Browsing by Author "Yen, Tzung-Hai"

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Calcitriol exerts a mineralization-inductive effect comparable to that of vitamin C in cultured human periodontium cells
(2019-01-01)
Hong, Hsiang-Hsi
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Hong, Adrienne
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Wang, Chun-Chieh
;
Huang, E-Wen
;
Chiang, Cheng-Cheng
This study inspected whether calcitriol could exert a mineralization-inductive effect comparable to that of vitamin C in cultured human periodontium cells (hPDCs). The mRNA expression of the mineralization-related biomarkers core-binding factor subunit alpha-1 (Cbfal), collagen 1 alpha l (Col-l), alkaline phosphatase (ALP), osteopontin (OPN), bone sialoprotein (BSP), osteocalcin (OCN), vitamin D receptor (VDR), cementum protein 1 (CEMP-1), cementum attachment protein (CAP), interleukin 6 (IL-6), transforming growth factor-beta 1 (TGF-beta 1) and osteoprotegerin (OPG) was surveyed after incubation of hPDCs with vitamin C and calcitriol for 2 weeks. Translational expression information from ALP activity and CEMP-1 and CAP immunofluorescence assays was acquired from hPDCs at the second and third weeks. Extracellular calcifications were confirmed by von Kossa staining, Alizarin Red staining and synchrotron transmission X-ray microscopy (TXM) at the fourth and fifth weeks. It was found that both vitamin C and calcitriol not only increased mineralization-related mRNA fold-changes but also enhanced ALP activity, CEMP1 immunofluorescence, von Kossa and Alizarin Red staining and TXM-associated calcifications. Generally, 10(-8) M calcitriol displayed greater mineralization significance than 10(-7) M calcitriol in the assays tested. However, vitamin C stimulated lower Cbfal, Col-1, ALP, OPN, BSP, OCN, VDR, CEMP-1 and IL-6 mRNA fold-changes than 10(-8) M calcitriol. Finally, TXM analysis indicated that a 10(-8) M calcitriol treatment stimulated greater calcifications than vitamin C treatment. Therefore, the analytical results confirmed the osteo-inductive potential of vitamin C in cultured hPDCs. In contrast, 10(-8) M calcitriol could potentially function as a substitute because it stimulates a greater mineralization effect than vitamin C or 10(-7) M calcitriol.
Roles of impaired intracellular calcium cycling in arrhythmogenicity of diabetic mouse model
(2017-10-01)
Chou, Chung-Chuan
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Ho, Chien-Te
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Lee, Hui-Ling
;
Chu, Yen
;
Yen, Tzung-Hai
BackgroundDiabetes mellitus is associated an increased risk of ventricular arrhythmias (VAs), but the underlying electrophysiological mechanisms are not fully explored. This study was aimed to test whether dynamic factors and Ca-i handling play roles in arrhythmogenesis of a diabetic animal model. Methods: We used 26 db/db type 2 diabetes mice and 28 control mice in this study. VA inducibility was evaluated in vivo under isoflurane general anesthesia. The intracellular Ca2+ (Ca-i) and membrane voltage (V-m) signals of the Langendorff-perfused mouse hearts were simultaneously recorded using the optical mapping technique. Action potential duration (APD), Ca-i dynamics conduction velocity (CV), and arrhythmogenic alternans were analyzed. Western blot was conducted to examine expressions of calcium handling and associated ion channels proteins. Results: The diabetic db/db mice showed significantly increased VA inducibility and severity. Longer APD and Ca-i transient duration and slower Ca-i decay and CV in the db/db mice than these in the control ones were observed. Dynamic pacing showed increased incidence of spatially discordant alternans leading to more VA inducibility in the db/db mice. Western blot analyses revealed increased phosphorylated-Ca2+/calmodulin-dependent protein kinase II protein expression and decreased ryanodine receptor protein expression, which probably underlay the molecular mechanisms of enhanced arrhythmogenicity in db/db mice. Conclusions: The type 2 diabetic mouse hearts show impaired repolarization, Ca-i handling homeostasis, and cardiac conduction reserve, leading to vulnerability of spatially discordant alternans development and induction of VA. Altered Ca-i-handling protein expressions probably underlie the molecular mechanisms of arrhythmogenicity in the type 2 diabetes animal model.