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Methotrexate attenuates vascular inflammation through an adenosine-microRNA dependent pathway

ABSTRACT: Methotrexate attenuates vascular inflammation through an adenosine-microRNA dependent pathway

PROVIDER: PRJNA689719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13357475_1.fastq.gz	Fastqsanger.gz
	SRR13357475_2.fastq.gz	Fastqsanger.gz
	SRR13357476_1.fastq.gz	Fastqsanger.gz
	SRR13357476_2.fastq.gz	Fastqsanger.gz
	SRR13357477_1.fastq.gz	Fastqsanger.gz

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Methotrexate attenuates vascular inflammation through an adenosine-microRNA dependent pathway

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Methotrexate attenuates vascular inflammation through an adenosine-microRNA-dependent pathway.

Project description:Endothelial cell (EC) activation is an early hallmark in the pathogenesis of chronic vascular diseases. MicroRNA-181b (Mir181b) is an important anti-inflammatory mediator in the vascular endothelium affecting endotoxemia, atherosclerosis, and insulin resistance. Herein, we identify that the drug methotrexate (MTX) and its downstream metabolite adenosine exert anti-inflammatory effects in the vascular endothelium by targeting and activating Mir181b expression. Both systemic and endothelial-specific Mir181a2b2-deficient mice develop vascular inflammation, white adipose tissue (WAT) inflammation, and insulin resistance in a diet-induced obesity model. Moreover, MTX attenuated diet-induced WAT inflammation, insulin resistance, and EC activation in a Mir181a2b2-dependent manner. Mechanistically, MTX attenuated cytokine-induced EC activation through a unique adenosine-adenosine receptor A3-SMAD3/4-Mir181b signaling cascade. These findings establish an essential role of endothelial Mir181b in controlling vascular inflammation and that restoring Mir181b in ECs by high-dose MTX or adenosine signaling may provide a potential therapeutic opportunity for anti-inflammatory therapy.

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CSF attenuates methotrexate efficacy

Project description:Treatment and prophylaxis of the central nervous system (CNS) is a critical component of acute lymphoblastic leukemia (ALL) therapy. However, CNS-directed therapies are a significant cause of morbidity and CNS relapse remains a cause of treatment failure. CNS-directed ALL therapies must target leukemia cells within cerebrospinal fluid (CSF), a fluid that is compositionally distinct from plasma and has been shown to impact leukemia biology. Herein, we demonstrate that human CSF attenuates the potency and efficacy of anti-folate drugs including methotrexate, the primary CNS-directed chemotherapeutic for over six decades. Importantly, this effect of CSF on leukemia methotrexate sensitivity was reversible. Additional mechanistic studies support that diminished proliferation and activation of the integrated stress response (ISR) in leukemia cells in CSF contribute to this resistance. Our findings suggest potential strategies to enhance methotrexate efficacy in CNS-directed ALL therapy and highlight the need to critically reassess even established standards of care.

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Caco2 response to methotrexate, lactoferrin, and methotrexate-lactoferrin co-exposure

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Methotrexate activates aspects of inflammation in EA.hy 926 cells

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