Induction of the Histamine-Forming Enzyme Histidine Decarboxylase in Skeletal Muscles by Prolonged Muscular Work: Histological Demonstration and Mediation by Cytokines

Ayada, Kentaro; Tsuchiya, Masahiro; Yoneda, Hikaru; Yamaguchi, Kohei; Kumamoto, Hiroyuki; Sasaki, Keiichi; Tadano, Takeshi; Watanabe, Makoto; Endo, Yasuo

doi:10.1248/bpb.b17-00112

Cited by 5 publications

(6 citation statements)

References 24 publications

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“…Histamine plays also an important role as a regulator of microcirculation in muscles during exercise and sustained post-exercise vasodilation [51,52]. Histidine decarboxylase expression is induced in mast cells, vascular endothelial cells, and muscle fibers themselves by cytokines (particularly IL-1 and TNF-α), increased temperature, decreased pH, and hypoxia-inducible factor 1 [53][54][55][56].…”

Section: Histaminementioning

confidence: 99%

Histidine in Health and Disease: Metabolism, Physiological Importance, and Use as a Supplement

2020

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L-histidine (HIS) is an essential amino acid with unique roles in proton buffering, metal ion chelation, scavenging of reactive oxygen and nitrogen species, erythropoiesis, and the histaminergic system. Several HIS-rich proteins (e.g., haemoproteins, HIS-rich glycoproteins, histatins, HIS-rich calcium-binding protein, and filaggrin), HIS-containing dipeptides (particularly carnosine), and methyl- and sulphur-containing derivatives of HIS (3-methylhistidine, 1-methylhistidine, and ergothioneine) have specific functions. The unique chemical properties and physiological functions are the basis of the theoretical rationale to suggest HIS supplementation in a wide range of conditions. Several decades of experience have confirmed the effectiveness of HIS as a component of solutions used for organ preservation and myocardial protection in cardiac surgery. Further studies are needed to elucidate the effects of HIS supplementation on neurological disorders, atopic dermatitis, metabolic syndrome, diabetes, uraemic anaemia, ulcers, inflammatory bowel diseases, malignancies, and muscle performance during strenuous exercise. Signs of toxicity, mutagenic activity, and allergic reactions or peptic ulcers have not been reported, although HIS is a histamine precursor. Of concern should be findings of hepatic enlargement and increases in ammonia and glutamine and of decrease in branched-chain amino acids (valine, leucine, and isoleucine) in blood plasma indicating that HIS supplementation is inappropriate in patients with liver disease.

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Section: Histaminementioning

confidence: 99%

Histidine in Health and Disease: Metabolism, Physiological Importance, and Use as a Supplement

2020

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“…In addition, our data suggested that bone marrow–derived HDC‐expressing CD11b + immune cells cannot be induced to transform into skeletal muscle or myoblasts. A recent study reported that prolonged muscular work (PMW) induces HDC expression in the endomysium and around blood vessels and some muscle fibres, using anti‐HDC IHC staining . PMW requires a large supply of O 2 and induces hypoxia in the tissue, which might cause slight inflammation in skeletal muscle and further recruit HDC‐expressing CD11b + myeloid cells.…”

Section: Discussionmentioning

confidence: 99%

Histamine deficiency delays ischaemic skeletal muscle regeneration via inducing aberrant inflammatory responses and repressing myoblast proliferation

Abudupataer

Zou

Zhang

et al. 2019

J Cellular Molecular Medi

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Histidine decarboxylase (HDC) catalyses the formation of histamine from L‐histidine. Histamine is a biogenic amine involved in many physiological and pathological processes, but its role in the regeneration of skeletal muscles has not been thoroughly clarified. Here, using a murine model of hindlimb ischaemia, we show that histamine deficiency in Hdc knockout (Hdc−/−) mice significantly reduces blood perfusion and impairs muscle regeneration. Using Hdc‐EGFP transgenic mice, we demonstrate that HDC is expressed predominately in CD11b+Gr‐1+ myeloid cells but not in skeletal muscles and endothelial cells. Large amounts of HDC‐expressing CD11b+ myeloid cells are rapidly recruited to injured and inflamed muscles. Hdc−/− enhances inflammatory responses and inhibits macrophage differentiation. Mechanically, we demonstrate that histamine deficiency decreases IGF‐1 (insulin‐like growth factor 1) levels and diminishes myoblast proliferation via H3R/PI3K/AKT‐dependent signalling. These results indicate a novel role for HDC‐expressing CD11b+ myeloid cells and histamine in myoblast proliferation and skeletal muscle regeneration.

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“…In resting skeletal muscle, HDC enzyme activity generates minute quantities of histamine (7). HDC mRNA expression, protein abundance, and activity are increased with exercise (1,2). HDC activity appears to be enhanced by increased temperature (7,8), decreased pH (8), hypoxia (6), and several signaling molecules such as interleukin-1 (2,9), all of which may play a role during repeated muscle contractions.…”

Section: Histamine In Exercise Responsesmentioning

confidence: 99%

“…Skeletal muscle interstitial histamine concentrations are low at rest, but increase in active musculature during moderate-intensity endurance exercise (1). Histamine is released by mast cell degranulation and produced through de novo synthesis (1), secondary to increased activity of the enzyme histidine decarboxylase (HDC) (1,2). Mast cell degranulation has been shown to occur with stimuli associated with exercise such as hypoxia, increased temperature, vibration, and hyperosmolality (3).…”

Section: Introductionmentioning

confidence: 99%

“…Mast cell degranulation has been shown to occur with stimuli associated with exercise such as hypoxia, increased temperature, vibration, and hyperosmolality (3). While HDC is present in high concentrations within mast cells, there is also evidence it may be expressed within skeletal muscle myocytes (2,4) and endothelial cells (4,5). HDC continually synthesizes minute quantities of histamine in resting muscle (4), but further activity can be induced by stimuli associated with exercise such as hypoxia (6), increased temperature (7,8), and decreased pH (8).…”

Section: Introductionmentioning

confidence: 99%

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Histamine-Receptor Antagonists Slow 10-km Cycling Performance in Competitive Cyclists

Ely

Sieck

Mangum

et al. 2019

Medicine &Amp; Science in Sports &Amp; Exercise

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Histamine‐receptor antagonists (“antihistamines”) are widely used among endurance athletes and are not currently banned by the World Anti‐Doping Agency. Our lab has recently shown that a single dose of antihistamines prior to muscle‐damaging exercise attenuates strength loss and muscle pain in the 72 hours following exercise. Histamine, produced within muscle, may be a factor in exercise‐induced muscle pain/discomfort and, therefore, perception of effort, as group III/IV muscle afferents (nociceptive neurons) are sensitized via activation of H1 and H2 receptors. Histamine may have more influence on muscle pain and effort sensations during long‐duration exercise than short‐duration, because the activity of histidine decarboxylase (the enzyme that creates histamine) increases with exercise duration. Therefore, the purpose of this experiment was to determine if combination H1/H2 antihistamines increase endurance exercise performance. It was hypothesized that H1/H2 antihistamines would decrease the time to completion of a fixed‐distance time‐trial compared to placebo, and the effect would be greater following an endurance‐exercise bout. Eleven (3F) highly competitive cyclists (Cat 1–3) performed six 10 km time‐trials on separate days. The first two trials served as a familiarization, and repeatability was assessed by calculating a coefficient of variation (CV) between times to completion. The next 4 trials were performed in a randomized‐block order. Two were preceded by 120 min of seated rest and two by 120 min of steady‐state cycling at 50% VO2peak. Within those blocks, volunteers consumed either antihistamines (540 mg fexofenadine; a H1 receptor blocker, and 300 mg of ranitidine; a H2 blocker) or placebo 60 min prior to the start of rest/exercise. The main outcome variable was 10 km time to completion. Additionally, rating of perceived exertion (RPE), isometric quadriceps muscle strength, blood glucose, and blood lactate were measured prior to and following the time‐trials. Conventional statistics (2‐Way Repeated Measures ANOVA), effect size (ES = Cohen's dz), 95% CI, and CV from familiarization trials were used to determine the presence, strength, and meaningfulness of differences, respectively, between the trials. There was a significant reduction in performance with antihistamines compared to placebo (+10.5 ± 3.8 s, mean±SEM, drug effect p=0.002), the reduced performance tended to be exacerbated by prior exercise (p=0.057) but there was no drug by prior exercise interaction (p=0.716) (Figure 1). The day‐to‐day 10 km performance variability (CV) was 0.98%. The percent change between placebo and antihistamine was likely trivial for time‐trials following rest (mean −0.87%, 95%CI −2.02 to 0.29%) (ES=0.505) and potentially harmful following exercise (mean −1.2%, 95%CI −2.45 to 0.05%) (ES=0.646). There were no drug effects on changes (pre to post time‐trial) in isometric muscle strength (p=0.607), RPE (p=0.828), blood glucose (p=0.964) or lactate (p=0.402) between antihistamine and placebo conditions. Thus, contrary t...

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Induction of the Histamine-Forming Enzyme Histidine Decarboxylase in Skeletal Muscles by Prolonged Muscular Work: Histological Demonstration and Mediation by Cytokines

Cited by 5 publications

References 24 publications

Histidine in Health and Disease: Metabolism, Physiological Importance, and Use as a Supplement

Histidine in Health and Disease: Metabolism, Physiological Importance, and Use as a Supplement

Histamine deficiency delays ischaemic skeletal muscle regeneration via inducing aberrant inflammatory responses and repressing myoblast proliferation

Histamine-Receptor Antagonists Slow 10-km Cycling Performance in Competitive Cyclists

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