Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126. Issue 12 (16th July 2019)
- Record Type:
- Journal Article
- Title:
- Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126. Issue 12 (16th July 2019)
- Main Title:
- Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126
- Authors:
- Song, Aiping
Feng, Rong
Gao, Jianying
Yang, Chunqing - Abstract:
- Abstract: Peripheral artery disease (PAD) is a serious hazard to the elderly in the lower extremity atherosclerotic plaque, accompanied by a large number of angiogenesis. Long noncoding RNA Alu‐mediated p21 transcriptional regulator (APTR) exerts important functions in promoting cell growth. Therefore, we planned to research the mechanism of APTR in angiogenesis in PAD. CCK‐8 assay, flow cytometry analysis, and migration assay were to detect cell viability, apoptosis, and migration respectively. The interaction between APTR and miR‐12 was tested through luciferase activity test. In vitro angiogenesis assay was used to test the number of tubular cells. qRT‐PCR and Western blot were to test expression of APTR, miR‐126, and angiogenesis relative factors. There was spontaneously pipe‐formation in HEMC‐1 cells under matrigel condition. Knockdown of APTR inhibited cell viability and migration and reduced the number of tubular cells. Further, APTR sponged miR‐126 and downregulating miR‐126 to promote angiogenesis. Overexpression of APTR promoted cell activity and migration and increased the number of tubular cells via negatively regulating miR‐126. APTR could elevate activating phosphatidylinositol 3 kinase/protein kinase B and mitogen extracellular kinase/extracellular signal‐regulated kinase signal pathways via negatively regulating miR‐126 to promote cell proliferation, migration, and pipe‐formation. We researched the mechanism of angiogenesis that APTR elevated proliferation,Abstract: Peripheral artery disease (PAD) is a serious hazard to the elderly in the lower extremity atherosclerotic plaque, accompanied by a large number of angiogenesis. Long noncoding RNA Alu‐mediated p21 transcriptional regulator (APTR) exerts important functions in promoting cell growth. Therefore, we planned to research the mechanism of APTR in angiogenesis in PAD. CCK‐8 assay, flow cytometry analysis, and migration assay were to detect cell viability, apoptosis, and migration respectively. The interaction between APTR and miR‐12 was tested through luciferase activity test. In vitro angiogenesis assay was used to test the number of tubular cells. qRT‐PCR and Western blot were to test expression of APTR, miR‐126, and angiogenesis relative factors. There was spontaneously pipe‐formation in HEMC‐1 cells under matrigel condition. Knockdown of APTR inhibited cell viability and migration and reduced the number of tubular cells. Further, APTR sponged miR‐126 and downregulating miR‐126 to promote angiogenesis. Overexpression of APTR promoted cell activity and migration and increased the number of tubular cells via negatively regulating miR‐126. APTR could elevate activating phosphatidylinositol 3 kinase/protein kinase B and mitogen extracellular kinase/extracellular signal‐regulated kinase signal pathways via negatively regulating miR‐126 to promote cell proliferation, migration, and pipe‐formation. We researched the mechanism of angiogenesis that APTR elevated proliferation, migration, and pipe‐formation via negatively regulating miR‐126. Abstract : Alu‐mediated p21 transcriptional regulator (APTR) overexpression promotes proliferation, migration, and pipe‐formation; APTR sponges miR‐126 to accelerate angiogenesis; phosphatidylinositol 3 kinase/protein kinase B and mitogen extracellular kinase/extracellular signal‐regulated kinase signal pathways are activated by APTR in promoting angiogenesis. … (more)
- Is Part Of:
- Journal of cellular biochemistry. Volume 120:Issue 12(2019)
- Journal:
- Journal of cellular biochemistry
- Issue:
- Volume 120:Issue 12(2019)
- Issue Display:
- Volume 120, Issue 12 (2019)
- Year:
- 2019
- Volume:
- 120
- Issue:
- 12
- Issue Sort Value:
- 2019-0120-0012-0000
- Page Start:
- 19858
- Page End:
- 19867
- Publication Date:
- 2019-07-16
- Subjects:
- Alu‐mediated p21 transcriptional regulator (APTR) -- angiogenesis -- miR‐126
Cytochemistry -- Periodicals
572 - Journal URLs:
- http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1097-4644 ↗
http://onlinelibrary.wiley.com/ ↗ - DOI:
- 10.1002/jcb.29291 ↗
- Languages:
- English
- ISSNs:
- 0730-2312
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 4955.010000
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- 11902.xml