Phoenixin-14 regulates proliferation and apoptosis of vascular smooth muscle cells by modulation of KCNQ1OT1/miR-183-3p/CTNNB1 axis

Ling, Cong; Hu, Xiling; Luo, Ling; Liang, Chaofeng; Wang, Hui; Chen, Chuan

doi:10.1016/j.etap.2021.103655

Cited by 15 publications

(13 citation statements)

References 41 publications

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“…KCNQ1OT1 could serve as an important mediator in endothelial cell physiologic processes, and endothelial dysfunction plays an crucial role in the pathogenesis of SS [46]. KCNQ1OT1 interacts with miR-183-3p to upregulate CTNNB1 in vascular smooth muscle cells (VSMCs) and further affects the proliferation and apoptosis of VSMCs [47]. Additionally, KCNQ1OT1 could suppress inflammation and proliferation of VSMCs in intimal hyperplasia [48].…”

Section: Discussionmentioning

confidence: 99%

Association of Circulating Biomarkers of lnc-IGSF3-1:1, SCOC-AS1, and SLC8A1-AS1 with Salt Sensitivity of Blood Pressure in Chinese Population

Peng

Xie

Xia

et al. 2021

J. of Cardiovasc. Trans. Res.

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Accumulating evidence suggested that long non-coding RNAs (lncRNAs) could play biological roles in cardiovascular diseases. We investigated whether lncRNAs can serve as biomarkers for salt sensitivity of blood pressure (SSBP). Participants were divided into salt-sensitive (SS) and salt-resistant (SR) ones by oral saline test. LncRNAs were tested by microarray (N = 20) and two-stage qRT-PCR (N = 89 and 228). We identified five differently expressed lncRNAs (lnc-IGSF3-1:1, SCOC-AS1, SLC8A1-AS1, KCNQ1OT1, and lnc-GNG-10-3:1) between SS and SR. In single-lncRNA analyses, lnc-IGSF3-1:1 displayed better diagnostic performance in hypertensive patients (AUC = 0.840), while SCOC-AS1 in normotensive (AUC = 0.810). In multi-lncRNA analyses, lnc-IGSF3-1:1 + SCOC-AS1 + SLC8A1-AS1 combination showed the best diagnostic performance in hypertensive (AUC = 0.853) and normotensive groups (AUC = 0.873). We constructed a lncRNA-mRNA-GO-KEGG-disease network by bioinformatic analysis; lnc-IGSF3-1:1 and SLC8A1-AS1 were identified as hub biomarkers. Our findings suggest that lnc-IGSF3-1:1, SCOC-AS1, and SLC8A1-AS1 may represent as genetic susceptible biomarkers for SSBP, and had different SS diagnostic performance in hypertensive patients and normotensive individuals.

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Section: Discussionmentioning

confidence: 99%

Association of Circulating Biomarkers of lnc-IGSF3-1:1, SCOC-AS1, and SLC8A1-AS1 with Salt Sensitivity of Blood Pressure in Chinese Population

Peng

Xie

Xia

et al. 2021

J. of Cardiovasc. Trans. Res.

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“…MiR-183-3p was reported to suppress the proliferation and migration of keratinocytes, 21 and KCNQ1OT1 could bind with miR-183-3p to regulate the proliferation and apoptosis of vascular smooth muscle cells. 20 Data from luciferase activity and RIP assays revealed the direct binding relationship between KCNQ1OT1 and miR-183-3p. Moreover, KCNQ1OT1 negatively regulated the expression of miR-183-3p in HaCaT cells, suggesting that KCNQ1OT1 might regulate negatively miR-183-3p expression and thus contribute to the proliferation and migration of keratinocytes.…”

Section: Kcnq1ot1 Contributed To the Proliferation And Migration Of Keratinocytes Through Regulation Of Mir-183-3p-gab1 Axismentioning

confidence: 99%

“…19 KCNQ1OT1-microRNA-183-3p (miR-183-3p) axis was involved in proliferation and apoptosis of vascular smooth muscle cells. 20 Since miR-183-3p has been reported to repress the migration and proliferation of keratinocytes in psoriasis, 21 KCNQ1OT1 was hypothesized to participate in migration and proliferation of keratinocytes through regulation of miR-183-3p.…”

Section: Introductionmentioning

confidence: 99%

KCNQ1OT1 promotes the proliferation and migration of psoriatic keratinocytes by regulating miR-183-3p/GAB1

Liu

Duan

et al. 2021

aei

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Background: Differentially expressed lncRNAs have been reported to be involved in keratinocyte proliferation and migration, and participate in the development of psoriasis. Potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) was implicated in the pathogenesis of various diseases, including cancer, sepsis, diabetic cardiomyopathy, and atherosclerosis. The influence of KCNQ1OT1 on proliferation and migration of psoriatic keratinocytes was unfolded in this study. Methods: Human keratinocyte cell line (HaCaT) was incubated with TNF-α to establish in vitro cell model of psoriasis. Cell viability and migration were assessed by MTT and wound healing, respectively. Target miRNA of KCNQ1OT1 was identified by luciferase activity and RNA immunoprecipitation (RIP) assays. Results: KCNQ1OT1 was up-regulated in TNF-α-induced HaCaT, and knockdown of KCNQ1OT1 reduced cell viability and suppressed migration of TNF-α-induced HaCaT. KCNQ1OT1 bind to miR-183-3p and negatively regulated expression of miR-183-3p. Over-expression of GAB1 (growth factor receptor binding 2-associated binding protein 1) counteracted with the suppressive effects of KCNQ1OT1 silence on cell viability and migration of TNF-α-induced HaCaT. Conclusion: Silence of KCNQ1OT1 suppressed proliferation and migration of TNF-α-induced HaCaT through regulation of miR-183-3p/GAB1, providing potential strategy for psoriasis.

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“…Exogenous phoenixin induced a reduction of contractility and relaxation of isolated Langendorff-perfused rat hearts, without affecting coronary artery pressure and heart rate, and these effects were accompanied by the increase in phosphorylation of Erk1/2, Akt, and eNOS; these changes may be the reason for alteration in cardiac contractility and diastole function ( Rocca et al, 2018 ). Phoenixin-14 inhibited cell proliferation and facilitated apoptosis of vascular smooth muscle cells under ox-LDL treatment by regulating the KCNQ1OT1/miR-183-3p/CTNNB1 axis ( Ling et al, 2021 ). In addition, phoenixin treatment of isolated hearts with ischemia/reperfusion (I/R) injury showed a smaller infarct area and better contraction recovery than the control group ( Rocca, et al, 2018 ).…”

Section: Function Of Phoenixinmentioning

confidence: 99%

Regulation and physiological functions of phoenixin

Liu

Zhao

et al. 2022

Front. Mol. Biosci.

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Phoenixin is a newly discovered neuropeptide generated from small integral membrane protein 20. Phoenixin is a ligand for the G protein-coupled receptor 173 (GPR173) and has been detected in central and peripheral tissues of human, rats, mice, bovine, and zebrafish. It was initially involved in regulating reproductive function by stimulating the luteinizing hormone release from pituitary cells by increasing the level of gonadotropin-releasing hormone. Recently, many functions of phoenixin have been generalized, including regulation of food intake, memory, Alzheimer’s disease, anxiety, inflammation, neuronal and microglial activity, energy metabolism and body fluid balance, cardiovascular function, and endocrine activity. In addition, the interaction between phoenixin and nesfatin-1 have been revealed. The present article summarized the latest research progress on physiological function of phoenixin, suggesting that it is a potential target for novel drug development and clinical application.

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Phoenixin-14 regulates proliferation and apoptosis of vascular smooth muscle cells by modulation of KCNQ1OT1/miR-183-3p/CTNNB1 axis

Cited by 15 publications

References 41 publications

Association of Circulating Biomarkers of lnc-IGSF3-1:1, SCOC-AS1, and SLC8A1-AS1 with Salt Sensitivity of Blood Pressure in Chinese Population

Association of Circulating Biomarkers of lnc-IGSF3-1:1, SCOC-AS1, and SLC8A1-AS1 with Salt Sensitivity of Blood Pressure in Chinese Population

KCNQ1OT1 promotes the proliferation and migration of psoriatic keratinocytes by regulating miR-183-3p/GAB1

Regulation and physiological functions of phoenixin

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