title: Effects of extracellular acid stimulation on rat vascular smooth muscle cell in Gas6/Axl or PI3K/Akt signaling pathway.
abstract: Recent studies have indicated that extracellular acid stimulation inhibited the calcification of vascular smooth muscle cells (VSMCs). Cell apoptosis played an important role in the occurrence and development of vascular calcification. We further explored the effects of Gas6/Axl or PI3K/Akt signaling pathway on the inhibition of rat VSMCs calcification in response to extracellular acid stimulation. Our study demonstrated that a high concentration of phosphorus induced apoptosis and calcification of VSMCs, decreased expression of Axl, and reduced phosphorylation of Akt. Stimulation of extracellular acid counteracted the effects as above by increasing the expression of Axl and Akt phosphorylation and decreasing the expression of activated Caspase3, which thereby decreased cell apoptosis and calcification. Moreover, the effects can be attenuated by PI3K inhibitor. Our study proved that extracellular acid stimulation played a vital role in the inhibition of rat VSMCs calcification and apoptosis in Gas6/Axl or PI3K/Akt signaling pathway.
authors.affiliation: a Department of Nephrology , The Fourth Affiliated Hospital of Hebei Medical University , Shijiazhuang City , Hebei Province , China.
authors.forename: Liwen
authors.initials: L
authors.lastname: Cui
authors.affiliation: a Department of Nephrology , The Fourth Affiliated Hospital of Hebei Medical University , Shijiazhuang City , Hebei Province , China.
authors.forename: Yaling
authors.initials: Y
authors.lastname: Bai
authors.affiliation: a Department of Nephrology , The Fourth Affiliated Hospital of Hebei Medical University , Shijiazhuang City , Hebei Province , China.
authors.forename: Junxia
authors.initials: J
authors.lastname: Zhang
authors.affiliation: a Department of Nephrology , The Fourth Affiliated Hospital of Hebei Medical University , Shijiazhuang City , Hebei Province , China.
authors.forename: Shenglei
authors.initials: S
authors.lastname: Zhang
authors.affiliation: a Department of Nephrology , The Fourth Affiliated Hospital of Hebei Medical University , Shijiazhuang City , Hebei Province , China.
authors.forename: Jinsheng
authors.initials: J
authors.lastname: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002114:Calcinosis / Q000517:prevention & control; D053148:Caspase 3 / Q000378:metabolism; D006973:Hypertension / Q000378:metabolism; D007202:Indicators and Reagents / Q000494:pharmacology*; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011804:Quinolines / Q000494:pharmacology*; D017207:Rats, Sprague-Dawley; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D000099255:Growth Arrest-Specific Protein 6
chemical_list: D053148:Caspase 3; D007202:Indicators and Reagents; D036341:Intercellular Signaling Peptides and Proteins; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D047428:Protein Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt; D011804:Quinolines; D020794:Receptor Protein-Tyrosine Kinases; D000099255:Growth Arrest-Specific Protein 6; C047117:bicinchoninic acid
keywords: Caspase3; Gas6/Axl; PI3K/Akt; extracellular acid stimulation; phosphate; vascular smooth muscle cell (VSMC)