The Experts below are selected from a list of 2100 Experts worldwide ranked by ideXlab platform
Jahar Bhattacharya - One of the best experts on this subject based on the ideXlab platform.
-
Mechano-oxidative coupling by mitochondria induces proinflammatory responses in Lung venular capillaries
The Journal of clinical investigation, 2003Co-Authors: Hideo Ichimura, Kaushik Parthasarathi, Sadiqa K. Quadri, Andrew C. Issekutz, Jahar BhattacharyaAbstract:Elevation of Lung Capillary Pressure causes exocytosis of the leukocyte adhesion receptor P-selectin in endothelial cells (ECs), indicating that Lung ECs generate a proinflammatory response to Pressureinduced stress. To define underlying mechanisms, we followed the EC signaling sequence leading to P-selectin exocytosis through application of real-time, in situ fluorescence microscopy in Lung capillaries. Pressure elevation increased the amplitude of cytosolic Ca2+ oscillations that triggered increases in the amplitude of mitochondrial Ca 2+ oscillations and in reactive oxygen species (ROS) production. Responses to blockers of the Ca2+ oscillations and of mitochondrial electron transport indicated that the ROS production was Ca 2+ dependent and of mitochondrial origin. A new proinflammatory mechanism was revealed in that Pressure-induced exocytosis of P-selectin was inhibited by both antioxidants and mitochondrial inhibitors, indicating that the exocytosis was driven by mitochondrial ROS. In this signaling pathway mitochondria coupled Pressure-induced Ca2+ oscillations to the production of ROS that in turn acted as diffusible messengers to activate P-selectin exocytosis. These findings implicate mitochondrial mechanisms in the Lung’s proinflammatory response to Pressure elevation and identify mitochondrial ROS as critical to P-selectin exocytosis in Lung Capillary ECs. J. Clin. Invest. 111:691‐699 (2003). doi:10.1172/JCI200317271.
-
Vascular regulation of type II cell exocytosis
American journal of physiology. Lung cellular and molecular physiology, 2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2+concentration ([Ca2+]i) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH2O increased septal Capillary diameter by 26% and induced marked alveolar [Ca2+]i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid-AM, the intracellular Ca2+ chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was comple...
-
Vascular regulation of type II cell exocytosis : Mechanotransduction in the Lung
American Journal of Physiology-lung Cellular and Molecular Physiology, 2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca 2+ concentration ([Ca 2+ ] i ) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH 2 O increased septal Capillary diameter by 26% and induced marked alveolar [Ca 2+ ] i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca 2+ ] i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, the intracellular Ca 2+ chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was completely inhibited. We conclude that Capillary Pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca 2+ -dependent manner but is sustained by Ca 2+ -independent mechanisms.
-
Mechanotransduction in the Lung Vascular regulation of type II cell exocytosis
2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:Wang, P. M., E. Fujita, and J. Bhattacharya. Vascular regulation of type II cell exocytosis. Am J Physiol Lung Cell Mol Physiol 282: L912–L916, 2002. First published January 4, 2002; 10.1152/ajpLung.00303.2001.—To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2 concentration ([Ca2 ]i) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH2O increased septal Capillary diameter by 26% and induced marked alveolar [Ca2 ]i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca2 ]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2aminophenoxy)ethane-N,N,N ,N -tetraacetic acid-AM, the intracellular Ca2 chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was completely inhibited. We conclude that Capillary Pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca2 -dependent manner but is sustained by Ca2 independent mechanisms.
Ping M Wang - One of the best experts on this subject based on the ideXlab platform.
-
Vascular regulation of type II cell exocytosis
American journal of physiology. Lung cellular and molecular physiology, 2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2+concentration ([Ca2+]i) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH2O increased septal Capillary diameter by 26% and induced marked alveolar [Ca2+]i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid-AM, the intracellular Ca2+ chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was comple...
-
Vascular regulation of type II cell exocytosis : Mechanotransduction in the Lung
American Journal of Physiology-lung Cellular and Molecular Physiology, 2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca 2+ concentration ([Ca 2+ ] i ) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH 2 O increased septal Capillary diameter by 26% and induced marked alveolar [Ca 2+ ] i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca 2+ ] i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, the intracellular Ca 2+ chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was completely inhibited. We conclude that Capillary Pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca 2+ -dependent manner but is sustained by Ca 2+ -independent mechanisms.
-
Mechanotransduction in the Lung Vascular regulation of type II cell exocytosis
2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:Wang, P. M., E. Fujita, and J. Bhattacharya. Vascular regulation of type II cell exocytosis. Am J Physiol Lung Cell Mol Physiol 282: L912–L916, 2002. First published January 4, 2002; 10.1152/ajpLung.00303.2001.—To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2 concentration ([Ca2 ]i) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH2O increased septal Capillary diameter by 26% and induced marked alveolar [Ca2 ]i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca2 ]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2aminophenoxy)ethane-N,N,N ,N -tetraacetic acid-AM, the intracellular Ca2 chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was completely inhibited. We conclude that Capillary Pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca2 -dependent manner but is sustained by Ca2 independent mechanisms.
Etsuo Fujita - One of the best experts on this subject based on the ideXlab platform.
-
Vascular regulation of type II cell exocytosis
American journal of physiology. Lung cellular and molecular physiology, 2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2+concentration ([Ca2+]i) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH2O increased septal Capillary diameter by 26% and induced marked alveolar [Ca2+]i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca2+]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid-AM, the intracellular Ca2+ chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was comple...
-
Vascular regulation of type II cell exocytosis : Mechanotransduction in the Lung
American Journal of Physiology-lung Cellular and Molecular Physiology, 2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca 2+ concentration ([Ca 2+ ] i ) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH 2 O increased septal Capillary diameter by 26% and induced marked alveolar [Ca 2+ ] i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca 2+ ] i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM, the intracellular Ca 2+ chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was completely inhibited. We conclude that Capillary Pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca 2+ -dependent manner but is sustained by Ca 2+ -independent mechanisms.
-
Mechanotransduction in the Lung Vascular regulation of type II cell exocytosis
2002Co-Authors: Ping M Wang, Etsuo Fujita, Jahar BhattacharyaAbstract:Wang, P. M., E. Fujita, and J. Bhattacharya. Vascular regulation of type II cell exocytosis. Am J Physiol Lung Cell Mol Physiol 282: L912–L916, 2002. First published January 4, 2002; 10.1152/ajpLung.00303.2001.—To determine whether Lung Capillary Pressure regulates surfactant secretion, we viewed alveoli of the constantly inflated, isolated blood-perfused rat Lung by fluorescence microscopy. By alveolar micropuncture we infused fura 2 and lamellar body (LB)-localizing dyes for fluorescence detection of, respectively, the alveolar cytosolic Ca2 concentration ([Ca2 ]i) and type II cell exocytosis. Increasing left atrial Pressure (Pla) from 5 to 10 cmH2O increased septal Capillary diameter by 26% and induced marked alveolar [Ca2 ]i oscillations that abated on relief of Pressure elevation. The rate of loss of LB fluorescence that reflects the LB exocytosis rate increased fourfold after the Pressure elevation and continued at the same rate even after Pressure and [Ca2 ]i oscillations had returned to baseline. In alveoli pretreated with either 1,2-bis(2aminophenoxy)ethane-N,N,N ,N -tetraacetic acid-AM, the intracellular Ca2 chelator, or heptanol, the gap junctional blocker, the Pressure-induced exocytosis was completely inhibited. We conclude that Capillary Pressure and surfactant secretion are mechanically coupled. The secretion initiates in a Ca2 -dependent manner but is sustained by Ca2 independent mechanisms.
Hermann Kuppe - One of the best experts on this subject based on the ideXlab platform.
-
Capillary Pressure-induced Lung injury: fact or fiction?
Current opinion in anaesthesiology, 2002Co-Authors: Wolfgang M. Kuebler, Hermann KuppeAbstract:Lung Capillary Pressure in healthy humans at rest ranges between 6 and 10 mmHg. At maximal effort or in pathophysiological conditions such as left sided heart disease or massive pulmonary vasoconstriction, for example in highaltitude pulmonary disease, Capillary Pressure may be markedly elevated. In
Wolfgang M. Kuebler - One of the best experts on this subject based on the ideXlab platform.
-
Capillary Pressure-induced Lung injury: fact or fiction?
Current opinion in anaesthesiology, 2002Co-Authors: Wolfgang M. Kuebler, Hermann KuppeAbstract:Lung Capillary Pressure in healthy humans at rest ranges between 6 and 10 mmHg. At maximal effort or in pathophysiological conditions such as left sided heart disease or massive pulmonary vasoconstriction, for example in highaltitude pulmonary disease, Capillary Pressure may be markedly elevated. In
-
Pressure-Induced Inflammatory Signaling in Lung Endothelial Cells
Cell Signaling in Vascular Inflammation, 1Co-Authors: Wolfgang M. KueblerAbstract:Elevation of Lung Capillary Pressure is a frequent clinical consequence of left-sided heart disease and characteristically results in the formation not only of pulmonary edema, but also of inflammatory reactions in the Lung. These processes are largely attributable to mechano-induced second-messenger responses in Lung Capillary endothelial cells. Pressure- and stretch-induced mobilization of intra- and extracellular calcium mediates an increase in Capillary permeability, thus contributing to pulmonary edema formation. In addition, endothelial calcium signaling promotes the exocytosis of endothelial Weibel-Palade bodies and, in consequence, vascular expression of P-selectin, thus initiating the sequestration of circulating leukocytes.
