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Pingjin Gao - One of the best experts on this subject based on the ideXlab platform.
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Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone Acetate-Salt hypertensive mice.
FEBS letters, 2016Co-Authors: Li-juan Sheng, Cheng-chao Ruan, Dong-rui Chen, Ling-ran Kong, Dingliang Zhu, Pingjin GaoAbstract:Beta3 adrenergic receptor (ADRB3) mediates vessel relaxation in the endothelium while it modulates lipolysis in the adipose tissue. However, the function and regulation mechanism of ADRB3 in the perivascular adipose tissue (PVAT), especially in hypertension, is still unclear. We show that ADRB3 protein is upregulated in the PVAT of deoxycorticosterone Acetate-Salt (DOCA-Salt) hypertensive mice, with the characteristics of PVAT browning and increased uncoupling protein 1 (UCP1) expression. Inhibition of ADRB3 with selective antagonist SR59230A caused serious vascular injury in vivo, even though UCP1 expression was downregulated. ADRB3 protein was regulated by let-7b, which was decreased in the PVAT of the DOCA-Salt group. These data reveal that ADRB3 in PVAT contributes to vascular function in the progression of hypertension.
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perivascular adipose tissue derived complement 3 is required for adventitial fibroblast functions and adventitial remodeling in deoxycorticosterone Acetate Salt hypertensive rats
Arteriosclerosis Thrombosis and Vascular Biology, 2010Co-Authors: Cheng-chao Ruan, Qizhi Chen, Jing Chen, Dingliang Zhu, Shujie Guo, Pingjin GaoAbstract:Objective— To examine the role of perivascular adipose tissue (PVAT)–derived factors in the regulation of adventitial fibroblast (AF) function in vitro and in vivo. Methods and Results— PVAT is an active component of blood vessels. Bioactive substances released from PVAT play regulatory roles in vascular function. However, their effects on vascular AFs remain unclear. PVAT-conditioned medium stimulated AF migration using a transwell technique, and differentiation was evaluated by α-smooth muscle–actin induction. We identified the secretome of PVAT by liquid chromatography–tandem mass spectrometry. One of the major secretory proteins in PVAT is complement 3 (C3). The C3 antagonist and neutralizing antibody attenuated PVAT-conditioned medium–induced AF migration and differentiation. Similar to PVAT-conditioned medium, C3 recombinant protein stimulated AF migration and differentiation. We demonstrated that the effects of PVAT-derived C3 were mediated by the c-Jun N-terminal kinase pathway. Moreover, we found morphological changes in perivascular adipocytes and increased expression of C3 in PVAT that was tightly associated with adventitial thickening and myofibroblast clustering around PVAT in deoxycorticosterone Acetate–Salt hypertensive rats. Conclusion— PVAT-derived C3 stimulated AF migration and differentiation via the c-Jun N-terminal kinase pathway. PVAT-derived C3 may contribute to adventitial remodeling in a deoxycorticosterone Acetate–Salt hypertensive model.
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Perivascular Adipose Tissue–Derived Complement 3 Is Required for Adventitial Fibroblast Functions and Adventitial Remodeling in Deoxycorticosterone Acetate–Salt Hypertensive Rats
Arteriosclerosis thrombosis and vascular biology, 2010Co-Authors: Cheng-chao Ruan, Qizhi Chen, Jing Chen, Dingliang Zhu, Shujie Guo, Pingjin GaoAbstract:Objective— To examine the role of perivascular adipose tissue (PVAT)–derived factors in the regulation of adventitial fibroblast (AF) function in vitro and in vivo. Methods and Results— PVAT is an active component of blood vessels. Bioactive substances released from PVAT play regulatory roles in vascular function. However, their effects on vascular AFs remain unclear. PVAT-conditioned medium stimulated AF migration using a transwell technique, and differentiation was evaluated by α-smooth muscle–actin induction. We identified the secretome of PVAT by liquid chromatography–tandem mass spectrometry. One of the major secretory proteins in PVAT is complement 3 (C3). The C3 antagonist and neutralizing antibody attenuated PVAT-conditioned medium–induced AF migration and differentiation. Similar to PVAT-conditioned medium, C3 recombinant protein stimulated AF migration and differentiation. We demonstrated that the effects of PVAT-derived C3 were mediated by the c-Jun N-terminal kinase pathway. Moreover, we found morphological changes in perivascular adipocytes and increased expression of C3 in PVAT that was tightly associated with adventitial thickening and myofibroblast clustering around PVAT in deoxycorticosterone Acetate–Salt hypertensive rats. Conclusion— PVAT-derived C3 stimulated AF migration and differentiation via the c-Jun N-terminal kinase pathway. PVAT-derived C3 may contribute to adventitial remodeling in a deoxycorticosterone Acetate–Salt hypertensive model.
Yi-ling Chen - One of the best experts on this subject based on the ideXlab platform.
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Renal Damages in Deoxycorticosterone Acetate–Salt Hypertensive Rats: Assessment with Diffusion Tensor Imaging and T2-mapping
Molecular Imaging and Biology, 2020Co-Authors: Sheung-fat Ko, Yen-yi Zhen, Chi-chih Hung, Chung-cheng Huang, Shu-hang Ng, Yi-ling ChenAbstract:Purpose This study aimed to investigate the feasibility of diffusion tensor imaging (DTI) and T2-mapping to assess temporal renal damage in deoxycorticosterone Acetate–Salt (DOCA-Salt) hypertensive rats and compare the results with histopathologic and immunohistochemical findings. Procedures After baseline renal magnetic resonance imaging (MRI), 24 out of 30 uninephrectomized Sprague-Dawley rats with DOCA-Salt-induced hypertension were divided equally into four groups. Group 1 had renal MRI at weeks 2, 4, 6, and 8, and groups 2, 3, and 4 had MRI at weeks 2, 4, and 6, respectively. The remaining 6 rats were used as sham controls. The renal cortex and outer and inner stripes of the outer medulla were examined over time using fractional anisotropy (FA), apparent diffusion coefficient (ADC), and T2-mapping, and the results were compared with baseline values. The degree of glomerular and tubular injury, endothelial cell thickening, hyaline arteriolosclerosis, macrophage infiltration, microcyst formation, and fibrosis in different zones at different time points in the DOCA-Salt rats were compared with controls. Results Compared with baseline values, DOCA-Salt rats demonstrated a significant decrease in renal cortical FA from week 4 to week 8 (0.244 ± 0.015 vs 0.172 ± 0.014–0.150 ± 0.016, P = 0.018–0.002), corresponding to significantly more glomerular damage, arteriolosclerosis, macrophage infiltration, and fibrosis. The DOCA-Salt rats had significantly increased cortical ADC and T2 values at weeks 6 and 8 (1.778 ± 0.051 × 10^−3 mm^2/s vs 1.872 ± 0.058–1.917 ± 0.066 × 10^−3 mm^2/s; 93.7 ± 4.9 ms vs 98.0 ± 2.9–100.7 ± 4.0 ms, respectively, all P
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renal damages in deoxycorticosterone Acetate Salt hypertensive rats assessment with diffusion tensor imaging and t2 mapping
Molecular Imaging and Biology, 2020Co-Authors: Honkan Yip, Yen-yi Zhen, Chi-chih Hung, Chung-cheng Huang, Yi-ling Chen, Chenchang Lee, Juiwei LinAbstract:PURPOSE This study aimed to investigate the feasibility of diffusion tensor imaging (DTI) and T2-mapping to assess temporal renal damage in deoxycorticosterone Acetate-Salt (DOCA-Salt) hypertensive rats and compare the results with histopathologic and immunohistochemical findings. PROCEDURES After baseline renal magnetic resonance imaging (MRI), 24 out of 30 uninephrectomized Sprague-Dawley rats with DOCA-Salt-induced hypertension were divided equally into four groups. Group 1 had renal MRI at weeks 2, 4, 6, and 8, and groups 2, 3, and 4 had MRI at weeks 2, 4, and 6, respectively. The remaining 6 rats were used as sham controls. The renal cortex and outer and inner stripes of the outer medulla were examined over time using fractional anisotropy (FA), apparent diffusion coefficient (ADC), and T2-mapping, and the results were compared with baseline values. The degree of glomerular and tubular injury, endothelial cell thickening, hyaline arteriolosclerosis, macrophage infiltration, microcyst formation, and fibrosis in different zones at different time points in the DOCA-Salt rats were compared with controls. RESULTS Compared with baseline values, DOCA-Salt rats demonstrated a significant decrease in renal cortical FA from week 4 to week 8 (0.244 ± 0.015 vs 0.172 ± 0.014-0.150 ± 0.016, P = 0.018-0.002), corresponding to significantly more glomerular damage, arteriolosclerosis, macrophage infiltration, and fibrosis. The DOCA-Salt rats had significantly increased cortical ADC and T2 values at weeks 6 and 8 (1.778 ± 0.051 × 10-3 mm2/s vs 1.872 ± 0.058-1.917 ± 0.066 × 10-3 mm2/s; 93.7 ± 4.9 ms vs 98.0 ± 2.9-100.7 ± 4.0 ms, respectively, all P < 0.05), consistent with excessively fluid-filled microcysts (aquaporin-2+). Despite DOCA-Salt rats harbored markedly increased fibrosis in outer and inner stripes of the outer medulla at weeks 6 and 8, only nonsignificant decreases in FA were observed in comparison with the controls suggesting that only limited microstructural changes were present. CONCLUSIONS Renal cortical FA is useful for the early detection and monitoring of renal damage in DOCA-Salt hypertensive rats.
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Renal Damages in Deoxycorticosterone Acetate-Salt Hypertensive Rats: Assessment with Diffusion Tensor Imaging and T2-mapping.
Molecular Imaging and Biology, 2019Co-Authors: Sheung-fat Ko, Yen-yi Zhen, Chi-chih Hung, Chung-cheng Huang, Shu-hang Ng, Yi-ling ChenAbstract:PURPOSE: This study aimed to investigate the feasibility of diffusion tensor imaging (DTI) and T2-mapping to assess temporal renal damage in deoxycorticosterone Acetate-Salt (DOCA-Salt) hypertensive rats and compare the results with histopathologic and immunohistochemical findings. PROCEDURES: After baseline renal magnetic resonance imaging (MRI), 24 out of 30 uninephrectomized Sprague-Dawley rats with DOCA-Salt-induced hypertension were divided equally into four groups. Group 1 had renal MRI at weeks 2, 4, 6, and 8, and groups 2, 3, and 4 had MRI at weeks 2, 4, and 6, respectively. The remaining 6 rats were used as sham controls. The renal cortex and outer and inner stripes of the outer medulla were examined over time using fractional anisotropy (FA), apparent diffusion coefficient (ADC), and T2-mapping, and the results were compared with baseline values. The degree of glomerular and tubular injury, endothelial cell thickening, hyaline arteriolosclerosis, macrophage infiltration, microcyst formation, and fibrosis in different zones at different time points in the DOCA-Salt rats were compared with controls. RESULTS: Compared with baseline values, DOCA-Salt rats demonstrated a significant decrease in renal cortical FA from week 4 to week 8 (0.244 ± 0.015 vs 0.172 ± 0.014-0.150 ± 0.016, P = 0.018-0.002), corresponding to significantly more glomerular damage, arteriolosclerosis, macrophage infiltration, and fibrosis. The DOCA-Salt rats had significantly increased cortical ADC and T2 values at weeks 6 and 8 (1.778 ± 0.051 × 10-3 mm2/s vs 1.872 ± 0.058-1.917 ± 0.066 × 10-3 mm2/s; 93.7 ± 4.9 ms vs 98.0 ± 2.9-100.7 ± 4.0 ms, respectively, all P
Cheng-chao Ruan - One of the best experts on this subject based on the ideXlab platform.
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Beta3 adrenergic receptor is involved in vascular injury in deoxycorticosterone Acetate-Salt hypertensive mice.
FEBS letters, 2016Co-Authors: Li-juan Sheng, Cheng-chao Ruan, Dong-rui Chen, Ling-ran Kong, Dingliang Zhu, Pingjin GaoAbstract:Beta3 adrenergic receptor (ADRB3) mediates vessel relaxation in the endothelium while it modulates lipolysis in the adipose tissue. However, the function and regulation mechanism of ADRB3 in the perivascular adipose tissue (PVAT), especially in hypertension, is still unclear. We show that ADRB3 protein is upregulated in the PVAT of deoxycorticosterone Acetate-Salt (DOCA-Salt) hypertensive mice, with the characteristics of PVAT browning and increased uncoupling protein 1 (UCP1) expression. Inhibition of ADRB3 with selective antagonist SR59230A caused serious vascular injury in vivo, even though UCP1 expression was downregulated. ADRB3 protein was regulated by let-7b, which was decreased in the PVAT of the DOCA-Salt group. These data reveal that ADRB3 in PVAT contributes to vascular function in the progression of hypertension.
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perivascular adipose tissue derived complement 3 is required for adventitial fibroblast functions and adventitial remodeling in deoxycorticosterone Acetate Salt hypertensive rats
Arteriosclerosis Thrombosis and Vascular Biology, 2010Co-Authors: Cheng-chao Ruan, Qizhi Chen, Jing Chen, Dingliang Zhu, Shujie Guo, Pingjin GaoAbstract:Objective— To examine the role of perivascular adipose tissue (PVAT)–derived factors in the regulation of adventitial fibroblast (AF) function in vitro and in vivo. Methods and Results— PVAT is an active component of blood vessels. Bioactive substances released from PVAT play regulatory roles in vascular function. However, their effects on vascular AFs remain unclear. PVAT-conditioned medium stimulated AF migration using a transwell technique, and differentiation was evaluated by α-smooth muscle–actin induction. We identified the secretome of PVAT by liquid chromatography–tandem mass spectrometry. One of the major secretory proteins in PVAT is complement 3 (C3). The C3 antagonist and neutralizing antibody attenuated PVAT-conditioned medium–induced AF migration and differentiation. Similar to PVAT-conditioned medium, C3 recombinant protein stimulated AF migration and differentiation. We demonstrated that the effects of PVAT-derived C3 were mediated by the c-Jun N-terminal kinase pathway. Moreover, we found morphological changes in perivascular adipocytes and increased expression of C3 in PVAT that was tightly associated with adventitial thickening and myofibroblast clustering around PVAT in deoxycorticosterone Acetate–Salt hypertensive rats. Conclusion— PVAT-derived C3 stimulated AF migration and differentiation via the c-Jun N-terminal kinase pathway. PVAT-derived C3 may contribute to adventitial remodeling in a deoxycorticosterone Acetate–Salt hypertensive model.
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Perivascular Adipose Tissue–Derived Complement 3 Is Required for Adventitial Fibroblast Functions and Adventitial Remodeling in Deoxycorticosterone Acetate–Salt Hypertensive Rats
Arteriosclerosis thrombosis and vascular biology, 2010Co-Authors: Cheng-chao Ruan, Qizhi Chen, Jing Chen, Dingliang Zhu, Shujie Guo, Pingjin GaoAbstract:Objective— To examine the role of perivascular adipose tissue (PVAT)–derived factors in the regulation of adventitial fibroblast (AF) function in vitro and in vivo. Methods and Results— PVAT is an active component of blood vessels. Bioactive substances released from PVAT play regulatory roles in vascular function. However, their effects on vascular AFs remain unclear. PVAT-conditioned medium stimulated AF migration using a transwell technique, and differentiation was evaluated by α-smooth muscle–actin induction. We identified the secretome of PVAT by liquid chromatography–tandem mass spectrometry. One of the major secretory proteins in PVAT is complement 3 (C3). The C3 antagonist and neutralizing antibody attenuated PVAT-conditioned medium–induced AF migration and differentiation. Similar to PVAT-conditioned medium, C3 recombinant protein stimulated AF migration and differentiation. We demonstrated that the effects of PVAT-derived C3 were mediated by the c-Jun N-terminal kinase pathway. Moreover, we found morphological changes in perivascular adipocytes and increased expression of C3 in PVAT that was tightly associated with adventitial thickening and myofibroblast clustering around PVAT in deoxycorticosterone Acetate–Salt hypertensive rats. Conclusion— PVAT-derived C3 stimulated AF migration and differentiation via the c-Jun N-terminal kinase pathway. PVAT-derived C3 may contribute to adventitial remodeling in a deoxycorticosterone Acetate–Salt hypertensive model.
Chien Wei Ooi - One of the best experts on this subject based on the ideXlab platform.
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Liquid–Liquid Equilibrium of Alcohols + Ammonium/Potassium/Sodium Acetate + Water Systems: Experimental and Correlation
Journal of Chemical & Engineering Data, 2015Co-Authors: Ramakrishnan Nagasundara Ramanan, Beng Ti Tey, Tau Chuan Ling, Pau Loke Show, Chien Wei OoiAbstract:Liquid–liquid equilibra of alcohol + Acetate Salt + water systems—namely, 2-butanol + ammonium Acetate + water, 1-propanol + sodium/potassium Acetate + water, and 2-propanol + sodium/potassium Acetate + water systems—were successfully determined. The ability of Acetate Salt to form aqueous two-phase system (ATPS) with alcohol was found to be mainly driven by a high Gibbs energy (i.e., greater than −1000 kJ/mol). The fitting of the experimental binodal data was done by using the Merchuk equations. The tie-line data were satisfactorily correlated by the Othmer–Tobias and Bancroft equations. The Salting-out strength of the Acetate Salts was evaluated based on the effective excluded volume theory and the Setschenow-type equation. The phase-forming abilities of the investigated alcohols were in the order of 2-butanol > 1-propanol > 2-propanol. For 2-propanol + Acetate Salt + water systems, the Salting-out strength of sodium Acetate was greater than that of potassium Acetate. In contrast, for 1-propanol + aceta...
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liquid liquid equilibrium of alcohols ammonium potassium sodium Acetate water systems experimental and correlation
Journal of Chemical & Engineering Data, 2015Co-Authors: Ramakrishnan Nagasundara Ramanan, Beng Ti Tey, Tau Chuan Ling, Pau Loke Show, Chien Wei OoiAbstract:Liquid–liquid equilibra of alcohol + Acetate Salt + water systems—namely, 2-butanol + ammonium Acetate + water, 1-propanol + sodium/potassium Acetate + water, and 2-propanol + sodium/potassium Acetate + water systems—were successfully determined. The ability of Acetate Salt to form aqueous two-phase system (ATPS) with alcohol was found to be mainly driven by a high Gibbs energy (i.e., greater than −1000 kJ/mol). The fitting of the experimental binodal data was done by using the Merchuk equations. The tie-line data were satisfactorily correlated by the Othmer–Tobias and Bancroft equations. The Salting-out strength of the Acetate Salts was evaluated based on the effective excluded volume theory and the Setschenow-type equation. The phase-forming abilities of the investigated alcohols were in the order of 2-butanol > 1-propanol > 2-propanol. For 2-propanol + Acetate Salt + water systems, the Salting-out strength of sodium Acetate was greater than that of potassium Acetate. In contrast, for 1-propanol + aceta...
Jing Chen - One of the best experts on this subject based on the ideXlab platform.
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anti stiffness effect of apocynin in deoxycorticosterone Acetate Salt hypertensive rats via inhibition of oxidative stress
Hypertension Research, 2013Co-Authors: Qizhi Chen, Jing ChenAbstract:Anti-stiffness effect of apocynin in deoxycorticosterone Acetate-Salt hypertensive rats via inhibition of oxidative stress
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perivascular adipose tissue derived complement 3 is required for adventitial fibroblast functions and adventitial remodeling in deoxycorticosterone Acetate Salt hypertensive rats
Arteriosclerosis Thrombosis and Vascular Biology, 2010Co-Authors: Cheng-chao Ruan, Qizhi Chen, Jing Chen, Dingliang Zhu, Shujie Guo, Pingjin GaoAbstract:Objective— To examine the role of perivascular adipose tissue (PVAT)–derived factors in the regulation of adventitial fibroblast (AF) function in vitro and in vivo. Methods and Results— PVAT is an active component of blood vessels. Bioactive substances released from PVAT play regulatory roles in vascular function. However, their effects on vascular AFs remain unclear. PVAT-conditioned medium stimulated AF migration using a transwell technique, and differentiation was evaluated by α-smooth muscle–actin induction. We identified the secretome of PVAT by liquid chromatography–tandem mass spectrometry. One of the major secretory proteins in PVAT is complement 3 (C3). The C3 antagonist and neutralizing antibody attenuated PVAT-conditioned medium–induced AF migration and differentiation. Similar to PVAT-conditioned medium, C3 recombinant protein stimulated AF migration and differentiation. We demonstrated that the effects of PVAT-derived C3 were mediated by the c-Jun N-terminal kinase pathway. Moreover, we found morphological changes in perivascular adipocytes and increased expression of C3 in PVAT that was tightly associated with adventitial thickening and myofibroblast clustering around PVAT in deoxycorticosterone Acetate–Salt hypertensive rats. Conclusion— PVAT-derived C3 stimulated AF migration and differentiation via the c-Jun N-terminal kinase pathway. PVAT-derived C3 may contribute to adventitial remodeling in a deoxycorticosterone Acetate–Salt hypertensive model.
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Perivascular Adipose Tissue–Derived Complement 3 Is Required for Adventitial Fibroblast Functions and Adventitial Remodeling in Deoxycorticosterone Acetate–Salt Hypertensive Rats
Arteriosclerosis thrombosis and vascular biology, 2010Co-Authors: Cheng-chao Ruan, Qizhi Chen, Jing Chen, Dingliang Zhu, Shujie Guo, Pingjin GaoAbstract:Objective— To examine the role of perivascular adipose tissue (PVAT)–derived factors in the regulation of adventitial fibroblast (AF) function in vitro and in vivo. Methods and Results— PVAT is an active component of blood vessels. Bioactive substances released from PVAT play regulatory roles in vascular function. However, their effects on vascular AFs remain unclear. PVAT-conditioned medium stimulated AF migration using a transwell technique, and differentiation was evaluated by α-smooth muscle–actin induction. We identified the secretome of PVAT by liquid chromatography–tandem mass spectrometry. One of the major secretory proteins in PVAT is complement 3 (C3). The C3 antagonist and neutralizing antibody attenuated PVAT-conditioned medium–induced AF migration and differentiation. Similar to PVAT-conditioned medium, C3 recombinant protein stimulated AF migration and differentiation. We demonstrated that the effects of PVAT-derived C3 were mediated by the c-Jun N-terminal kinase pathway. Moreover, we found morphological changes in perivascular adipocytes and increased expression of C3 in PVAT that was tightly associated with adventitial thickening and myofibroblast clustering around PVAT in deoxycorticosterone Acetate–Salt hypertensive rats. Conclusion— PVAT-derived C3 stimulated AF migration and differentiation via the c-Jun N-terminal kinase pathway. PVAT-derived C3 may contribute to adventitial remodeling in a deoxycorticosterone Acetate–Salt hypertensive model.