Survival and cellular immune functions in septic mice treated with growth hormone (GH) and insulin-like growth factor-I (IGF-I)

Schmitz, Daniel; Kobbe, Phillip; Lendemanns, Sven; Wilsenack, Klaus; Exton, Michael S.; Schedlowski, Manfred; Oberbeck, Reiner

doi:10.1016/j.ghir.2007.10.002

Cited by 11 publications

(9 citation statements)

References 50 publications

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“…Transgenic mice with cardiac-specific overexpression of IGF-1 display reduced cardiomyocyte apoptosis, lessened ventricular wall stress, and chamber dilatation after myocardial infarction or during aging (13-15), indicating a critical role of this essential cardiac survival factor in the maintenance of cardiac morphology and function. It has been shown that circulating IGF-1 levels are drastically reduced in patients with sepsis, which is in line with the beneficial role of IGF-1 supplementation on the overall survival rate in sepsis, possibly via a facilitated hepatic bacterial clearance and improved cellular immune response (16, 17). However, little is known with regards to the impact of IGF-1 on sepsis-induced cardiac contractile dysfunction.…”

Section: Introductionmentioning

confidence: 55%

CARDIAC-SPECIFIC OVEREXPRESSION OF INSULIN-LIKE GROWTH FACTOR I (IGF-1) RESCUES lIPOPOLYSACCHARIDE-INDUCED CARDIAC DYSFUNCTION AND ACTIVATION OF STRESS SIGNALING IN MURINE CARDIOMYOCYTES

Zhao¹,

Turdi

Dong

et al. 2009

Shock

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LPS, a component of the outer membrane of Gram-negative bacteria, plays a key role in cardiac dysfunction in sepsis. Low circulating levels of insulin-like growth factor 1 (IGF-1) are found in sepsis, although the influence of IGF-1 on septic cardiac defect is unknown. This study was designed to examine the impact of IGF-1 on LPS-induced cardiac contractile and intracellular Ca2+ dysfunction, activation of stress signal, and endoplasmic reticulum (ER) stress. Mechanical and intracellular Ca2+ properties were examined in cardiomyocytes from Fast Violet B and cardiac-specific IGF-1 overexpression mice treated with or without LPS (4 mg kg-1, 6 h). Reactive oxygen species (ROS), protein carbonyl formation, and apoptosis were measured. Activation of mitogen-activated protein kinase pathways (p38, c-jun N-terminal kinase [JNK] and extracellular signal-related kinase [ERK]), ER stress, and apoptotic markers were evaluated using Western blot analysis. Our results revealed decreased peak shortening and maximal velocity of shortening/relengthening and prolonged duration of relengthening in LPS-treated Fast Violet B cardiomyocytes associated with reduced intracellular Ca2+ decay. Accumulation of ROS protein carbonyl and apoptosis were elevated after LPS treatment. Western blot analysis revealed activated p38 and JNK, up-regulated Bax, and the ER stress markers GRP78 and Gadd153 in LPS-treated mouse hearts without any change in ERK and Bcl-2. Total protein expression of p38, JNK, and ERK was unaffected by either LPS or IGF-1. Interestingly, these LPS-induced changes in mechanical and intracellular Ca2+ properties, ROS, protein carbonyl, apoptosis, stress signal activation, and ER stress markers were effectively ablated by IGF-1. In vitro LPS exposure (1 μg mL-1) produced cardiomyocyte mechanical dysfunction reminiscent of the in vivo setting, which was alleviated by exogenous IGF-1 (50 nM). These data collectively suggested a beneficial of IGF-1 in the management of cardiac dysfunction under sepsis.

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Section: Introductionmentioning

confidence: 55%

CARDIAC-SPECIFIC OVEREXPRESSION OF INSULIN-LIKE GROWTH FACTOR I (IGF-1) RESCUES lIPOPOLYSACCHARIDE-INDUCED CARDIAC DYSFUNCTION AND ACTIVATION OF STRESS SIGNALING IN MURINE CARDIOMYOCYTES

Zhao¹,

Turdi

Dong

et al. 2009

Shock

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“…Serum levels of IL-6 were assayed with a high sensitivity enzyme-linked immunoassay kit (R&D Systems, Inc., MN). IL-6, a pro-inflammatory cytokine, and IGF-1, a stimulator of systemic cell growth, have both been used in prior studies of allostatic load, and are both considered correlates of immune status [32]. IGF-1 is thought to play a role in resistance to oxidative stress [33], is crucial in the neurogenesis process [34], and has been used previously in studies of allostatic load [35].…”

Section: Methodsmentioning

confidence: 99%

Depressive symptoms are associated with allostatic load among community-dwelling older adults

Kobrosly

Wijngaarden

Seplaki

et al. 2014

Physiology & Behavior

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The allostatic load model has been used to quantify the physiological costs of the body’s response to repeated stressful demands and may provide a useful, integrative perspective on the various correlates of late-life depressive symptoms. We interviewed 125 Rochester, NY adults, ranging in age from 67 to 94 years. We employed an allostatic load score as a measure of multisystem dysfunction in hypothalamic-pituitary-adrenal axis function, immune function, anabolic activity, and cardiovascular activity. Overall, affective, and somatic depressive symptom scores were computed using the 20-item Center for Epidemiologic Studies Depression Scale. Multiple linear regression models were used to estimate associations between allostatic load scores and affective, somatic, and overall depressive symptoms. Among our sample of mean age 76.1 years, the one-week prevalence of clinically significant depressive symptoms was 12.8%. In models adjusting for demographic, socioeconomic, and health-related factors, higher allostatic load scores were associated with elevated scores for overall, affective, and somatic depressive symptoms: beta = 1.21 (95% CI = 0.38, 2.05); beta = 0.14 (95% CI = 0.040, 0.24); beta = 0.60 (95% CI = 0.23, 0.97), respectively. Our results suggest that allostatic load measure is associated with late-life depressive symptoms. This association appears to be of clinical significance, as the magnitude of the effect size was comparable (but opposite in direction) to that of antidepressant use. Future research should examine the inter-relationships of allostatic load, psychological stress, and late-life depressive symptoms.

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“…However, both studies found that RA at concentrations from 10 À8 to 10 À6 M induced the inhibition of cell viability. IGF-I is an important survival hormone that is known to inhibit apoptosis in various cell types [35,36]. We found that RA decreased IGF-I secretion and synthesis, which is analogous to the decrease in cell viability with increasing RA concentration, with opposite results for PKC-d activity.…”

Section: Discussionmentioning

confidence: 66%

Oxidative stress in MCF-7 cells is involved in the effects of retinoic acid-induced activation of protein kinase C-δ on insulin-like growth factor-I secretion and synthesis

Kim

Kang

2010

Growth Hormone & IGF Research

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Survival and cellular immune functions in septic mice treated with growth hormone (GH) and insulin-like growth factor-I (IGF-I)

Cited by 11 publications

References 50 publications

CARDIAC-SPECIFIC OVEREXPRESSION OF INSULIN-LIKE GROWTH FACTOR I (IGF-1) RESCUES lIPOPOLYSACCHARIDE-INDUCED CARDIAC DYSFUNCTION AND ACTIVATION OF STRESS SIGNALING IN MURINE CARDIOMYOCYTES

CARDIAC-SPECIFIC OVEREXPRESSION OF INSULIN-LIKE GROWTH FACTOR I (IGF-1) RESCUES lIPOPOLYSACCHARIDE-INDUCED CARDIAC DYSFUNCTION AND ACTIVATION OF STRESS SIGNALING IN MURINE CARDIOMYOCYTES

Depressive symptoms are associated with allostatic load among community-dwelling older adults

Oxidative stress in MCF-7 cells is involved in the effects of retinoic acid-induced activation of protein kinase C-δ on insulin-like growth factor-I secretion and synthesis

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