The Experts below are selected from a list of 24939 Experts worldwide ranked by ideXlab platform
Angela Bandeira - One of the best experts on this subject based on the ideXlab platform.
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transforming growth factor β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background—The pathogenic mechanisms underlying pulmonary arterial hypertension resulting from schistosomiasis, one of the most common causes of pulmonary hypertension worldwide, remain unknown. We hypothesized that transforming growth factor-β (TGF-β) signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results—Mice sensitized and subsequently challenged with Schistosoma mansoni eggs developed pulmonary hypertension associated with an increase in right ventricular systolic pressure, thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase–dependent vasoconstriction accounted for ≈60% of the increase in right ventricular systolic pressure. The pulmonary vascular remodeling and pulmonary hypertension were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma-induced pulmonary hypertension. Blockade of TGF-...
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tgf β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background —The pathogenic mechanisms underlying pulmonary arterial hypertension (PAH) due to schistosomiasis, one of the most common causes of pulmonary hypertension (PH) worldwide, remains unknown. We hypothesized that TGF-β signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results —Mice sensitized and subsequently challenged with S. mansoni eggs developed PH associated with an increase in right ventricular systolic pressure (RVSP), thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase dependent vasoconstriction accounted for about 60% of the increase in RVSP. The pulmonary vascular remodeling and PH were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma -induced PH. Blockade of TGF-β signaling also led to a decrease in IL4 and IL13 concentrations, which drive the Th2 responses characteristic of schistosomiasis lung pathology. Lungs of patients with schistosomiasis-associated PAH have evidence of TGF-β signaling in their remodeled pulmonary arteries. Conclusions —Experimental S. mansoni -induced pulmonary vascular disease relies on canonical TGF-β signaling.
Brian B Graham - One of the best experts on this subject based on the ideXlab platform.
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transforming growth factor β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background—The pathogenic mechanisms underlying pulmonary arterial hypertension resulting from schistosomiasis, one of the most common causes of pulmonary hypertension worldwide, remain unknown. We hypothesized that transforming growth factor-β (TGF-β) signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results—Mice sensitized and subsequently challenged with Schistosoma mansoni eggs developed pulmonary hypertension associated with an increase in right ventricular systolic pressure, thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase–dependent vasoconstriction accounted for ≈60% of the increase in right ventricular systolic pressure. The pulmonary vascular remodeling and pulmonary hypertension were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma-induced pulmonary hypertension. Blockade of TGF-...
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tgf β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background —The pathogenic mechanisms underlying pulmonary arterial hypertension (PAH) due to schistosomiasis, one of the most common causes of pulmonary hypertension (PH) worldwide, remains unknown. We hypothesized that TGF-β signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results —Mice sensitized and subsequently challenged with S. mansoni eggs developed PH associated with an increase in right ventricular systolic pressure (RVSP), thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase dependent vasoconstriction accounted for about 60% of the increase in RVSP. The pulmonary vascular remodeling and PH were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma -induced PH. Blockade of TGF-β signaling also led to a decrease in IL4 and IL13 concentrations, which drive the Th2 responses characteristic of schistosomiasis lung pathology. Lungs of patients with schistosomiasis-associated PAH have evidence of TGF-β signaling in their remodeled pulmonary arteries. Conclusions —Experimental S. mansoni -induced pulmonary vascular disease relies on canonical TGF-β signaling.
Jennifer Poole - One of the best experts on this subject based on the ideXlab platform.
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transforming growth factor β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background—The pathogenic mechanisms underlying pulmonary arterial hypertension resulting from schistosomiasis, one of the most common causes of pulmonary hypertension worldwide, remain unknown. We hypothesized that transforming growth factor-β (TGF-β) signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results—Mice sensitized and subsequently challenged with Schistosoma mansoni eggs developed pulmonary hypertension associated with an increase in right ventricular systolic pressure, thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase–dependent vasoconstriction accounted for ≈60% of the increase in right ventricular systolic pressure. The pulmonary vascular remodeling and pulmonary hypertension were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma-induced pulmonary hypertension. Blockade of TGF-...
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tgf β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background —The pathogenic mechanisms underlying pulmonary arterial hypertension (PAH) due to schistosomiasis, one of the most common causes of pulmonary hypertension (PH) worldwide, remains unknown. We hypothesized that TGF-β signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results —Mice sensitized and subsequently challenged with S. mansoni eggs developed PH associated with an increase in right ventricular systolic pressure (RVSP), thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase dependent vasoconstriction accounted for about 60% of the increase in RVSP. The pulmonary vascular remodeling and PH were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma -induced PH. Blockade of TGF-β signaling also led to a decrease in IL4 and IL13 concentrations, which drive the Th2 responses characteristic of schistosomiasis lung pathology. Lungs of patients with schistosomiasis-associated PAH have evidence of TGF-β signaling in their remodeled pulmonary arteries. Conclusions —Experimental S. mansoni -induced pulmonary vascular disease relies on canonical TGF-β signaling.
Linda Sanders - One of the best experts on this subject based on the ideXlab platform.
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transforming growth factor β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background—The pathogenic mechanisms underlying pulmonary arterial hypertension resulting from schistosomiasis, one of the most common causes of pulmonary hypertension worldwide, remain unknown. We hypothesized that transforming growth factor-β (TGF-β) signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results—Mice sensitized and subsequently challenged with Schistosoma mansoni eggs developed pulmonary hypertension associated with an increase in right ventricular systolic pressure, thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase–dependent vasoconstriction accounted for ≈60% of the increase in right ventricular systolic pressure. The pulmonary vascular remodeling and pulmonary hypertension were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma-induced pulmonary hypertension. Blockade of TGF-...
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tgf β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background —The pathogenic mechanisms underlying pulmonary arterial hypertension (PAH) due to schistosomiasis, one of the most common causes of pulmonary hypertension (PH) worldwide, remains unknown. We hypothesized that TGF-β signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results —Mice sensitized and subsequently challenged with S. mansoni eggs developed PH associated with an increase in right ventricular systolic pressure (RVSP), thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase dependent vasoconstriction accounted for about 60% of the increase in RVSP. The pulmonary vascular remodeling and PH were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma -induced PH. Blockade of TGF-β signaling also led to a decrease in IL4 and IL13 concentrations, which drive the Th2 responses characteristic of schistosomiasis lung pathology. Lungs of patients with schistosomiasis-associated PAH have evidence of TGF-β signaling in their remodeled pulmonary arteries. Conclusions —Experimental S. mansoni -induced pulmonary vascular disease relies on canonical TGF-β signaling.
Jacob J Chabon - One of the best experts on this subject based on the ideXlab platform.
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transforming growth factor β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background—The pathogenic mechanisms underlying pulmonary arterial hypertension resulting from schistosomiasis, one of the most common causes of pulmonary hypertension worldwide, remain unknown. We hypothesized that transforming growth factor-β (TGF-β) signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results—Mice sensitized and subsequently challenged with Schistosoma mansoni eggs developed pulmonary hypertension associated with an increase in right ventricular systolic pressure, thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase–dependent vasoconstriction accounted for ≈60% of the increase in right ventricular systolic pressure. The pulmonary vascular remodeling and pulmonary hypertension were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma-induced pulmonary hypertension. Blockade of TGF-...
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tgf β signaling promotes pulmonary hypertension caused by schistosoma mansoni
Circulation, 2013Co-Authors: Brian B Graham, Jacob J Chabon, Liya Gebreab, Jennifer Poole, Elias Debella, Laura Davis, Takeshi Tanaka, Linda Sanders, Nina Dropcho, Angela BandeiraAbstract:Background —The pathogenic mechanisms underlying pulmonary arterial hypertension (PAH) due to schistosomiasis, one of the most common causes of pulmonary hypertension (PH) worldwide, remains unknown. We hypothesized that TGF-β signaling as a consequence of Th2 inflammation is critical for the pathogenesis of this disease. Methods and Results —Mice sensitized and subsequently challenged with S. mansoni eggs developed PH associated with an increase in right ventricular systolic pressure (RVSP), thickening of the pulmonary Artery Media, and right ventricular hypertrophy. Rho-kinase dependent vasoconstriction accounted for about 60% of the increase in RVSP. The pulmonary vascular remodeling and PH were dependent on increased TGF-β signaling, as pharmacological blockade of the TGF-β ligand and receptor, and mice lacking Smad3 were significantly protected from Schistosoma -induced PH. Blockade of TGF-β signaling also led to a decrease in IL4 and IL13 concentrations, which drive the Th2 responses characteristic of schistosomiasis lung pathology. Lungs of patients with schistosomiasis-associated PAH have evidence of TGF-β signaling in their remodeled pulmonary arteries. Conclusions —Experimental S. mansoni -induced pulmonary vascular disease relies on canonical TGF-β signaling.
