Role of circular RNA cdr1as in modulation of macrophage phenotype

González, Carolina; Cimini, Maria; Cheng, Zhongjian; Benedict, Cindy; Wang, Chunlin; Trungcao, May; Mallaredy, Vandana; Rajan, Sudarsan; Garikipati, Venkata Naga Srikanth; Kishore, Raj

doi:10.1016/j.lfs.2022.121003

Cited by 6 publications

(3 citation statements)

References 61 publications

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“…Suppressed p21 expression implies that cell stress is relieved, thus leading to a reduction in macrophage infiltration in tissues. The TGF-β/p-smad3 pathway plays pivotal roles in cardiac damage induced by DOX [28], and tissue-resident macrophages secrete pro-inflammatory and fibrotic factors, such as TGF-β1, which can promote the activation of stromal cells, synthesis of collagen and release of cytokines like TNF-α and IL-1 in chronic inflammatory conditions, which contribute to EMT [62,63]. In vivo, we found that supplementing NMN suppresses the TGF-β/p-smad3 pathway and reduces macrophage infiltration.…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis

Wen,

Xu,

Wei

et al. 2024

IJMS

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Doxorubicin (DOX) is a potent chemotherapeutic agent known for its multi-organ toxicity, especially in the heart, which limits its clinical application. The toxic side effects of DOX, including DNA damage, oxidative stress, mitochondrial dysfunction and cell apoptosis, are intricately linked to the involvement of nicotinamide adenine dinucleotide (NAD+). To assess the effectiveness of the NAD+ precursor nicotinamide mononucleotide (NMN) in counteracting the multi-organ toxicity of DOX, a mouse model was established through DOX administration, which led to significant reductions in NAD+ in tissues with evident injury, including the heart, liver and lungs. NMN treatment alleviated both multi-organ fibrosis and mortality in mice. Mechanistically, tissue fibrosis, macrophage infiltration and DOX-related cellular damage, which are potentially implicated in the development of multi-organ fibrosis, could be attenuated by NAD+ restoration. Our findings provide compelling evidence for the benefits of NMN supplementation in mitigating the adverse effects of chemotherapeutic drugs on multiple organs.

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Section: Discussionmentioning

confidence: 99%

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis

Wen,

Xu,

Wei

et al. 2024

IJMS

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“…Another in vitro study revealed that circCdr1 overexpression enhanced the transcription of IL-10 both in naïve and pro-inflammatory macrophages (Ref. 200). CircCHST15 was recently reported to possess an oncogenic role by promoting immune escape through upregulating the expression of IL-10 and a sponging effect on miR-155 and miR-194 in lung cancer (Ref.…”

Section: The Tumour Microenvironmentmentioning

confidence: 99%

Pharmacogenomic and epigenomic approaches to untangle the enigma of IL-10 blockade in oncology

Elemam,

Mekky,

Rashid

et al. 2024

Expert Rev. Mol. Med.

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The host immune system status remains an unresolved mystery among several malignancies. An immune-compromised state or smart immune-surveillance tactics orchestrated by cancer cells are the primary cause of cancer invasion and metastasis. Taking a closer look at the tumour-immune microenvironment, a complex network and crosstalk between infiltrating immune cells and cancer cells mediated by cytokines, chemokines, exosomal mediators and shed ligands are present. Cytokines such as interleukins can influence all components of the tumour microenvironment (TME), consequently promoting or suppressing tumour invasion based on their secreting source. Interleukin-10 (IL-10) is an interlocked cytokine that has been associated with several types of malignancies and proved to have paradoxical effects. IL-10 has multiple functions on cellular and non-cellular components within the TME. In this review, the authors shed the light on the regulatory role of IL-10 in the TME of several malignant contexts. Moreover, detailed epigenomic and pharmacogenomic approaches for the regulation of IL-10 were presented and discussed.

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“…CircRNAs play a role in the activation of macrophages ( 135 ). CircCdr1as was found to be downregulated in proinflammatory macrophages and increased in anti-inflammatory macrophages, and overexpression of circCdr1as induced the expression of anti-inflammatory markers and enhanced the percentage of CD206+ cells in naïve and proinflammatory macrophages ( 136 ).…”

Section: Roles Of Circrnas In Ibdmentioning

confidence: 99%

Circular RNAs in inflammatory bowel disease

Lun,

Guo,

et al. 2023

Front. Immunol.

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Inflammatory bowel disease (IBD) is a term encompassing a few chronic inflammatory disorders that leads to damage of the intestinal tract. Although much progress has been made in understanding the pathology of IBD, the precise pathogenesis is not completely understood. Circular RNAs (circRNAs) are single-stranded, covalently closed, endogenous molecules in eukaryotes with a variety of biological functions. CircRNAs have been shown to have regulatory effects in many diseases, such as cancer, cardiovascular disease, and neurological disorders. CircRNAs have also been found to play important roles in IBD, and although they are not sufficiently investigated in the context of IBD, a few circRNAs have been identified as potential biomarkers for the diagnosis and prognosis of IBD and as potential therapeutic targets for IBD. Herein, we survey recent progress in understanding the functions and roles of circRNAs in IBD and discuss their potential clinical applications.

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Role of circular RNA cdr1as in modulation of macrophage phenotype

Cited by 6 publications

References 61 publications

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis

Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis

Pharmacogenomic and epigenomic approaches to untangle the enigma of IL-10 blockade in oncology

Circular RNAs in inflammatory bowel disease

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