vitamin-k-1 and Rheumatic-Heart-Disease

vitamin-k-1 has been researched along with Rheumatic-Heart-Disease* in 2 studies

Other Studies

2 other study(ies) available for vitamin-k-1 and Rheumatic-Heart-Disease

Article	Year
Low-level overexpression of p53 promotes warfarin-induced calcification of porcine aortic valve interstitial cells by activating The Journal of biological chemistry, 2018, 03-09, Volume: 293, Issue:10 The most frequently used oral anti-coagulant warfarin has been implicated in inducing calcification of aortic valve interstitial cells (AVICs), whereas the mechanism is not fully understood. The low-level activation of p53 is found to be involved in osteogenic transdifferentiation and calcification of AVICs. Whether p53 participates in warfarin-induced AVIC calcification remains unknown. In this study, we investigated the role of low-level p53 overexpression in warfarin-induced porcine AVIC (pAVIC) calcification. Immunostaining, quantitative PCR, and Western blotting revealed that p53 was expressed in human and pAVICs and that p53 expression was slightly increased in calcific human aortic valves compared with non-calcific valves. Terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling staining indicated that apoptosis slightly increased in calcific aortic valves than in non-calcific valves. Warfarin treatment led to a low-level increase of p53 mRNA and protein in both pAVICs and mouse aortic valves. Low-level overexpression of p53 in pAVICs via an adenovirus vector did not affect pAVIC apoptosis but promoted warfarin-induced calcium deposition and expression of osteogenic markers. shRNA-mediated p53 knockdown attenuated the pAVIC calcium deposition and osteogenic marker expression. Moreover, ChIP and luciferase assays showed that p53 was recruited to the Topics: Animals; Anticoagulants; Antifibrinolytic Agents; Aortic Valve; Atrial Fibrillation; Calcinosis; Cells, Cultured; Disease Models, Animal; Epigenesis, Genetic; Gene Expression Regulation; Genes, Reporter; Heart Valve Diseases; Humans; Male; Mice, Inbred C57BL; Promoter Regions, Genetic; Recombinant Proteins; Rheumatic Heart Disease; RNA Interference; Snail Family Transcription Factors; Sus scrofa; Tumor Suppressor Protein p53; Vitamin K 1; Warfarin	2018
[Peptic ulcer hemorrhage due to anticoagulants]. Deutsche medizinische Wochenschrift (1946), 1973, Sep-14, Volume: 98, Issue:37 Topics: Anticoagulants; Aspirin; Atrial Fibrillation; Blood Transfusion; Coumarins; Digitalis Glycosides; Dose-Response Relationship, Drug; Duodenal Ulcer; Humans; Male; Middle Aged; Peptic Ulcer Hemorrhage; Rheumatic Heart Disease; Vitamin K 1	1973

Article

Year

Low-level overexpression of p53 promotes warfarin-induced calcification of porcine aortic valve interstitial cells by activating

The Journal of biological chemistry, 2018, 03-09, Volume: 293, Issue:10

The most frequently used oral anti-coagulant warfarin has been implicated in inducing calcification of aortic valve interstitial cells (AVICs), whereas the mechanism is not fully understood. The low-level activation of p53 is found to be involved in osteogenic transdifferentiation and calcification of AVICs. Whether p53 participates in warfarin-induced AVIC calcification remains unknown. In this study, we investigated the role of low-level p53 overexpression in warfarin-induced porcine AVIC (pAVIC) calcification. Immunostaining, quantitative PCR, and Western blotting revealed that p53 was expressed in human and pAVICs and that p53 expression was slightly increased in calcific human aortic valves compared with non-calcific valves. Terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling staining indicated that apoptosis slightly increased in calcific aortic valves than in non-calcific valves. Warfarin treatment led to a low-level increase of p53 mRNA and protein in both pAVICs and mouse aortic valves. Low-level overexpression of p53 in pAVICs via an adenovirus vector did not affect pAVIC apoptosis but promoted warfarin-induced calcium deposition and expression of osteogenic markers. shRNA-mediated p53 knockdown attenuated the pAVIC calcium deposition and osteogenic marker expression. Moreover, ChIP and luciferase assays showed that p53 was recruited to the

Topics: Animals; Anticoagulants; Antifibrinolytic Agents; Aortic Valve; Atrial Fibrillation; Calcinosis; Cells, Cultured; Disease Models, Animal; Epigenesis, Genetic; Gene Expression Regulation; Genes, Reporter; Heart Valve Diseases; Humans; Male; Mice, Inbred C57BL; Promoter Regions, Genetic; Recombinant Proteins; Rheumatic Heart Disease; RNA Interference; Snail Family Transcription Factors; Sus scrofa; Tumor Suppressor Protein p53; Vitamin K 1; Warfarin

2018

[Peptic ulcer hemorrhage due to anticoagulants].

Deutsche medizinische Wochenschrift (1946), 1973, Sep-14, Volume: 98, Issue:37

Topics: Anticoagulants; Aspirin; Atrial Fibrillation; Blood Transfusion; Coumarins; Digitalis Glycosides; Dose-Response Relationship, Drug; Duodenal Ulcer; Humans; Male; Middle Aged; Peptic Ulcer Hemorrhage; Rheumatic Heart Disease; Vitamin K 1

1973