Neurotrophic factors decrease the release of creatine kinase and prostaglandin E2 from metabolically stressed muscle

Lian, Jidong; Aljumah, Mohammed; Cwik, Valerie; Brooke, Michael H.

doi:10.1016/s0960-8966(97)00122-3

Cited by 10 publications

(6 citation statements)

References 30 publications

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“…Additional data showing increased mitochondrial ROS and decreased glutathione levels in GHRKO osteocytes favors the latter. Our data are consistent with previous reports showing the protective effects of GH or IGF‐1 on mitochondrial function, specifically with regard to ROS metabolism …”

Section: Discussionsupporting

confidence: 93%

Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice

Liu

Solesio

Schaffler

et al. 2018

Journal of Bone and Mineral Research

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Despite increased longevity and resistance to multiple stressors, growth hormone receptor null (GHRKO) mice exhibit severe skeletal impairment. The role of GHR in maintaining osteocyte mitochondrial function is unknown. We found that GHR ablation was detrimental to osteocyte mitochondrial function. In vivo multiphoton microscopy revealed significant reductions of >10% in mitochondrial membrane potential (MMP) in GHRKO osteocytes and reduced mitochondrial volumetric density. Reductions in MMP were accompanied by reductions in glucose transporter-1 levels, steady state ATP, NADH redox index, oxygen consumption rate, and mitochondrial reserve capacity in GHRKO osteocytes. Glycolytic capacity did not differ between control and GHRKO males' osteocytes. However, osteocytes from aged female GHRKO mice exhibited reductions in glycolytic parameters, indicating impairments in glucose metabolism, which may be sex dependent. GHRKO osteocytes exhibited increased levels of cytoplasmic reactive oxygen species (ROS) (both basal and in response to high glucose), insulin-like growth factor-1 (IGF-1), and insulin. Mitochondrial ROS levels were increased and correlated with reduced glutathione in GHRKO osteocytes. Overall, the compromised osteocyte mitochondrial function and responses to metabolic insults strongly correlated with skeletal impairments, suggesting that despite increased life span of the GHRKO mice, skeletal health span is decreased. © 2018 American Society for Bone and Mineral Research.

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Section: Discussionsupporting

confidence: 93%

Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice

Liu

Solesio

Schaffler

et al. 2018

Journal of Bone and Mineral Research

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“…Among other effects, ovariectomy can stimulate an increase in growth hormone release and IGF-1 production (11). IGF-1 has been shown to attenuate injury after I/R in the heart (6, 14) and brain (16) and in skeletal muscle exposed to oxidants in vivo (21). Hence, serum was analyzed not only for 17␤-estradiol content but also for IGF-1 content; results were further interpreted by taking into account the potentially protective effects of both estrogen and IGF-1.…”

Section: Discussionmentioning

confidence: 99%

Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

Stupka

Tiidus

2001

Journal of Applied Physiology

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The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17beta-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater (P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats (P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower (P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater (P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower (P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower (P < 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content (P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

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“…Likewise, hearts of IGF-1 transgenic mice were protected from ischemia and reperfusion [83], and streptozotocin-induced diabetic cardiomyopathy in mice resulted in accumulation of nitrotyrosine (a reactive oxygen product) in vivo and the formation of H 2 O 2 in myocytes in vitro that were rescued in IGF-1 transgenic mice [84]. Additionally, IGF-1 protected from 2:4 dinitrophenol-induced oxidative stress in rat muscle in vitro [85] and myoblasts protected from H 2 O 2 stress-induced apoptosis [86].…”

Section: Gh/igf-1 Effects On Oxidative Stress During Agingmentioning

confidence: 99%

Effects of GH/IGF on the Aging Mitochondria

Poudel

Dixit

Neginskaya

et al. 2020

Cells

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The mitochondria are key organelles regulating vital processes in the eukaryote cell. A decline in mitochondrial function is one of the hallmarks of aging. Growth hormone (GH) and the insulin-like growth factor-1 (IGF-1) are somatotropic hormones that regulate cellular homeostasis and play significant roles in cell differentiation, function, and survival. In mammals, these hormones peak during puberty and decline gradually during adulthood and aging. Here, we review the evidence that GH and IGF-1 regulate mitochondrial mass and function and contribute to specific processes of cellular aging. Specifically, we discuss the contribution of GH and IGF-1 to mitochondrial biogenesis, respiration and ATP production, oxidative stress, senescence, and apoptosis. Particular emphasis was placed on how these pathways intersect during aging.

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Neurotrophic factors decrease the release of creatine kinase and prostaglandin E2 from metabolically stressed muscle

Cited by 10 publications

References 30 publications

Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice

Mitochondrial Function Is Compromised in Cortical Bone Osteocytes of Long-Lived Growth Hormone Receptor Null Mice

Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

Effects of GH/IGF on the Aging Mitochondria

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