Post-transcriptional silencing of TRPC1 ion channel gene by RNA interference upregulates TRPC6 expression and store-operated Ca2+ entry in A7r5 vascular smooth muscle cells

2009 ◽  
Vol 51 (2-3) ◽  
pp. 96-100 ◽  
Author(s):  
Cigdem Selli ◽  
Yasemin Erac ◽  
Buket Kosova ◽  
Metiner Tosun
Keyword(s):  
Smooth Muscle ◽  
Rna Interference ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Ion Channel ◽  
Vascular Smooth Muscle Cells ◽  
Transcriptional Silencing ◽  
Muscle Cells ◽  
Channel Gene ◽  
Ion Channel Gene

Lentivirus-mediated RNA Interference Targeting STAT4 Inhibits the Proliferation of Vascular Smooth Muscle Cells

2008 ◽  
Vol 39 (6) ◽  
pp. 582-589 ◽  
Author(s):  
Lei Lv ◽  
Jiwei Zhang ◽  
Xiaozhong Huang ◽  
Yiping Zhao ◽  
Zhaoxiong Zhou ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Rna Interference ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells

scholarly journals RNA interference-mediated survivin gene knockdown induces growth arrest and reduced migration of vascular smooth muscle cells

2011 ◽  
Vol 301 (5) ◽  
pp. H1841-H1849 ◽  
Author(s):  
Christoph S. Nabzdyk ◽  
Hope Lancero ◽  
Khanh P. Nguyen ◽  
Sherveen Salek ◽  
Michael S. Conte
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Smooth Muscle ◽  
Rna Interference ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Neointimal Hyperplasia ◽  
Muscle Cells ◽  
Rnai Treatment

Survivin (SVV) is a multifunctional protein that has been implicated in the development of neointimal hyperplasia. Nuclear SVV is essential for mitosis, whereas in mitochondria SVV has a cytoprotective function. Here, we investigated the effects of RNA interference (RNAi)-mediated SVV knockdown on cell cycle kinetics, apoptosis, migration, and gene expression in primary cultured vascular smooth muscle cells (VSMCs) from the human saphenous vein. Primary Human VSMCs were obtained from saphenous veins and cultured under standard conditions. SVV knockdown was achieved by either small interfering RNA or lentiviral transduction of short hairpin RNA, reducing SVV gene expression by quantitative PCR (>75%, P < 0.01) without a loss of cell viability. Subcellular fractionation revealed that RNAi treatment effectively targeted the nuclear SVV pool, whereas the larger mitochondrial pool was much less sensitive to transient knockdown. Both p53 and p27 protein levels were notably increased. SVV RNAi treatment significantly blocked VSMC proliferation in response to serum and PDGF-AB, arresting VSMC growth. Cell cycle analysis revealed an increased G2/M fraction consistent with a mitotic defect; 4′,6-diamidino-2-phenylindole staining confirmed an increased frequency of polyploid and abnormal nuclei. In a transwell assay, SVV knockdown reduced migration to PDGF-AB, and actin-phalloidin staining revealed disorganized actin filaments and polygonal cell shape. However, apoptosis (DNA content and annexin V flow cytometry) was not directly induced by SVV RNAi, and sensitivity to apoptotic agonists (e.g., staurosporine and cytokines) was unchanged. In conclusion, RNAi-mediated SVV knockdown in VSMCs leads to profound cell cycle arrest at G2/M and impaired chemotaxis without cytotoxicity. The regulation of mitosis and apoptosis in VSMC involves differentially regulated subcellular pools of SVV. Thus, treatment of VSMC with RNAi targeting SVV might limit the response to vascular injury without destabilizing the vessel wall.

scholarly journals AAV transduction of the MaxiK channel gene in vascular smooth muscle cells for the long‐term control of hypertension

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Dinesh K Hirenallur S ◽  
Nancy J. Rusch ◽  
Yong Liu ◽  
Paul L. Hermonat ◽  
Dazhi Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Channel Gene ◽  
Maxik Channel
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