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Vitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway

Overview of attention for article published in Molecular and Cellular Biochemistry, April 2017
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  • Good Attention Score compared to outputs of the same age (67th percentile)
  • High Attention Score compared to outputs of the same age and source (94th percentile)

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2 X users
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12 patents

Citations

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40 Dimensions

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28 Mendeley
Title
Vitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway
Published in
Molecular and Cellular Biochemistry, April 2017
DOI 10.1007/s11010-017-3023-z
Pubmed ID
Authors

Cuiting Qiu, Haijun Zheng, Huiren Tao, Wenjun Yu, Xiaoyu Jiang, Aiqin Li, Hui Jin, Anlin Lv, Huan Li

Abstract

Vascular calcification is associated with cardiovascular disease as a complication of hypertension, hyperlipidemia, diabetes mellitus, and chronic kidney disease. Vitamin K2 (VK2) delays vascular calcification by an unclear mechanism. Moreover, apoptosis modulates vascular smooth muscle cell (VSMC) calcification. This paper aimed to study VK2-modified VSMC calcification and survival cell signaling mediated by growth arrest-specific gene 6 (Gas6) and its tyrosine kinase receptor Axl. Primary-cultured VSMCs were dose-dependently treated with VK2 in the presence of calcification medium for 8 days, or pre-treated for 1 h with/without the Axl inhibitor R428 (2 μmol/L) or the caspase inhibitor Z-VAD-fmk (20 μmol/L) followed by treatment with VK2 (10 μmol/L) or rmGas6 (200 nmol/L) in calcification medium for 8 days. Calcium deposition was determined by the o-cresolphthalein complexone assay and Alizarin Red S staining. Apoptosis was determined by TUNEL and flow cytometry using Annexin V-FITC and propidium iodide staining. Western blotting detected the expressions of Axl, Gas6, p-Akt, Akt, and Bcl2. VK2 significantly inhibited CaCl2- and β-sodium glycerophosphate (β-GP)-induced VSMC calcification and apoptosis, which was dependent on restored Gas6 expression and activated downstream signaling by Axl, p-Akt, and Bcl2. Z-VAD-fmk significantly inhibited CaCl2- and β-GP-induced VSMC calcification and apoptosis. Augmented recombinant mouse Gas6 protein (rmGas6) expression significantly reduced VSMC calcification and apoptosis. Furthermore, the Gas6/Axl interaction was inhibited by R428, which abolished the preventive effect of VK2 on CaCl2- and β-GP-induced apoptosis and calcification. These results suggest that Gas6 is critical in VK2-mediated functions that attenuate CaCl2- and β-GP-induced VSMC calcification by blocking apoptosis.

X Demographics

X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 28 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 18%
Other 3 11%
Student > Doctoral Student 3 11%
Student > Bachelor 2 7%
Researcher 2 7%
Other 6 21%
Unknown 7 25%
Readers by discipline Count As %
Medicine and Dentistry 7 25%
Biochemistry, Genetics and Molecular Biology 5 18%
Pharmacology, Toxicology and Pharmaceutical Science 3 11%
Agricultural and Biological Sciences 2 7%
Earth and Planetary Sciences 1 4%
Other 3 11%
Unknown 7 25%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 5. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 24 October 2023.
All research outputs
#6,815,157
of 24,727,020 outputs
Outputs from Molecular and Cellular Biochemistry
#359
of 2,449 outputs
Outputs of similar age
#101,961
of 314,301 outputs
Outputs of similar age from Molecular and Cellular Biochemistry
#4
of 53 outputs
Altmetric has tracked 24,727,020 research outputs across all sources so far. This one has received more attention than most of these and is in the 72nd percentile.
So far Altmetric has tracked 2,449 research outputs from this source. They receive a mean Attention Score of 4.0. This one has done well, scoring higher than 85% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 314,301 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 67% of its contemporaries.
We're also able to compare this research output to 53 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 94% of its contemporaries.