CCR5 antagonist treatment inhibits vascular injury by regulating NADPH oxidase 1

Singh, Shubhnita; Bruder‐Nascimento, Ariane; Chantemèle, Eric J. Belin de; Bruder‐Nascimento, Thiago

doi:10.1016/j.bcp.2021.114859

Cited by 12 publications

(23 citation statements)

References 66 publications

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“…Corresponding pathological examination exhibited depletion of CCL5, revised neuronal degeneration, and microglia activation (Figure S2D,E). It has been reported that CCL5 induces cell migration via binding to the corresponding receptor, CCR5 41,42 . We blocked the interaction between CCL5 and CCR5 by using maraviroc, 42,43 an FDA‐approved CCR5 antagonist, to inhibit the biological function of CCL5.…”

Section: Resultsmentioning

confidence: 99%

Targeting CCL5 signaling attenuates neuroinflammation after seizure

Zhang

Jiang

et al. 2022

CNS Neurosci Ther

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Section: Resultsmentioning

confidence: 99%

Targeting CCL5 signaling attenuates neuroinflammation after seizure

Zhang

Jiang

et al. 2022

CNS Neurosci Ther

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“…Our results suggest that during a neuroendocrine stress condition, RANTES concentration rises independently from migraine diagnosis. Increased RANTES is suggested to play a role in dysfunctional vascular regulation by the modulation of perivascular inflammation [ 89 , 93 ], so the increasing RANTES concentration might be a part of the vascular response in neuroendocrine stress. However, in our study, RANTES concentration remained lower in migraine patients (median: 10,580 pg/mL (13,292–5882) 95% CI) compared to controls (median: 14,340 pg/mL (20,233–7260) 95% CI), even during the neuroendocrine stress challenge.…”

Section: Discussionmentioning

confidence: 99%

Citalopram Neuroendocrine Challenge Shows Altered Tryptophan and Kynurenine Metabolism in Migraine

Gecse

Édes

Nagy

et al. 2022

Cells

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Altered tryptophan (TRP) metabolism may have an important role in migraine susceptibility through its main metabolites, serotonin and kynurenine (KYN). Both affect pain processing and stress response by interfering with neural and brain hypersensitivity and by interacting with chemokines and cytokines that control vascular and inflammatory processes. The involvement of these pathways in migraine has been widely studied, but acute citalopram neuroendocrine challenge on TRP metabolism and cytokine profile has not been investigated yet. In our study, females with episodic migraine without aura and healthy controls were studied before and after acute citalopram or placebo in a double-blind setting. At baseline, increased TRP/large neutral amino acid (LNAA) ratio and decreased RANTES chemokine concentration were detected in migraine patients compared to controls. The challenge induced a significant increase in TRP, KYN, and TRP/LNAA in healthy controls, but not in migraine patients. Furthermore, migraine attack frequency negatively correlated with KYN/TRP ratio and positively correlated with the neuroendocrine-challenge-induced KYN concentration increase. Our results support a decreased breakdown of TRP via KYN pathway and a failure to modulate TRP–KYN pathway during citalopram-induced acute stress together with an increased vascular sensitivity in migraine. These mechanisms may provide useful drug targets for future drug development.

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“…Firstly, we performed a time course with CAWS to analyze whether it can change Nox1 and 4 and COXs expressions in VSMC, we did not analyze Nox2 in RASMC because its expression is very low 33 . We observed no differences in Nox1 and 4 enzymes expression (Fig.…”

Section: Caws Evokes Coxs Expression Via Tlr4 In Vsmcmentioning

confidence: 99%

“…As described by our previous studies 26,33 , Rat Aortic Smooth Muscle cells (RASMC, Lonza, Walkersville, MD, USA) were maintained in Dulbecco's Modified Eagle Medium (DMEM) (Gibco from Thermo Fisher Scientific, Waltham, MA, USA) containing 10% fetal bovine serum (FBS, HyClone Logan UT, USA), 100 U/ml penicillin and 100 μg/ml streptomycin (Gibco from Thermo Fisher Scientific, Waltham, MA, USA).…”

Section: Culture Of Vascular Smooth Muscle Cellsmentioning

confidence: 99%

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Progression of vascular function and blood pressure in a mouse model of Kawasaki disease

DelVechio

Alves

Saiyi

et al. 2022

Preprint

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Background: Kawasaki disease (KD) is a systemic vasculitis of childhood characterized by vascular damage in the acute stage, which can persist into the late stage. Aneurysms, myocardial infarction, and death are long-standing complications associated with KD. The vascular mechanisms in the cardiovascular risk of KD are not fully studied. Herein, we investigated the vascular function and blood pressure regulation in a murine model of KD. Material and methods: We used the Candida albicans water soluble (CAWS) fraction model. Mice were injected with 4 mg CAWS for five consecutive days and separated into 3 groups. Control (Ctrl): water injected for 5 days; CAWS 7 days (C7): CAWS injected for 5 days plus 2 additional days of wait; CAWS 28 days (C28): CAWS injected for 5 days plus 23 additional days of wait. Blood pressure was analyzed via radiotelemetry. In the end, the heart and arteries were harvested for vasculitis characterization and vascular function in a wire myograph. Rat Aortic Vascular Smooth Muscle cells (RASMC) were used to dissect the molecular mechanisms in vitro. Main findings: C7 presented elevated inflammatory markers in the coronary area (CA) and abdominal aortae (AA), whereas C28 showed severe vasculitis in CA and AA. No difference was found in blood pressure and heart rate. Vascular dysfunction characterized by higher contractility to norepinephrine (NA) in C7 and C28 was abolished by blocking nitric oxide (NO) production, reactive oxygen species (ROS), and cyclooxygenase (COX)-derived products. RASMC treated with CAWS (10ug/mL) presented an increase in COX2 expression, which was prevented by pre-treating the cells with TAK-242 [Toll like receptor 4 (TLR4) antagonist, 3x10-5M]. Conclusion: Our data indicate that the murine model of KD is associated with vascular dysfunction likely dependent on COX-derived products, oxidant properties, and NO bioavailability. Furthermore, VSMC may present an important role in the genesis of vascular dysfunction and vasculitis via the TLR4 pathway. Finally, the CAWS model seems not to be appropriate to study KD-associated shock. More studies are necessary to understand whether vascular dysfunction and COXs are triggers for vasculitis.

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CCR5 antagonist treatment inhibits vascular injury by regulating NADPH oxidase 1

Cited by 12 publications

References 66 publications

Targeting CCL5 signaling attenuates neuroinflammation after seizure

Targeting CCL5 signaling attenuates neuroinflammation after seizure

Citalopram Neuroendocrine Challenge Shows Altered Tryptophan and Kynurenine Metabolism in Migraine

Progression of vascular function and blood pressure in a mouse model of Kawasaki disease

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