A Human Long Non-Coding RNA ALT1 Controls the Cell Cycle of Vascular Endothelial Cells Via ACE2 and Cyclin D1 Pathway

Li, Wen; Wang, Rui; Ma, Jiachi; Wang, Mian; Cui, Jin; Wu, Weibin; Liu, Rui-Ming; Zhang, Chunxiang; Wang, Shenming

doi:10.1159/000481756

Cited by 17 publications

(14 citation statements)

References 34 publications

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“…Non-coding RNAs are important cell cycle modulators and levels of miR-138, miR-195, and miR-206 have been predicted to promote CCND1 expression, which regulates the progression from G1 phase to S phase of the cell cycle (26) (27). There is evidence that long non-coding RNA ALT1 controls the cell cycle progression via ACE2 and Cyclin D1 pathway (28). In the present study, we report that the lncRNA CRYBG3 regulates cell division and its expression is dynamically associated with cell cycle progression, being lowest in M phase and highest in G1 phase.…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA CRYBG3 Blocks Cytokinesis by Directly Binding G-Actin

Pei

Guo

et al. 2018

Cancer Research

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The dynamic interchange between monomeric globular actin (G-actin) and polymeric filamentous actin filaments (F-actin) is fundamental and essential to many cellular processes, including cytokinesis and maintenance of genomic stability. Here, we report that the long noncoding RNA LNC CRYBG3 directly binds G-actin to inhibit its polymerization and formation of contractile rings, resulting in M-phase cell arrest. Knockdown of LNC CRYBG3 in tumor cells enhanced their malignant phenotypes. Nucleotide sequence 228-237 of the full-length LNC CRYBG3 and the ser domain of β-actin is essential for their interaction, and mutation of either of these sites abrogated binding of LNC CRYBG3 to G-actin. Binding of LNC CRYBG3 to G-actin blocked nuclear localization of MAL, which consequently kept serum response factor (SRF) away from the promoter region of several immediate early genes, including JUNB and Arp3, which are necessary for cellular proliferation, tumor growth, adhesion, movement, and metastasis. These findings reveal a novel lncRNA-actin-MAL-SRF pathway and highlight LNC CRYBG3 as a means to block cytokinesis and to treat cancer by targeting the actin cytoskeleton. Identification of the long noncoding RNA LNC CRYBG3 as a mediator of microfilament disorganization marks it as a novel therapeutic antitumor strategy. .

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA CRYBG3 Blocks Cytokinesis by Directly Binding G-Actin

Pei

Guo

et al. 2018

Cancer Research

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“…Li and colleagues showed that lncRNA ALT1 directly interacts with ACE2 in HUVECs cells. ALT1 knockdown decreases ACE2 level thereby inhibiting cell proliferation via promotion of cyclin D1 ubiquitination 92 . Several studies have also addressed that lncRNAs control cell proliferation, autophagy, or colony formation through DPP4 93‐95 .…”

Section: Lncrnas and Sars‐cov‐2mentioning

confidence: 99%

Diverse roles of long non‐coding RNAs in viral diseases

Ginn

Montagna

et al. 2020

Reviews in Medical Virology

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Summary Viral infection leads to large alterations in the host transcriptome and stimulates an antiviral host immune response involving numerous proteins and signalling pathways. Long non‐coding RNAs (lncRNAs) have emerged as important regulators during viral infection. Emerging data demonstrates that lncRNAs play essential roles at the host pathogen interface modulating viral infection by either antiviral response at distinct level including pathogen recognition receptors or by epigenetic, transcriptional, and post‐transcriptional effects. Furthermore, differentially expressed lncRNAs may be employed as prognostic and diagnostic biomarkers for viral diseases. Here, we summarize the current knowledge of lncRNAs and their functions in viral infections with a specific focus on host‐virus responses. In addition, the potential implications of lncRNAs in severe acute respiratory syndrome coronavirus 2 will be discussed.

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“…injections, Ang (1‐7) and A779 were dissolved in Ringer 's solution (Fuso Pharmaceutical Industries, Japan). The specificity of the anti‐Mas receptor and anti‐ACE2 antibodies used in this study has been demonstrated using Mas receptor knockout mice (Freund et al, ) and ACE2‐siRNA transfected cells (Li et al, ), respectively. The antibody against the membrane‐bound anti‐Na + /K + ‐ATPase used in our study has been reported to selectively bind the protein in membrane fractions but not in cytoplasmic fractions (Aravena et al, ; Planès et al, ).…”

Section: Methodsmentioning

confidence: 94%

Anti‐hypersensitive effect of angiotensin (1‐7) on streptozotocin‐induced diabetic neuropathic pain in mice

Okita

Nemoto

Yamagata

et al. 2018

European Journal of Pain

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Background We have recently reported that the spinal angiotensin (Ang) converting enzyme (ACE)/Ang II/AT1 receptor axis and downstream p38 MAPK phosphorylation are activated in streptozotocin (STZ)‐induced diabetic mice and lead to tactile hypersensitivity. Moreover, our previous results suggested that the intrathecal (i.t.) administration of Ang (1‐7), an N‐terminal fragment of Ang II, may attenuate the Ang II‐induced nociceptive behaviour through the inhibition of p38 MAPK phosphorylation via Mas receptors. Here, we investigated whether the i.t. administration of Ang (1‐7) can attenuate STZ‐induced diabetic neuropathic pain. Methods Tactile and thermal hypersensitivities were determined using the von Frey filament and Hargreaves tests, respectively. The protein expression of ACE2, Mas receptors and phospho‐p38 MAPK was measured by western blotting. Spinal ACE2 activity was determined using ACE2 activity assay kit. Results The i.t. administration of Ang (1‐7) significantly reduced the tactile and thermal hypersensitivities on day 14 after STZ injection, and these effects were significantly prevented by the Mas receptor antagonist A779. The expression of ACE2 and Mas receptors in the plasma membrane fraction of the lumbar dorsal spinal cord was both significantly decreased in STZ mice. Spinal ACE2 activity was also decreased while p38 MAPK phosphorylation was increased in the lumbar dorsal region of these mice. This phosphorylation was attenuated by the injection of Ang (1‐7), whose effect was reversed by A779. Conclusions Our data demonstrate that Ang (1‐7) attenuates STZ‐induced diabetic neuropathic pain and that this occurs through a mechanism involving spinal Mas receptors and he inhibition of p38 MAPK phosphorylation. Significance The ACE2/Ang (1‐7)/Mas receptor axis was down‐regulated in the spinal cord of STZ mice and the i.t. administration of Ang (1‐7) attenuated the STZ‐induced diabetic neuropathic pain via Mas receptors. Therefore, the activation of this axis could be an effective therapeutic target to alleviate the neuropathic pain in diabetic patients.

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A Human Long Non-Coding RNA ALT1 Controls the Cell Cycle of Vascular Endothelial Cells Via ACE2 and Cyclin D1 Pathway

Cited by 17 publications

References 34 publications

Long Noncoding RNA CRYBG3 Blocks Cytokinesis by Directly Binding G-Actin

Long Noncoding RNA CRYBG3 Blocks Cytokinesis by Directly Binding G-Actin

Diverse roles of long non‐coding RNAs in viral diseases

Anti‐hypersensitive effect of angiotensin (1‐7) on streptozotocin‐induced diabetic neuropathic pain in mice

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