Dopamine Alters Lipopolysaccharide-Induced Nitric Oxide Production in Microglial Cells via Activation of D1-Like Receptors

Wang, Biao; Chen, Teng; Li, Guodong; Jia, Yuwei; Wang, Jing; Li, Xue; Chen, Yanjiong

doi:10.1007/s11064-019-02730-7

Cited by 20 publications

(18 citation statements)

References 50 publications

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“…For example, bradykinesia generally responds very well to levodopa (Nutt et al, 2011), while tremor does not (Yahr et al, 1969). Anti-parkinsonian drugs may produce effects on inflammatory factors, like IL-6, IL-8 and NO (Parrado et al, 2012; Wang et al, 2019). For example, it has been found that DA alone does not regulate the inflammatory factors directly, like IL-6, TNF-α or NO, but it inhibits lipopolysaccharide-induced NO production in microglial cells.…”

Section: Discussionmentioning

confidence: 99%

Tremor-Dominant in Parkinson Disease: The Relevance to Iron Metabolism and Inflammation

et al. 2019

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Background: Tremor is one of the most predominant symptoms of patients with Parkinson disease (PD), but the underlying mechanisms for tremor relating to iron and its metabolism-related proteins and the inflammatory factors in cerebrospinal fluid (CSF) and serum have not been fully elucidated. Methods: A total of 135 PD patients were divided into a tremor-dominant (PD-TD) group ( N = 74) and a postural instability and gait difficulty-dominant (PD-PIGD) group ( N = 39) based on the ratio of mean tremor score to the mean bradykinesia/rigid score of the Unified Parkinson’s Disease Rating Scale (UPDRS) III. Age and sex-matched healthy controls were recruited ( N = 35). Demographic variables were evaluated; iron and its metabolism-related proteins and the inflammatory mediators in both CSF and serum were measured in these groups. The relevance of iron metabolism, inflammation and PD-TD were analyzed. Results: (1) The PD-TD group had significantly decreased L -ferritin, increased iron levels in CSF and increased ferritin levels in the serum compared with the PD-PIGD and control groups ( P < 0.05). (2) The PD-TD group had significantly enhanced IL-6 levels in both CSF and serum compared with the PD-PIGD and control groups ( P < 0.05). (3) In CSF, the IL-6 level was increased as the iron level was elevated in the PD-TD group ( r = 0.308, P = 0.022). In serum, the IL-6 level was increased as the ferritin level was elevated in the PD-TD group ( r = 0.410, P = 0.004). Conclusion: The interplay between disturbed iron metabolism and relevant inflammation might modulate clinical phenotypes of PD.

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Section: Discussionmentioning

confidence: 99%

Tremor-Dominant in Parkinson Disease: The Relevance to Iron Metabolism and Inflammation

et al. 2019

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“…Consistent with the previous report that DA-DRD5 signaling suppresses macrophage-mediated inflammation 18 , we revealed that DA-DRD5 signaling is likely to play an important role in controlling the balance of colonic macrophage polarization, which is required for colonic homeostasis and prevent colitis. Notably, DA has recently been reported to inhibit LPS-induced NO production and inflammation in microglia, a type of central nervous system (CNS) macrophage, through DRD5-mediated signaling 38 , further suggesting an inhibitory role of DRD5 signaling in macrophage inflammation.…”

Section: Discussionmentioning

confidence: 99%

DA-DRD5 signaling controls colitis by regulating colonic M1/M2 macrophage polarization

Lü

Wang

et al. 2021

Cell Death Dis

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The decrease of neurotransmitter dopamine (DA) levels in the intestine is closely related to the development of inflammatory bowel disease (IBD). However, the functional relevance and underlying mechanistic basis of the effects of DA signaling on IBD remains unclear. Here, we observed that the DRD5 receptor is highly expressed in colonic macrophages, and the deficiency of DA-DRD5 signaling exacerbated experimental colitis. Moreover, DA-DRD5 signaling can inhibit M1 by negatively regulating NF-κB signaling but promote M2 macrophage polarization through activation of the CREB pathway, respectively. The deficiency of DRD5 signaling increased colonic M1 macrophages but reduced M2 cells during colitis. Additionally, the administration of a D1-like agonist that has a higher affinity to DRD5 can attenuate the colitogenic phenotype of mice. Collectively, these findings provide the first demonstration of DA-DRD5 signaling in colonic macrophages controlling the development of colitis by regulating M1/M2 macrophage polarization.

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“…Dopamine prevented cartilage degradation in a DMM-induced OA mouse model and reduced MMPs expression and elevated Col II expression in IL-1β-treated chondrocytes via NF-κB and JAK2/STAT3 signaling pathway [ 22 ]. In lipopolysaccharide-stimulated microglia cells, dopamine suppressed nitric oxide production [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Norepinephrine modulates IL-1β-induced catabolic response of human chondrocytes

Hwang

Lee²,

Go³

et al. 2021

BMC Musculoskelet Disord

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Background The influence of the sympathetic nervous system (SNS) on metabolism of bone and cartilage expressing β-adrenergic receptors (AR) was suggested. Here, we investigated whether the SNS functions as a modulator of cartilage metabolism induced by interleukin-1beta (IL-1β). Methods Human articular chondrocytes and articular cartilage were collected from patients with osteoarthritis (OA). Chondrocyte monolayer and cartilage explant culture were stimulated with IL-1β. The activity of β-ARs was modulated by an agonist, norepinephrine (NE), and antagonists, including propranolol, atenolol, nebivolol, and nadolol. Results The levels of β1-, β2-, and β3-AR in OA cartilage and IL-1β-treated chondrocytes were lower than normal cartilage and untreated cells. Treatment of chondrocytes with IL-1β and β-blockers, including propranolol, atenolol, nebivolol, and nadolol, for 6 h significantly upregulated IL-1β-induced expression of MMP-1, -3, and − 13, compared to chondrocytes treated with IL-1β alone, indicating that antagonism of β-AR confers catabolic signals. On the other hand, NE antagonized IL-1β-induced catabolic response. In addition, NE significantly inhibited IL-1β-induced release of glycosaminoglycan (GAG) from cartilage explant culture. In addition, β-AR activity significantly affected IL-1β-stimulated phosphorylation of JNK and ERK. These results indicate that β-AR signal is associated with cartilage metabolism. Conclusions Our findings showed that β-ARs is a regulator of cartilage catabolism induced with IL-1β.

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Dopamine Alters Lipopolysaccharide-Induced Nitric Oxide Production in Microglial Cells via Activation of D1-Like Receptors

Cited by 20 publications

References 50 publications

Tremor-Dominant in Parkinson Disease: The Relevance to Iron Metabolism and Inflammation

Tremor-Dominant in Parkinson Disease: The Relevance to Iron Metabolism and Inflammation

DA-DRD5 signaling controls colitis by regulating colonic M1/M2 macrophage polarization

Norepinephrine modulates IL-1β-induced catabolic response of human chondrocytes

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