Biosynthesis of prostaglandins in microsomes of human skeletal muscle and kidney

Nowak, Jacek; Bohman, Sven‐Olof; Alster, Pawel; Berlin, Tomas; Cronestrand, R; Sonnenfeld, T

doi:10.1016/0262-1746(83)90040-9

Cited by 11 publications

(9 citation statements)

References 23 publications

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“…Muscle biopsy-derived measures of PGs that regulate protein turnover show PGE 2 to be the dominant PG in young and old human muscle (11,33,51,74,126). Intramuscular PGE 2 levels are three to four times higher than PGF 2␣ at rest and after resistance exercise in young individuals, suggesting equivalent, relative increases in both PGs after exercise (126).…”

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confidence: 99%

“…Whereas PGs were reported to be in resting human skeletal muscle as early as 1967 (51), Berlin et al (11) showed in 1979, with radiolabeled arachidonic acid added to homogenates of skeletal muscle biopsy samples, that skeletal muscle could produce PGD 2 , PGE 2 , PGF 2␣ , and PGI 2 . PGE 2 was the predominant PG produced (11), but this could be shifted to PGF 2␣ if the assay environment was altered (74). (53,107,108).…”

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Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Trappe

Liu

2013

Journal of Applied Physiology

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Trappe TA, Liu SZ. Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise. J Appl Physiol 115: 909 -919, 2013. First published March 28, 2013 doi:10.1152/japplphysiol.00061.2013.-It has been ϳ40 yr since the discovery that PGs are produced by exercising skeletal muscle and since the discovery that inhibition of PG synthesis is the mechanism of action of what are now known as cyclooxygenase (COX)-inhibiting drugs. Since that time, it has been established that PGs are made during and after aerobic and resistance exercise and have a potent paracrine and autocrine effect on muscle metabolism. Consequently, it has also been determined that orally consumed doses of COX inhibitors can profoundly influence muscle PG synthesis, muscle protein metabolism, and numerous other cellular processes that regulate muscle adaptations to exercise loading. Although data from acute human exercise studies, as well as animal and cell-culture data, would predict that regular consumption of a COX inhibitor during exercise training would dampen the typical muscle adaptations, the chronic data do not support this conjecture. From the studies in young and older individuals, lasting from 1.5 to 4 mo, no interfering effects of COX inhibitors on muscle adaptations to resistance-exercise training have been noted. In fact, in older individuals, a substantial enhancement of muscle mass and strength has been observed. The collective findings of the PG/COX-pathway regulation of skeletal muscle responses and adaptations to exercise are compelling. Considering the discoveries in other areas of COX regulation of health and disease, there is certainly an interesting future of investigation in this re-emerging area, especially as it pertains to older individuals and the condition of sarcopenia, as well as exercise training and performance of individuals of all ages. PGE 2; PGF2␣; acetaminophen; ibuprofen; sarcopenia PGS PRODUCED BY the cyclooxygenase (COX) enzyme are ubiquitous in human physiology and regulate numerous processes (105, 108), including muscle protein metabolism (78,93,106,126,128). As a result, PGs regulate adaptations to muscular exercise, and COX-inhibiting drugs can alter the acute and chronic responses to exercise. Because of the continuum of acute responses and chronic adaptations that exists from lowerintensity, longer-duration exercise to higher-intensity, shorterduration exercise, it is difficult to adopt a "one-mechanismfits-all" approach to PG and COX involvement in skeletal muscle exercise adaptations. This is also true when distinguishing between muscle injury and muscular exercise for health and performance.COX-inhibiting drugs are one of the most commonly consumed classes of drugs in the world. In the United States, the COX inhibitors, acetaminophen, ibuprofen, and aspirin, are the top three consumed drugs of young, middle-aged, and older individuals, with ϳ50 million individuals using each of these drugs during any given week (52, 129). Interestingly, two of these drugs (acetaminophen...

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Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Trappe

Liu

2013

Journal of Applied Physiology

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“…1 Several PGs have been implicated in multiple phases of myogenesis. [1][2][3][4] For example, prostaglandin F2a (PGF2a) is secreted by skeletal muscle cells in vitro and in vivo 5,6 and promotes myotube growth during later stages of myogenesis by increasing the number of nuclei within myotubes. 3 PGF2a signals by the FP receptor to increase levels of intracellular calcium, activating the nuclear factor of activated T cells 2 (NFATC2) transcription factor in muscle cells.…”

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Prostaglandin F2α promotes muscle cell survival and growth through upregulation of the inhibitor of apoptosis protein BRUCE

Jansen

Pavlath

2008

Cell Death Differ

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During skeletal muscle growth and regeneration, the majority of differentiating myoblasts undergoes cell-cell fusion to form multinucleated myofibers, whereas a proportion of myoblasts undergoes apoptosis. The treatment of myoblasts with prostaglandin F2a (PGF2a) during myogenesis in vitro leads to the formation of large myotubes, but the mechanism by which PGF2a promotes myotube growth has not been investigated. Here, we demonstrate that PGF2a reduces cell death during myogenesis in vitro and in vivo. In addition, we show that PGF2a increases expression of the inhibitor of apoptosis protein (IAP) BRUCE through a pathway dependent on the nuclear factor of activated T cell 2 transcription factor. Importantly, PGF2a-mediated reduction in muscle cell death is dependent on BRUCE, and overexpression of BRUCE is sufficient to promote muscle cell survival and growth. These results establish a previously unrecognized link between NFAT signaling and regulation of IAP expression and are the first to identify a signaling pathway that increases BRUCE expression. In addition, our results provide evidence that increasing the pool of muscle cells available for fusion by inhibiting cell death enhances myotube growth.

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“…Muscles were preincubated for 30 min at 34"C, then transferred to fresh media and incubated for a further 3 h. PGE, production was estimated by radioimmunoassay of the incubation medium as described previously (Strelksv et al 1989;Tian and Baracos 1989). The cross-reactivity of the anti-PGE, antibody (HCN Immunobiologicals, Costa Mesa, @A) with PGE, is > 1W%, but with PGF,, less than 2%-Since skeletal muscle does not appear to synthesize PGE, (Nowak et al 1983), the crossreactivity would not interfere with the assay of To determine tissue protein content, MG, L muscles were dissected intact. Tissues were solubilized in 1.8 M NaOH at room temperature and protein was determined according to the Bradford method using bovine semm albumin as standard ( ford 1974).…”

Section: Experiments 11mentioning

confidence: 99%

“…Skeletal muscles of humans and rats can produce metabolites of arachidonic acid including PG12, PGE2, PGF2,, and thromboxane B2 (Nowak et al 1983;Smith et al 1983;Rodemann and Goldberg 1982). In addition to PC3 production by muscle cells, mononuclear phagocytes, which participate in the inflammatory response following tissue injury, produce P G , particularly PGE2 (Male et al 1988).…”

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confidence: 97%

Effect of systemic inhibition of prostaglandin synthesis on muscle protein balance after trauma in the rat

Fisher¹,

Baracos²,

Reid³

1991

Can. J. Physiol. Pharmacol.

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Anaesthetized rats were subjected to a single impact trauma to the medial aspect of the right hindlimb (gastrocnemius muscle), and were compared with sham-treated controls. For 3 days after injury, muscles of the traumatized limb showed a marked catabolic response. Muscle protein repletion commenced after day 3, however, this process was not complete until 21 days after injury. Muscles of the uninjured limb of the traumatized rats also showed a distinct catabolic response, compared with rats that were never injured, although this response was less in magnitude than that of the injured limb. At 3 days after trauma, augmented synthesis of prostaglandin (PG)E2 by muscles of the injured and uninjured limb provided evidence of a local and systemic inflammatory response. Inhibition of PG synthesis by the systemic administration of naproxen (6-methoxy-alpha-methyl-2-napthaleneacetic acid) significantly reduced the catabolic loss of muscle protein seen locally and peripherally to the injury site.

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Biosynthesis of prostaglandins in microsomes of human skeletal muscle and kidney

Cited by 11 publications

References 23 publications

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Prostaglandin F2α promotes muscle cell survival and growth through upregulation of the inhibitor of apoptosis protein BRUCE

Effect of systemic inhibition of prostaglandin synthesis on muscle protein balance after trauma in the rat

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