Overexpression of mimecan in human aortic smooth muscle cells inhibits cell proliferation and enhances apoptosis and migration

Background Sporadic non-syndromic thoracic aortic aneurysms (SNSTAAs) are less well understood than familial non-syndromic or syndromic ones. The study aimed at defining the peculiar morphologic and molecular changes occurring in the media layer of SNSTAAs. Design This study was based on a single centre design. Methods Media layer samples taken from seven carefully selected SNSTAAs and seven reference patients (controls) were investigated via quantitative polymerase chain reaction, proteomics-bioinformatics, immunoblotting, quantitative histology, and immunohistochemistry/immunofluorescence. Results In SNSTAAs media, aortic smooth muscle cells numbers were halved due to an apoptotic process coupled with a negligible cell proliferation. Cystathionine γ-lyase was diffusely up-regulated. Surviving aortic smooth muscle cells exhibited diverging phenotypes: in inner- and outer-media contractile cells prevailed, having higher contents of smooth-muscle-α-actin holoprotein (45-kDa) and of caspase-3-cleaved smooth-muscle-α-actin 25-kDa fragments; in mid-media, aortic smooth muscle cells exhibited a synthetic/secretor phenotype, down-regulating vimentin, but up-regulating glial fibrillary acidic protein, trans-Golgi network 46 protein, Jagged1 (172-kDa) holoprotein, and Jagged1’s receptor Notch1. Extracellular soluble Jagged1 (42-kDa) fragments accumulated. Conclusions In SNSTAAs, there is a relentless aortic smooth muscle cells attrition caused by the up-regulated cystathionine γ-lyase. In mid-media, synthetic/secretor aortic smooth muscle cells intensify Jagged1/NOTCH1 signalling in the attempt to counterbalance the weakened aortic wall, due to aortic smooth muscle cells net loss and mechanical stress. Synthetic/secretor aortic smooth muscle cells are apoptosis-prone, and the accruing thrombin-cleaved Jagged1 fragments counteract the otherwise useful effects of Jagged1/NOTCH1 signalling, thus hampering tissue homeostasis/remodelling, and aortic smooth muscle cells adhesion, differentiation, and migration.

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Differential Effects of Vasodilatory Prostaglandins on Focal Adhesions, Cytoskeletal Architecture, and Migration in Human Aortic Smooth Muscle Cells

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/01.atv.0000146814.81581.68 ◽

2005 ◽

Vol 25 (1) ◽

pp. 84-89 ◽

Cited By ~ 35

Author(s):

C. Bulin ◽

U. Albrecht ◽

J.G. Bode ◽

A.-A. Weber ◽

K. Schrör ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Focal Adhesions ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Differential Effects ◽

Aortic Smooth Muscle ◽

And Migration

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Activation of PKCβII and PKCθ is essential for LDL-induced cell proliferation of human aortic smooth muscle cells via Gi-mediated Erk1/2 activation and Egr-1 upregulation

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2008.01.050 ◽

2008 ◽

Vol 368 (1) ◽

pp. 126-131 ◽

Cited By ~ 13

Author(s):

Kyung-Sun Heo ◽

Dong-Uk Kim ◽

Lila Kim ◽

Miyoung Nam ◽

Seung-Tae Baek ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle

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Metformin-induced activation of AMPK inhibits the proliferation and migration of human aortic smooth muscle cells through upregulation of p53 and IFI16

International Journal of Molecular Medicine ◽

10.3892/ijmm.2017.3346 ◽

2017 ◽

Cited By ~ 8

Author(s):

Biao Hao ◽

Yan Xiao ◽

Fang Song ◽

Xiangshu Long ◽

Jing Huang ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle ◽

And Migration ◽

Proliferation And Migration

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Brahma-related gene 1 inhibits proliferation and migration of human aortic smooth muscle cells by directly up-regulating Ras-related associated with diabetes in the pathophysiologic processes of aortic dissection

Journal of Thoracic and Cardiovascular Surgery ◽

10.1016/j.jtcvs.2015.08.010 ◽

2015 ◽

Vol 150 (5) ◽

pp. 1292-1301.e2 ◽

Cited By ~ 10

Author(s):

Wei-Lin Liao ◽

Meng-Wei Tan ◽

Yang Yuan ◽

Guo-Kun Wang ◽

Chong Wang ◽

...

Keyword(s):

Smooth Muscle ◽

Aortic Dissection ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Related Gene ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle ◽

And Migration ◽

Proliferation And Migration

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Tangeretin, a citrus flavonoid, inhibits PGDF-BB-induced proliferation and migration of aortic smooth muscle cells by blocking AKT activation

European Journal of Pharmacology ◽

10.1016/j.ejphar.2011.10.011 ◽

2011 ◽

Vol 673 (1-3) ◽

pp. 56-64 ◽

Cited By ~ 41

Author(s):

Juhee Seo ◽

Hyun Sun Lee ◽

Sungwoo Ryoo ◽

Jee Hee Seo ◽

Byung-Sun Min ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Akt Activation ◽

Aortic Smooth Muscle ◽

And Migration ◽

Proliferation And Migration

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Cyclic tensile strain facilitates proliferation and migration of human aortic smooth muscle cells and reduces their apoptosis via miRNA-187-3p

Bioengineered ◽

10.1080/21655979.2021.2009321 ◽

2021 ◽

Vol 12 (2) ◽

pp. 11439-11450

Author(s):

Di Yang ◽

Guang-Yuan Wei ◽

Min Li ◽

Ming-Sheng Peng ◽

Yuan Sun ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Tensile Strain ◽

Muscle Cells ◽

Cyclic Tensile Strain ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle ◽

And Migration ◽

Proliferation And Migration

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Influence of Iron and Magnesium on Cell Proliferation, Glucose Consumption and Lactate Production in Cultured Rat Aortic Smooth Muscle Cells

The Journal of Japan Atherosclerosis Society ◽

10.5551/jat1973.11.5_1147 ◽

1983 ◽

Vol 11 (5) ◽

pp. 1147-1152

Author(s):

Takashi SUZUKI ◽

Eiichi KAYAMA ◽

Haruhisa ICHINARI ◽

Shigenobu KASAGI ◽

Yasuko TOYODA ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Lactate Production ◽

Glucose Consumption ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle

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LncRNA SCIRT is downregulated in atherosclerosis and suppresses the proliferation of human aortic smooth muscle cells (HAOSMCs) by sponging miR-146a in cytoplasm

Journal of Cardiothoracic Surgery ◽

10.1186/s13019-021-01700-x ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Wenhui Gao ◽

Rong Li ◽

Jingjing Yu ◽

Xijie He ◽

Duo Xu ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Cancer Biology ◽

Direct Interaction ◽

Muscle Cells ◽

Aortic Smooth Muscle Cells ◽

Aortic Smooth Muscle ◽

Brdu Assay

Abstract Background SCIRT has been characterized as a key player in cancer biology, while its role in other human diseases is unclear. This study explored its role in atherosclerosis, with a specific focus on its interaction with SCIRT and miR-146a. Methods The expression of SCIRT and miR-146a in atherosclerosis-affected tissues and healthy tissues from 56 atherosclerosis patients were analyzed by RT-qPCR. The expression of SCIRT in nuclear and cytoplasm samples was detected by RNA fractionation assay. The direct interaction between SCIRT and miR-146a was detected by RNA pull-down assay. SCIRT and miR-146a were overexpressed in human aortic smooth muscle cells (HAOSMCs) to study the crosstalk between them. The role of SCIRT and miR-146a in the proliferation of HAOSMCs was analyzed with BrdU assay. Results SCIRT was downregulated by atherosclerosis, while miR-146a was upregulated by atherosclerosis. SCIRT was detected in both cytoplasm and nuclear samples, and it directly interacted with miR-146a. In HAOSMCs, overexpression of SCIRT and miR-146a did not affect the expression of each other. Interestingly, SCIRT suppressed the proliferation of HAOSMCs and reduced the enhancing effects of miR-146a on cell proliferation. Conclusion Therefore, SCIRT is downregulated in atherosclerosis and it suppresses the proliferation of HAOSMCs by sponging miR-146a in cytoplasm.

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