IL-1β and TNF-α Modulation of Proliferated and Committed Myoblasts: IL-6 and COX-2-Derived Prostaglandins as Key Actors in the Mechanisms Involved

Alvarez, Angela M.; DeOcesano-Pereira, Carlos; Teixeira, Catarina; Moreira, Vanessa

doi:10.3390/cells9092005

Cited by 53 publications

(36 citation statements)

References 75 publications

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“…Inflammatory prostaglandin signaling plays a role in the preclinical development of neurodegenerative diseases [ 29 , 30 , 54 ]. COX-2, the inducible form of the COX enzyme involved in prostaglandin synthesis, is rarely expressed in steady state but is induced rapidly following stimulation by a mitogen, cytokine, or lipopolysaccharide [ 28 , 31 , 55 ]. Here, we found that COX-2 expression was increased following treatment of BV2 and HT22 cells with IL-22, and there was a time difference between the responses of the BV2 and HT22 cell lines at the transcriptional ( Figure 2 B) and translational levels ( Figure 2 C).…”

Section: Discussionmentioning

confidence: 99%

“…Activated microglia release various bioactive molecules, including nitric oxide and reactive oxygen species. In addition, cyclooxygenase-2 (COX-2) is an enzyme that produces prostaglandin E2 (PGE2), a major inducer of inflammatory processes in the hippocampus [ 28 , 29 , 30 , 31 ]. Hence, we examined the effects of IL-22 on IL-6, TNF-α, COX-2, and PGE2 expression in mouse brain cell lines.…”

Section: Introductionmentioning

confidence: 99%

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The Roles of IL-22 and Its Receptor in the Regulation of Inflammatory Responses in the Brain

Lee

et al. 2022

IJMS

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Interleukin (IL)-22 is a potent mediator of inflammatory responses. The IL-22 receptor consists of the IL-22Rα and IL-10Rβ subunits. Previous studies have shown that IL-22Rα expression is restricted to non-hematopoietic cells in the skin, pancreas, intestine, liver, lung, and kidney. Although IL-22 is involved in the development of inflammatory responses, there have been no reports of its role in brain inflammation. Here, we used RT-PCR, Western blotting, flow cytometry, immunohistochemical, and microarray analyses to examine the role of IL-22 and expression of IL-22Rα in the brain, using the microglial cell line, hippocampal neuronal cell line, and inflamed mouse brain tissue. Treatment of BV2 and HT22 cells with recombinant IL-22 increased the expression levels of the pro-inflammatory cytokines IL-6 and TNF-α, as well as cyclooxygenase (COX)-2 and prostaglandin E2. We also found that the JNK and STAT3 signaling pathways play an important role in IL-22-mediated increases in inflammatory mediators. Microarray analyses revealed upregulated expression of inflammation-related genes in IL-22-treated HT22 cells. Finally, we found that IL-22Rα is spontaneously expressed in the brain and is upregulated in inflamed mouse brain. Overall, our results demonstrate that interaction of IL-22 with IL-22Rα plays a role in the development of inflammatory responses in the brain.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Roles of IL-22 and Its Receptor in the Regulation of Inflammatory Responses in the Brain

Lee

et al. 2022

IJMS

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“…showed that inflammation induced by atrophy triggers the activation of COX-2 to promote proliferation via interleukin-1β and tumor necrosis factor-α 28 . We postulated that the activity of COX-2 might increase in the later phase of immobilization.…”

Section: Discussionmentioning

confidence: 99%

Lipid Dynamics due to Muscle Atrophy Induced by Immobilization

et al. 2021

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Muscle atrophy refers to skeletal muscle loss and dysfunction that affects glucose and lipid metabolism. Moreover, muscle atrophy is manifested in cancer, diabetes, and obesity. In this study, we focused on lipid metabolism during muscle atrophy. We observed that the gastrocnemius muscle was associated with significant atrophy with 8 days of immobilization of hind limb joints and that muscle atrophy occurred regardless of the muscle fiber type. Further, we performed lipid analyses using thin layer chromatography, liquid chromatography-mass spectrometry, and mass spectrometry imaging. Total amounts of triacylglycerol, phosphatidylserine, and sphingomyelin were found to be increased in the immobilized muscle. Additionally, we found that specific molecular species of phosphatidylserine, phosphatidylcholine, and sphingomyelin were increased by immobilization. Furthermore, the expression of adipose triglyceride lipase and the activity of cyclooxygenase-2 were significantly reduced by atrophy. From these results, it was revealed that lipid accumulation and metabolic changes in specific fatty acids occur during disuse muscle atrophy. The present study holds implications in validating preventive treatment strategies for muscle atrophy.

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“…TNFα ↓MyoD (Li and Reid, 2001;Alvarez et al, 2020) ↓Myoblast differentiation (Alvarez et al, 2020) ↓Myosin, actin, and sarcoplasmic proteins (Alvarez et al, 2020) ↑Protein catabolism (Cheema et al, 2000;Popa et al, 2007) ↑Glycolysis (Boscá and Corredor, 1984;Rhoades et al, 2005;Remels et al, 2015) ↓Glucose oxidation in β cells (Oleson et al, 2015) ↓Glucose-stimulated insulin secretion (Oleson et al, 2015) ↓Insulin sensitivity (Youd et al, 2000;Li and Reid, 2001) ↑Lipolysis in fat deposits (Cheema et al, 2000;Popa et al, 2007) IL-6 ↓Muscle hypertrophy (Haddad et al, 2005;Bodell et al, 2009) ↓Myoblast differentiation (Haddad et al, 2005;Posont et al, 2018) ↑Muscle atrophy (Haddad et al, 2005;Bodell et al, 2009) Altered islet structure (Campbell et al, 1994) ↑Fibrosis (Campbell et al, 1994) Impaired insulin signaling (Bruce and Dyck, 2004;Wolsk et al, 2010;Knudsen et al, 2017) ↓GH and IGF-1 secretion and sensitivity, multiple tissues (Haddad et al, 2005;Bodell et al, 2009) IL-1β ↑Protein catabolism (Nawabi et al, 1990;Dinarello, 2000;Li et al, 2009) ↓Myofiber width (Li et al, 2009) ↓Actin content (Li et al, 2009) ↑β cell apoptosis (Harms et al, 2015;Oleson et al, 2015) ↓Glucose-stimulated insulin sec...…”

Section: Skeletal Muscle Pancreatic Islets Othermentioning

confidence: 99%

Going Up Inflame: Reviewing the Underexplored Role of Inflammatory Programming in Stress-Induced Intrauterine Growth Restricted Livestock

Hicks

Yates

2021

Front. Anim. Sci.

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The impact of intrauterine growth restriction (IUGR) on health in humans is well-recognized. It is the second leading cause of perinatal mortality worldwide, and it is associated with deficits in metabolism and muscle growth that increase lifelong risk for hypertension, obesity, hyperlipidemia, and type 2 diabetes. Comparatively, the barrier that IUGR imposes on livestock production is less recognized by the industry. Meat animals born with low birthweight due to IUGR are beset with greater early death loss, inefficient growth, and reduced carcass merit. These animals exhibit poor feed-to-gain ratios, less lean mass, and greater fat deposition, which increase production costs and decrease value. Ultimately, this reduces the amount of meat produced by each animal and threatens the economic sustainability of livestock industries. Intrauterine growth restriction is most commonly the result of fetal programming responses to placental insufficiency, but the exact mechanisms by which this occurs are not well-understood. In uncompromised pregnancies, inflammatory cytokines are produced at modest rates by placental and fetal tissues and play an important role in fetal development. However, unfavorable intrauterine conditions can cause cytokine activity to be excessive during critical windows of fetal development. Our recent evidence indicates that this impacts developmental programming of muscle growth and metabolism and contributes to the IUGR phenotype. In this review, we outline the role of inflammatory cytokine activity in the development of normal and IUGR phenotypes. We also highlight the contributions of sheep and other animal models in identifying mechanisms for IUGR pathologies.

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IL-1β and TNF-α Modulation of Proliferated and Committed Myoblasts: IL-6 and COX-2-Derived Prostaglandins as Key Actors in the Mechanisms Involved

Cited by 53 publications

References 75 publications

The Roles of IL-22 and Its Receptor in the Regulation of Inflammatory Responses in the Brain

The Roles of IL-22 and Its Receptor in the Regulation of Inflammatory Responses in the Brain

Lipid Dynamics due to Muscle Atrophy Induced by Immobilization

Going Up Inflame: Reviewing the Underexplored Role of Inflammatory Programming in Stress-Induced Intrauterine Growth Restricted Livestock

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