IGF-I system, atrogenes and myogenic regulatory factors in arthritis induced muscle wasting

Castillero, Estíbaliz; Martín, Ana Isabel; López-Menduiña, María; Granado, Miriam; Villanúa, María Ángeles; López-Calderón, Asunción

doi:10.1016/j.mce.2009.05.017

Cited by 45 publications

(97 citation statements)

References 48 publications

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“…As previously reported (8), arthritis induced an increase in PCNA mRNA (P Ͻ 0.01) and PCNA protein (P Ͻ 0.05) in the rats that received coconut oil (Fig. 5, A and B).…”

Section: Resultssupporting

confidence: 85%

“…Although the maximal external signs have their maximum value around day 21 after adjuvant injection (31), rats were killed on day 15, since we had previously observed a high increase in atrogin-1 and MuRF1 mRNA as well as the myogenic regulatory factors PCNA, MyoD, and myogenin on this day in the gastrocnemius of the arthritic rats (8). Immediately after decapitation, gastrocnemius muscle was removed and weighed.…”

Section: Methodsmentioning

confidence: 99%

“…Similarly, a decrease in the relative skeletal muscle mass is observed in arthritic rats but not in pair-fed rats (8).…”

mentioning

confidence: 88%

“…Proliferation and differentiation of muscular precursor cells, or satellite cells, into mature muscular cells depends on hormones and growth factors such as PCNA, MyoD, and myogenin. Because adjuvant-induced arthritis also increases the expression of the myogenic regulatory factors PCNA, MyoD, and myogenin (8), their response to EPA administration was also analyzed.…”

mentioning

confidence: 99%

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Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

Castillero

Martín

López-Menduiña

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Castillero E, Martín AI, López-Menduiña M, Villanúa MA, López-Calderón A. Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors. Am J Physiol Regul Integr Comp Physiol 297: R1322-R1331, 2009. First published September 9, 2009 doi:10.1152/ajpregu.00388.2009.-Eicosapentaenoic acid (EPA) is an omega-3 polyunsaturated fatty acid that has anti-inflammatory and anticachectic actions. The aim of this work was to elucidate whether EPA administration is able to prevent an arthritis-induced decrease in body weight and muscle wasting in rats. Arthritis was induced by intradermal injection of Freund's adjuvant; 3 days later, nine rats received 1 g/kg EPA or coconut oil daily. All rats were killed 15 days after adjuvant injection. EPA administration decreased the external signs of arthritis and paw volume as well as liver TNF-␣ mRNA. EPA did not modify arthritis-induced decrease in food intake or body weight gain. However, EPA treatment prevented arthritis-induced increase in muscle TNF-␣ and atrogin-1, whereas it attenuated the decrease in gastrocnemius weight and the increase in MuRF1 mRNA. Arthritis not only decreased myogenic regulatory factors but also increased PCNA, MyoD, and myogenin mRNA in the gastrocnemius. Western blot analysis showed that changes in protein content followed the pattern seen with mRNA. In the control rats, EPA administration increased PCNA and MyoD mRNA and protein.In arthritic rats, EPA did not modify the stimulatory effect of arthritis on these myogenic regulatory factors. The results suggest that in experimental arthritis, in addition to its anti-inflammatory effect, EPA treatment attenuates muscle wasting by decreasing atrogin-1 and MuRF1 gene expression and increasing the transcription factors that regulate myogenesis. adjuvant-induced arthritis; ubiquitin-proteasome system; MyoD; myogenin; proliferating cell nuclear antigen CHRONIC INFLAMMATORY DISEASES such as cancer, sepsis, and rheumatoid arthritis are associated with a decrease in body weight, skeletal muscle atrophy, and cachexia. Cachexia is a complex metabolic syndrome associated with underlying

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“…As previously reported (8), arthritis induced an increase in PCNA mRNA (P Ͻ 0.01) and PCNA protein (P Ͻ 0.05) in the rats that received coconut oil (Fig. 5, A and B).…”

Section: Resultssupporting

confidence: 85%

Section: Methodsmentioning

confidence: 99%

“…Similarly, a decrease in the relative skeletal muscle mass is observed in arthritic rats but not in pair-fed rats (8).…”

mentioning

confidence: 88%

mentioning

confidence: 99%

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Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

Castillero

Martín

López-Menduiña

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Adjuvant‐induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and skeletal muscle wasting. Although inflammation and arthritis induce anorexia, skeletal muscle wasting in arthritic rats is not secondary to the decrease in food intake 1, 2. Similarly, loss of fat‐free mass in rheumatoid arthritis patients is not attributable to reduced food intake 3.…”

Section: Introductionmentioning

confidence: 99%

The melanocortin receptor type 3 agonistd-Trp(8)-γMSH decreases inflammation and muscle wasting in arthritic rats

Gómez-SanMiguel

Martín

Nieto-Bona

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

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BackgroundChronic inflammatory diseases induce cachexia that increases mortality and morbidity of the illness. Adjuvant‐induced arthritis is an experimental model of rheumatoid arthritis that is associated with body weight loss and muscle wasting. Alpha‐melanocyte stimulating hormone has an anti‐inflammatory effect in arthritic rats and decreases muscle wasting. The aim of this work was to elucidate whether the anti‐cachectic action of alpha‐melanocyte stimulating hormone is mediated by the melanocortin receptor type 3 pathway.MethodsArthritis was induced in male Wistar rats by intradermal injection of Freund's adjuvant, and 6 days afterwards, arthritic rats were injected with the selective melanocortin receptor type 3 agonist d‐Trp(8)‐gammaMSH ( d‐Trp(8)‐γMSH) 500 µg/kg subcutaneously. or saline twice a day, for 10 days.Results d‐Trp(8)‐γMSH decreased the external signs of inflammation and body weight loss, but it was not able to modify the anorexigenic effect of arthritis or the increase in hypothalamic cyclooxygenase‐2 (COX‐2) expression. In contrast, d‐Trp(8)‐γMSH prevented arthritis‐induced increase in hypothalamic IL‐1β and serum corticosterone levels and the decrease in serum IGF‐I levels. d‐Trp(8)‐γMSH treatment also prevented arthritis‐induced NF‐kB(p65) phosphorylation and tumour necrosis factor‐α mRNA increase in the gastrocnemius. d‐Trp(8)‐γMSH administration to arthritic rats increased gastrocnemius mass, its cross‐sectional area, and mean fast fibre area. Those effects of d‐Trp(8)‐γMSH were associated with a decreased expression of atrogin‐1 and muscle ring‐finger protein‐1 in the gastrocnemius. In rats treated with saline, arthritis increased the expression of autophagy marker genes LC3b, Bnip‐3, and Gabarap1 as well as the conversion of LC3b I to LC3b II by lipidation in the gastrocnemius. d‐Trp(8)‐γMSH decreased gastrocnemius LC3b, Bnip‐3, and Gabarap1 mRNA expression and prevented the increase in LC3b II in arthritic rats.ConclusionThese data suggest that d‐Trp(8)‐γMSH administration prevents the effect of arthritis on corticosterone and insulin‐like growth factor‐I serum levels and decreases muscle wasting, by down‐regulating atrogenes and autophagy through modifying the NF‐kB(p65)/tumour necrosis factor‐α signalling transduction pathway.

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Upregulation of Systemic Inflammatory Pathways Following Anterior Cruciate Ligament Injury Relates to Both Cartilage and Muscular Changes: A Pilot Study

Hunt

Villasanta‐Tezanos

Butterfield

et al. 2019

Journal Orthopaedic Research

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In conjunction with cartilage breakdown, muscle maladaptation including atrophy and increased fibrosis have been observed in the quadriceps following anterior cruciate ligament (ACL) injury. Previously observed upregulated muscle-related proteins in the synovial fluid following ACL rupture allude to cellular communication between the joint and muscle. Therefore, the purpose of this study was to determine whether muscle-related analytes are differentially expressed in the serum. Sixteen patients with an acute ACL tear participated in this IRB-approved study. Serum was obtained at two different time points at a mean of 6 and 14 days post-injury, and serum was analyzed by a highly multiplexed assay of 1,300 proteins. Pathway analysis using DAVID was performed; genes included met three criteria: significant change between the two study time points using a paired t test, significant change between the two study time points using a Mann-Whitney non-parametric test, and significant Benjamini post hoc analysis. Twelve analytes significantly increased between time points. Proteins chitinase-3-like protein 1 (p = 0.01), insulin-like growth factor binding protein 1 (p = 0.01), insulin-like growth factor binding protein 5 (p = 0.02), renin (p = 0.004), and lymphotoxin alpha 1: beta 2 (p = 0.03) were significantly upregulated in serum following acute ACL injury. The current results confirm the inflammatory pattern previously seen in the synovial fluid thought to play a role in the progression of post-traumatic osteoarthritis after ACL injury, and this data also provides further insights into important communication between the joint and quadriceps group, whose function is important in long term health.

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IGF-I system, atrogenes and myogenic regulatory factors in arthritis induced muscle wasting

Cited by 45 publications

References 48 publications

Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

Eicosapentaenoic acid attenuates arthritis-induced muscle wasting acting on atrogin-1 and on myogenic regulatory factors

The melanocortin receptor type 3 agonistd-Trp(8)-γMSH decreases inflammation and muscle wasting in arthritic rats

Upregulation of Systemic Inflammatory Pathways Following Anterior Cruciate Ligament Injury Relates to Both Cartilage and Muscular Changes: A Pilot Study

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