Activation of PPAR-γ induces macrophage polarization and reduces neutrophil migration mediated by heme oxygenase 1

Abdalla, Henrique Ballassini; Napimoga, Marcelo Henrique; Lopes, Alexandre H.; Maganin, Alexandre Gomes de Macedo; Cunha, Thiago M.; Dyke, Thomas E. Van; Clemente-Napimoga, Juliana Trindade

doi:10.1016/j.intimp.2020.106565

Cited by 44 publications

(27 citation statements)

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“…It has been confirmed that SIRT1 and PPAR-γ drive M2 polarization. 8 , 9 Decreased expression of mRNA SIRT1, PPAR-γ and IL-10, and increased expression of IL-1β and iNOS suggest that macrophages resided in AIA WAT tend to differentiate into inflammatory phenotype. QLY effectively promoted PPAR-γ expression in the treated rats, but exerted no obvious effects on NAMPT and SIRT1.…”

Section: Resultsmentioning

confidence: 99%

“…6 Metabolic regulators such as NAMPT, SIRT1 and PPARγ are deeply involved in monocytes/macrophages polarization. [7][8][9] M1 and M2 cell subsets have distinctly different metabolic profiles. 6 More importantly, high prevalence of metabolic complication is observed in inflammatory diseases, while metabolic disorders are always associated with low-grade inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Qing-Luo-Yin Alleviated Monocytes/Macrophages-Mediated Inflammation in Rats with Adjuvant-Induced Arthritis by Disrupting Their Interaction with (Pre)-Adipocytes Through PPAR-γ Signaling

Wang

Li²,

Hu³

et al. 2021

DDDT

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Background:The Chinese herbal formula Qing-Luo-Yin (QLY) has been successfully used in rheumatoid arthritis treatment for decades. It exhibits notable immune and metabolism regulatory properties. Thereby, we investigated its effects on the interplay between (pre)adipocytes and monocytes/macrophages under adjuvant-induced arthritis (AIA) circumstances. Methods: Fat reservoir and histological characteristics of white fat tissues (WAT) in AIA rats receiving QLY treatment were examined upon sacrifice. Metabolic parameters, clinical indicators, and oxidative stress levels were determined using corresponding kits, while mRNA/protein expression was investigated by PCR and immunoblotting methods. M1 macrophage distribution in WAT was assessed by flow cytometry. The effects of QLY on (pre)-adipocytes were further validated by experiments in vitro. Results: Compared with normal healthy controls, body weight and circulating triglyceride were declined in AIA rats, but serological levels of free fatty acids and low-density lipoprotein cholesterol were increased. mRNA IL-1β and iNOS expression in white blood cells and rheumatoid factor, C-reactive protein, anti-cyclic citrullinated peptide antibody, MCP-1 and IL-1β production in serum/WAT were up-regulated. Obvious CD86 + CD11b + macrophages were enriched in WAT. Meanwhile, expression of PPAR-γ and SIRT1 and secretion of adiponectin and leptin in these AIA rats were impaired. QLY restored all these pathological changes. Of note, it significantly stimulated PPAR-γ expression in the treated AIA rats. Accordingly, QLY-containing serum promoted SCD-1, PPAR-γ, and SIRT1 expression in pre-adipocytes cultured in vitro. AIA rats-derived peripheral blood mononuclear cells suppressed PPAR-γ and SCD-1 expression in co-cultured pre-adipocytes, but serum from AIA rats receiving QLY treatment did not exhibit this potential. The changes on PPAR-γ expression eventually resulted in varied adipocyte differentiation statuses. PPAR-γ selective inhibitor T0070907 abrogated QLY-induced MCP-1 production decline in LPS-primed preadipocytes and reduced adiponectin secretion. Conclusion: QLY was potent in promoting PPAR-γ expression and consequently disrupted inflammatory feedback in WAT by altering monocytes/macrophages polarization and adipocytes differentiation.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Qing-Luo-Yin Alleviated Monocytes/Macrophages-Mediated Inflammation in Rats with Adjuvant-Induced Arthritis by Disrupting Their Interaction with (Pre)-Adipocytes Through PPAR-γ Signaling

Wang

Li²,

Hu³

et al. 2021

DDDT

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“…Intratympanic injection of pioglitazone suppressed inflammatory and oxidative responses by attenuating the expression of NF-κB and interleukin (IL)-1β in the cochlea [ 30 ]. PPARγ is a ligand-activated transcription factor that activates anti-inflammatory cascades through HO-dependent signaling [ 31 ]. HO1 has been reported to activate macrophages and reduce neutrophil responses [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

“…PPARγ is a ligand-activated transcription factor that activates anti-inflammatory cascades through HO-dependent signaling [ 31 ]. HO1 has been reported to activate macrophages and reduce neutrophil responses [ 31 ]. The increased level of HO1 in KM rats implied a reactive anti-inflammatory response following KM ototoxicity.…”

Section: Discussionmentioning

confidence: 99%

Telmisartan Attenuates Kanamycin-Induced Ototoxicity in Rats

Lee

Kim

2021

IJMS

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Telmisartan (TM) has been proposed to relieve inflammatory responses by modulating peroxisome proliferator activator receptor-γ (PPARγ) signaling. This study aimed to investigate the protective effects of TM on kanamycin(KM)-induced ototoxicity in rats. Forty-eight, 8-week-old female Sprague Dawley rats were divided into four groups: (1) control group, (2) TM group, (3) KM group, and (4) TM + KM group. Auditory brainstem response was measured. The histology of the cochlea was examined. The protein expression levels of angiotensin-converting enzyme 2 (ACE2), HO1, and PPARγ were measured by Western blotting. The auditory threshold shifts at 4, 8, 16, and 32 kHz were lower in the TM + KM group than in the KM group (all p < 0.05). The loss of cochlear outer hair cells and spiral ganglial cells was lower in the TM + KM group than in the KM group. The protein expression levels of ACE2, PPARγ, and HO1 were higher in the KM group than in the control group (all p < 0.05). The TM + KM group showed lower expression levels of PPARγ and HO1 than the KM group.TM protected the cochlea from KM-induced injuries in rats. TM preserved hearing levels and attenuated the increase in PPARγ and HO1 expression levels in KM-exposed rat cochleae.

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“…It has been reported that activation of LXR α and HO-1 not only increases ABCA1 and ABCG1 expression but also inhibits proinflammatory cytokine secretion [ 13 – 15 ]. Interestingly, PPAR γ serves as an upstream effector of LXR α and HO-1 [ 12 , 16 , 17 ]. These findings suggest that PPAR γ functions as a crosstalk between lipid metabolism and inflammation.…”

Section: Introductionmentioning

confidence: 99%

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

Chen

Deng

et al. 2020

Oxidative Medicine and Cellular Longevity

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Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms. Our results showed that administration of BCA promoted reverse cholesterol transport (RCT), improved plasma lipid profile, and decreased serum proinflammatory cytokine levels and atherosclerotic lesion area in apoE-/- mice fed a Western diet. In THP-1 macrophage-derived foam cells, treatment with BCA upregulated ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 expression and facilitated subsequent cholesterol efflux and diminished intracellular cholesterol contents by activating the peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) and PPARγ/heme oxygenase 1 (HO-1) pathways. BCA also activated these two signaling pathways to inhibit the secretion of proinflammatory cytokines. Taken together, these findings suggest that BCA is protective against atherosclerosis by inhibiting lipid accumulation and inflammatory response through the PPARγ/LXRα and PPARγ/HO-1 pathways. BCA may be an attractive drug for the prevention and treatment of atherosclerotic cardiovascular disease.

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Activation of PPAR-γ induces macrophage polarization and reduces neutrophil migration mediated by heme oxygenase 1

Cited by 44 publications

References 45 publications

Qing-Luo-Yin Alleviated Monocytes/Macrophages-Mediated Inflammation in Rats with Adjuvant-Induced Arthritis by Disrupting Their Interaction with (Pre)-Adipocytes Through PPAR-γ Signaling

Qing-Luo-Yin Alleviated Monocytes/Macrophages-Mediated Inflammation in Rats with Adjuvant-Induced Arthritis by Disrupting Their Interaction with (Pre)-Adipocytes Through PPAR-γ Signaling

Telmisartan Attenuates Kanamycin-Induced Ototoxicity in Rats

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response

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