schliessen

Filtern

 

Bibliotheken

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

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)... Full description

Journal Title: Molecular and Cellular Biochemistry 2017, Vol.433(1), pp.149-159
Main Author: Qiu, Cuiting
Other Authors: Zheng, Haijun , Tao, Huiren , Yu, Wenjun , Jiang, Xiaoyu , Li, Aiqin , Jin, Hui , Lv, Anlin , Li, Huan
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0300-8177 ; E-ISSN: 1573-4919 ; DOI: 10.1007/s11010-017-3023-z
Link: http://dx.doi.org/10.1007/s11010-017-3023-z
Zum Text:
SendSend as email Add to Book BagAdd to Book Bag
Staff View
recordid: springer_jour10.1007/s11010-017-3023-z
title: Vitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway
format: Article
creator:
  • Qiu, Cuiting
  • Zheng, Haijun
  • Tao, Huiren
  • Yu, Wenjun
  • Jiang, Xiaoyu
  • Li, Aiqin
  • Jin, Hui
  • Lv, Anlin
  • Li, Huan
subjects:
  • Vitamin K2
  • Growth arrest-specific gene 6 (Gas-6)
  • Apoptosis
  • Vascular calcification
  • Vascular smooth muscle cells
ispartof: Molecular and Cellular Biochemistry, 2017, Vol.433(1), pp.149-159
description: 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 CaCl 2 - 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 CaCl 2 - 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 CaCl 2 - and β-GP-induced apoptosis and calcification. These results suggest that Gas6 is critical in VK2-mediated functions that attenuate CaCl 2 - and β-GP-induced VSMC calcification by blocking apoptosis.
language: eng
source:
identifier: ISSN: 0300-8177 ; E-ISSN: 1573-4919 ; DOI: 10.1007/s11010-017-3023-z
fulltext: fulltext
issn:
  • 1573-4919
  • 15734919
  • 0300-8177
  • 03008177
url: Link


@attributes
ID1182426254
RANK0.07
NO1
SEARCH_ENGINEprimo_central_multiple_fe
SEARCH_ENGINE_TYPEPrimo Central Search Engine
LOCALfalse
PrimoNMBib
record
control
sourcerecordid10.1007/s11010-017-3023-z
sourceidspringer_jour
recordidTN_springer_jour10.1007/s11010-017-3023-z
sourcesystemPC
pqid1928140546
galeid501298063
display
typearticle
titleVitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway
creatorQiu, Cuiting ; Zheng, Haijun ; Tao, Huiren ; Yu, Wenjun ; Jiang, Xiaoyu ; Li, Aiqin ; Jin, Hui ; Lv, Anlin ; Li, Huan
ispartofMolecular and Cellular Biochemistry, 2017, Vol.433(1), pp.149-159
identifier
subjectVitamin K2 ; Growth arrest-specific gene 6 (Gas-6) ; Apoptosis ; Vascular calcification ; Vascular smooth muscle cells
descriptionVascular 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 CaCl 2 - 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 CaCl 2 - 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 CaCl 2 - and β-GP-induced apoptosis and calcification. These results suggest that Gas6 is critical in VK2-mediated functions that attenuate CaCl 2 - and β-GP-induced VSMC calcification by blocking apoptosis.
languageeng
source
version6
lds50peer_reviewed
links
openurl$$Topenurl_article
openurlfulltext$$Topenurlfull_article
backlink$$Uhttp://dx.doi.org/10.1007/s11010-017-3023-z$$EView_full_text_in_Springer_(Subscribers_only)
search
creatorcontrib
0Qiu, Cuiting
1Zheng, Haijun
2Tao, Huiren
3Yu, Wenjun
4Jiang, Xiaoyu
5Li, Aiqin
6Jin, Hui
7Lv, Anlin
8Li, Huan
titleVitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway
descriptionVascular 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 CaCl 2 - 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 CaCl 2 - 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 CaCl 2 - and β-GP-induced apoptosis and calcification. These results suggest that Gas6 is critical in VK2-mediated functions that attenuate CaCl 2 - and β-GP-induced VSMC calcification by blocking apoptosis.
subject
0Vitamin K2
1Growth arrest-specific gene 6 (Gas-6)
2Apoptosis
3Vascular calcification
4Vascular smooth muscle cells
general
010.1007/s11010-017-3023-z
1English
2Springer Science & Business Media B.V.
3SpringerLink
sourceidspringer_jour
recordidspringer_jour10.1007/s11010-017-3023-z
issn
01573-4919
115734919
20300-8177
303008177
rsrctypearticle
creationdate2017
addtitle
0Molecular and Cellular Biochemistry
1An International Journal for Chemical Biology in Health and Disease
2Mol Cell Biochem
searchscopespringer_journals_complete
scopespringer_journals_complete
lsr30VSR-Enriched:[galeid, pqid, pages, issue]
sort
titleVitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway
authorQiu, Cuiting ; Zheng, Haijun ; Tao, Huiren ; Yu, Wenjun ; Jiang, Xiaoyu ; Li, Aiqin ; Jin, Hui ; Lv, Anlin ; Li, Huan
creationdate20170900
facets
frbrgroupid-718429310455844407
frbrtype5
newrecords20170815
languageeng
creationdate2017
topic
0Vitamin K2
1Growth Arrest-Specific Gene 6 (Gas-6)
2Apoptosis
3Vascular Calcification
4Vascular Smooth Muscle Cells
collectionSpringerLink
prefilterarticles
rsrctypearticles
creatorcontrib
0Qiu, Cuiting
1Zheng, Haijun
2Tao, Huiren
3Yu, Wenjun
4Jiang, Xiaoyu
5Li, Aiqin
6Jin, Hui
7Lv, Anlin
8Li, Huan
jtitleMolecular And Cellular Biochemistry
toplevelpeer_reviewed
delivery
delcategoryRemote Search Resource
fulltextfulltext
addata
aulast
0Qiu
1Zheng
2Tao
3Yu
4Jiang
5Li
6Jin
7Lv
aufirst
0Cuiting
1Haijun
2Huiren
3Wenjun
4Xiaoyu
5Aiqin
6Hui
7Anlin
8Huan
au
0Qiu, Cuiting
1Zheng, Haijun
2Tao, Huiren
3Yu, Wenjun
4Jiang, Xiaoyu
5Li, Aiqin
6Jin, Hui
7Lv, Anlin
8Li, Huan
atitleVitamin K2 inhibits rat vascular smooth muscle cell calcification by restoring the Gas6/Axl/Akt anti-apoptotic pathway
jtitleMolecular and Cellular Biochemistry
stitleMol Cell Biochem
addtitleAn International Journal for Chemical Biology in Health and Disease
risdate201709
volume433
issue1-2
spage149
epage159
issn0300-8177
eissn1573-4919
genrearticle
ristypeJOUR
abstractVascular 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 CaCl 2 - 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 CaCl 2 - 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 CaCl 2 - and β-GP-induced apoptosis and calcification. These results suggest that Gas6 is critical in VK2-mediated functions that attenuate CaCl 2 - and β-GP-induced VSMC calcification by blocking apoptosis.
copNew York
pubSpringer US
doi10.1007/s11010-017-3023-z
pages149-159
date2017-09