A long noncoding RNA regulates inflammation resolution by mouse macrophages through fatty acid oxidation activation

Nakayama, Y.; Fujiu, Katsuhito; Yuki, Ryuzaburo; Oishi, Yumiko; Morioka, M.; Isagawa, Takayuki; Matsuda, Jun; Oshima, Tomokazu; Matsubara, Takumi; Sugita, Junichi; Kudo, Fujimi; Kaneda, Atsushi; Endo, Yusuke; Nakayama, Toshinori; Nagai, Ryozo; Komuro, Issei; Manabe, Ichiro

doi:10.1073/pnas.2005924117

Cited by 43 publications

(34 citation statements)

References 80 publications

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“…LncRNA-Mirt2 inhibits the NF-κB and MAPK pathways activation and limits the production of pro-in ammatory cytokines through negative feedback 38 . In addition, lncRNAs can participate in in ammatory progression by regulating macrophage oxidative stress and metabolism 39,40 . Our study found that LINC01126 silencing signi cantly reduced expression of proin ammatory cytokines in LPS-induced HGFs, particularly IL-6.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Tang¹,

Li²,

Yu³

et al. 2021

Preprint

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Background Periodontitis is a serious threat to oral quality of life and overall health. Although our previous studies confirmed that long intergenic non-coding RNA 01126 (LINC01126) is aberrantly expressed in periodontitis tissues, there are few reports on the pathogenesis of LINC01126 in periodontitis. Our study investigated the biological functions of LINC01126 in periodontitis and the potential mechanism. Results An inflammatory model of human gingival fibroblasts (HGFs) was successfully established. LINC01126 silencing can alleviate lipopolysaccharide (LPS) induced cell inflammation, reduce cell apoptosis, and promote cell migration. As a "sponge" for miR-655-3p, LINC01126 inhibits its binding to mRNA of IL-6, thereby promoting inflammation progression and JAK2/STAT3 pathway activation. qRT- PCR, WB, and IHC results of clinical tissue samples further confirmed that miR-655-3p expression was down-regulated and IL-6/JAK/STAT3 was abnormally activated in periodontitis tissues. Conclusions Our results indicate that LINC01126, as an endogenous competitive RNA (ceRNA) of miR-655-3p, can promote IL-6/JAK3/STAT3 pathway activation, thereby promoting periodontitis pathogenesis. And this is the first study of miR-655-3p in inflammatory periodontal diseases. Our study reveales a new pathogenesis of periodontitis, and provides a new strategy for preventing and treating periodontitis.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Tang¹,

Li²,

Yu³

et al. 2021

Preprint

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“…In recent years there has been considerable interest in the regulation of signaling pathways by non-coding RNAs in various human diseases [ 188 ]. Targeting non-coding RNAs, such as long non-coding RNAs (lncRNAS) [ [189] , [190] , [191] ] and miRNAs [ 192 , 193 ] can modulate inflammation and the associated immune responses [ 191 ]. Non-coding RNAs are a large class of RNA molecules with new members being identified regularly.…”

Section: Epigenetic Regulation Of Inflammationmentioning

confidence: 99%

“…For example, lncRNAs, the non-coding RNAs longer than 200 nuceotides, can enhance or suppress transcription of inflammatory responses [ 194 ]. lncRNA HIX003209 [ 195 ], ROCKI [ 196 ], Rpph1 [ 197 ], HOTAIR [ 198 ] are some of the lncRNAs that promote inflammation while lncFAO [ 190 ], Mirt2 [ 199 ], PMS2L2 [ 200 ], AF131217.1 [ 201 ] are some of the lncRNAs that inhibit inflammation. These lncRNAs bring about their physiological effects by interacting with multiple molecular targets.…”

Section: Epigenetic Regulation Of Inflammationmentioning

confidence: 99%

Epigenetic underpinnings of inflammation: Connecting the dots between pulmonary diseases, lung cancer and COVID-19

Ahmad

Manzoor

Siddiqui

et al. 2022

Seminars in Cancer Biology

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Inflammation is an essential component of several respiratory diseases, such as chronic obstructive pulmonary disease (COPD), asthma and acute respiratory distress syndrome (ARDS). It is central to lung cancer, the leading cancer in terms of associated mortality that has affected millions of individuals worldwide. Inflammation and pulmonary manifestations are also the major causes of COVID-19 related deaths. Acute hyperinflammation plays an important role in the COVID-19 disease progression and severity, and development of protective immunity against the virus is greatly sought. Further, the severity of COVID-19 is greatly enhanced in lung cancer patients, probably due to the genes such as ACE2, TMPRSS2, PAI-1 and furin that are commonly involved in cancer progression as well as SAR-CoV-2 infection. The importance of inflammation in pulmonary manifestations, cancer and COVID-19 calls for a closer look at the underlying processes, particularly the associated increase in IL-6 and other cytokines, the dysregulation of immune cells and the coagulation pathway. Towards this end, several reports have identified epigenetic regulation of inflammation at different levels. Expression of several key inflammation-related cytokines, chemokines and other genes is affected by methylation and acetylation while non-coding RNAs, including microRNAs as well as long non-coding RNAs, also affect the overall inflammatory responses. Select miRNAs can regulate inflammation in COVID-19 infection, lung cancer as well as other inflammatory lung diseases, and can serve as epigenetic links that can be therapeutically targeted. Furthermore, epigenetic changes also mediate the environmental factors-induced inflammation. Therefore, a better understanding of epigenetic regulation of inflammation can potentially help develop novel strategies to prevent, diagnose and treat chronic pulmonary diseases, lung cancer and COVID-19.

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“…We have dissected the pathogenesis of heart failure and uncovered a variety of molecular mechanisms involved in ischemia [104][105][106][107][108][109][110][111][112][113][114][115], inflammation [116][117][118][119][120][121][122][123][124][125], metabolism [107,126,127], catecholamines [128][129][130], calcium handling [52,54,[131][132][133][134][135][136], signaling [30,41,108,[137][138][139][140][141][142], oxidative stress [143][144][145][146]…”

Section: Heart Failurementioning

confidence: 99%

Precision medicine for heart failure based on molecular mechanisms: The 2019 ISHR Research Achievement Award Lecture

Nomura

Komuro

2021

Journal of Molecular and Cellular Cardiology

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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A long noncoding RNA regulates inflammation resolution by mouse macrophages through fatty acid oxidation activation

Cited by 43 publications

References 80 publications

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Long non-coding RNA 01126 activates IL-6/JAK2/STAT3 pathway via serving as a sponge of miR-655-3p in periodontitis

Epigenetic underpinnings of inflammation: Connecting the dots between pulmonary diseases, lung cancer and COVID-19

Precision medicine for heart failure based on molecular mechanisms: The 2019 ISHR Research Achievement Award Lecture

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