited by 35 publications

(23 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Skeletal muscle aging also causes large reductions in the expression of nNOS (Richmonds et al ., 1999; Samengo et al ., 2012) that accompany the increase in fibrosis and the reduction in regenerative capacity experienced during muscle senescence. Thus, it is feasible that the age-related decrease in muscle nNOS expression contributes to an increase in the numbers and activation of leukocytes that promote muscle fibrosis while also leading to a reduction in the numbers of satellite cells, which would reduce the regenerative capacity of aging muscle.…”

Section: Introductionmentioning

confidence: 99%

Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle‐derived nitric oxide

et al. 2015

View full text Add to dashboard Cite

Muscle aging is associated with changes in myeloid cell phenotype that may influence age-related changes in muscle structure. We tested whether preventing age-related reductions in muscle neuronal nitric oxide synthase (nNOS) would obviate age-related changes in myeloid cells in muscle. Our findings show that muscle aging is associated with elevations of anti-inflammatory M2a macrophages that can increase muscle fibrosis. Expression of a muscle-specific nNOS transgene in mice prevented age-related increases in M2a macrophages. Transgene expression also reduced expression of collagens and decreased muscle fibrosis. The nNOS transgene prevented age-related increases in arginase-1 but did not influence TGFβ expression, indicating that the transgene may prevent age-related muscle fibrosis by inhibiting the arginase-dependent profibrotic pathway. Although aged satellite cells or fibro-adipogenic precursor (FAPs) cells also promote fibrosis, transgene expression had no effect on the expression of key signaling molecules that regulate fibrogenic activity of those cells. Finally, we tested whether increases in M2a macrophages and the associated increase in fibrosis were attributable to aging of myeloid lineage cells. Young bone marrow cells (BMCs) were transplanted into young or old mice, and muscles were collected 8 months later. Muscles of young mice receiving young BMCs showed no effect on M2a macrophage number or collagen accumulation compared to age-matched, nontransplanted controls. However, muscles of old mice receiving young BMCs showed fewer M2a macrophages and less accumulation of collagen. Thus, the age-related increase in M2a macrophages in aging muscle and the associated muscle fibrosis are determined in part by the age of bone marrow cells.

show abstract

Section: Introductionmentioning

confidence: 99%

Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle‐derived nitric oxide

et al. 2015

View full text Add to dashboard Cite

show abstract

“…A color figure is freely accessible via the website of the book: http://www.springer.com/1-4020-5176-x. heat shock proteins are increased following exercise, and this response has been shown to be blunted in aged muscle fibers (Spiers, 2000) relationship with the reduced levels of either NOS expression or activity in the rat limb and respiratory muscles (Richmonds, 1999). Lawler et al (1997) also demonstrated in their study that the response to oxidant challenge and increased contractile demand was impaired in the aging rat diaphragm.…”

Section: Oxidative Stressmentioning

confidence: 92%

“…Levels of both antioxidants and as aforementioned, NO is normally synthesized by NOS in the muscle fibers and its derivatives can also interact with ROS leading to the formation of highly reactive species such as peroxynitrite. As shown by Richmonds et al 1999 aging seems to have opposite effects on NO synthesis compared to its effects on ROS cascade ( Figure 11). Specifically, both NOS expression and enzyme activity were shown to be reduced in aged muscle fibers of rats (Richmonds, 1999).…”

Section: Respiratory Disorders Related To Sleep (The Sleep Apnea-hypomentioning

confidence: 96%

“…As shown by Richmonds et al 1999 aging seems to have opposite effects on NO synthesis compared to its effects on ROS cascade ( Figure 11). Specifically, both NOS expression and enzyme activity were shown to be reduced in aged muscle fibers of rats (Richmonds, 1999). Reports from the literature with regard to oxidative stress are still controversial and no clear conclusions have been reached yet.…”

Section: Respiratory Disorders Related To Sleep (The Sleep Apnea-hypomentioning

confidence: 96%

See 1 more Smart Citation

Skeletal Muscle Plasticity in Health and Disease

Bottinelli¹,

Reggiani²

2006

Advances in Muscle Research

View full text Add to dashboard Cite

“…Of these substances, age‐related differences have been reported only with respect to expression of nNOS in animals. For example, in senescent rats, the percentage of nNOS‐containing fibers is significantly reduced with age in both the soleus and the extensor digitorum longus ( 87 ). Additionally, ovariectomized rats exhibit reduced nNOS and enhanced sympathetic vasoconstriction, which can be prevented by chronic treatment of 17β‐estradiol ( 32 ).…”

Section: Potential Mechanisms Underlying Age‐related Differences In Ementioning

confidence: 99%

Vasodilation and Vascular Control in Contracting Muscle of the Aging Human

2006

View full text Add to dashboard Cite

There is accumulating evidence in humans that the control of blood flow to dynamically contracting skeletal muscle is altered with normal aging. Despite some inconsistencies in the literature, most healthy older subject groups studied to date (approximately 55-75 years) exhibited attenuated leg blood flow responses to moderate intensity leg exercise in comparison to younger (approximately 20-30 years) controls. In most cases, older subjects also have higher arterial perfusion pressures at rest and at any submaximal workload than their younger counterparts, suggesting a heightened level of vasoconstriction in the legs that could result from structural and/or functional alterations within the arterial vasculature. The influence of age on vasodilator responsiveness in the contracting limbs of humans remains an open question, with reports of blunted, similar, and augmented increases in local vascular conductance during graded exercise in older vs. younger adults. Recent results from the authors' laboratory suggest that the ability of vascular smooth muscle in the legs to dilate in response to physiological and pharmacological stimuli is relatively well preserved with advancing age in men; however, a sex difference may exist in that older estrogen-deficient women exhibit blunted leg vasodilator responses compared to younger women. Potential mechanisms underlying altered vascular control within the resistance vasculature of contracting muscles of older men and women remain to be determined, but could include (1) fewer, smaller, and/or stiffer vessels, (2) impaired endothelium-dependent vasodilation, (3) augmented sympathetic vasoconstriction, (4) alterations in metabolic or myogenic control, and (5) reduced effectiveness of the skeletal muscle pump. Systematic research involving both humans and animal models will be necessary to fully elucidate the mechanisms underlying compromised muscle blood flow in old age.

show abstract

Nitric oxide synthase in aging rat skeletal muscle

Cited by 35 publications

References 35 publications

Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle‐derived nitric oxide

Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle‐derived nitric oxide

Skeletal Muscle Plasticity in Health and Disease

Vasodilation and Vascular Control in Contracting Muscle of the Aging Human

Contact Info

Product

Resources

About