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Source: Am J Physiol Lung Ce...
Condition: Hypertension

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Total 17 results found since Jan 2013.

Contribution of TRPC channels in human and experimental pulmonary arterial hypertension
Am J Physiol Lung Cell Mol Physiol. 2023 Jun 27. doi: 10.1152/ajplung.00011.2023. Online ahead of print.ABSTRACTPulmonary arterial hypertension (PAH) is due to progressive distal pulmonary artery (PA) obstruction leading to right ventricular hypertrophy and failure. Exacerbated store-operated Ca2+ entry (SOCE) contributes to PAH pathogenesis, mediating human PA smooth muscle cells (hPASMCs) abnormalities. The transient receptor potential canonical channels (TRPC family) are Ca2+-permeable channels contributing to SOCE in different cell types, including PASMCs. However, the properties, signaling pathways, and contribution t...
Source: Am J Physiol Lung Ce... - June 27, 2023 Category: Respiratory Medicine Authors: Bastien Masson Ana ïs Saint-Martin Willer Mary Dutheil Lucille Penalva H élène Le Ribeuz Kristelle El Jekmek Yann Ruchon Sylvia Cohen-Kaminsky Jessica Sabourin Marc Humbert Olaf Mercier David Montani V éronique Capuano Fabrice Antigny Source Type: research

Mechanosensitive channel Piezo1 is required for pulmonary artery smooth muscle cell proliferation
Am J Physiol Lung Cell Mol Physiol. 2022 Mar 23. doi: 10.1152/ajplung.00447.2021. Online ahead of print.ABSTRACTConcentric pulmonary vascular wall thickening due partially to increased PASMC proliferation contributes to elevating PVR in patients with pulmonary hypertension (PH). While pulmonary vasoconstriction may be an early contributor to increasing PVR, the transition of contractile PASMCs to proliferative PASMCs may play an important role in the development and progression of pulmonary vascular remodeling in PH. A rise in cytosolic Ca2+ concentration ([Ca2+]cyt) is a trigger for PASMC contraction and proliferation. He...
Source: Am J Physiol Lung Ce... - March 23, 2022 Category: Respiratory Medicine Authors: Jiyuan Chen Marisela Rodriguez Jinrui Miao Jing Liao Pritesh Prakash Jain Manjia Zhao Tengteng Zhao Aleksandra Babicheva Ziyi Wang Sophia Parmisano Ryan Powers Moreen Matti Cole Paquin Zahra Soroureddin John Y-J Shyy Patricia A Thistlethwaite Ayako Makino Source Type: research

Pulmonary artery smooth muscle cell HIF-1 α regulates endothelin expression via microRNA-543.
Pulmonary artery smooth muscle cell HIF-1α regulates endothelin expression via microRNA-543. Am J Physiol Lung Cell Mol Physiol. 2018 May 10;: Authors: Wang CC, Ying L, Barnes EA, Adams ES, Kim FY, Engel KW, Alvira CM, Cornfield DN Abstract Pulmonary artery smooth muscle cells (PASMC) express endothelin (ET-1) which modulates the pulmonary vascular response to hypoxia. Although cross-talk between hypoxia-inducible factor-1α (HIF-1α), an O2-sensitive transcription factor, and ET-1 is established, the cell-specific relationship between HIF-1α and ET-1 expression remains incompletely understood. We t...
Source: Am J Physiol Lung Ce... - May 10, 2018 Category: Respiratory Medicine Authors: Wang CC, Ying L, Barnes EA, Adams ES, Kim FY, Engel KW, Alvira CM, Cornfield DN Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPK α1 signaling.
Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPKα1 signaling. Am J Physiol Lung Cell Mol Physiol. 2017 Feb 17;:ajplung.00117.2016 Authors: Xue J, Nelin LD, Chen B Abstract Pulmonary artery smooth muscle cell (PASMC) proliferation is one of the hallmark features of hypoxia-induced pulmonary hypertension. With only supportive treatment options available for this life threatening disease, treating and preventing the proliferation of PASMCs is a viable therapeutic option. A key promoter of hypoxia-induced increases in the number of via...
Source: Am J Physiol Lung Ce... - February 16, 2017 Category: Respiratory Medicine Authors: Xue J, Nelin LD, Chen B Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Histone deacetylation contributes to low extracellular superoxide dismutase expression in human idiopathic pulmonary arterial hypertension.
Abstract Epigenetic mechanisms, including DNA methylation and histone acetylation, regulate gene expression in idiopathic pulmonary arterial hypertension (IPAH). These mechanisms can modulate expression of extracellular superoxide dismutase (SOD3 or EC-SOD), a key vascular antioxidant enzyme, and loss of vascular SOD3 worsens outcomes in animal models of PAH. We hypothesized that SOD3 gene expression is decreased in patients with IPAH due to aberrant DNA methylation and/or histone deacetylation. We used lung tissue and pulmonary artery smooth muscle cells (PASMC) from subjects with IPAH at transplantation and fail...
Source: Am J Physiol Lung Ce... - May 26, 2016 Category: Respiratory Medicine Authors: Nozik-Grayck E, Woods C, Stearman RS, Venkataraman S, Ferguson BS, Swain K, Bowler RP, Geraci MW, Ihida-Stansbury K, Stenmark KR, McKinsey TA, Domann FE Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells.
This study examined the non-canonical signaling consequences of BMPR2 silencing in human pulmonary artery endothelial cells to identify potential therapeutic targets. BMPR2 siRNA silencing resulted in a proliferative, pro-migratory pulmonary artery endothelial cell phenotype and disruption of cytoskeletal architecture. Expression profiling closely reflected these phenotypic changes. Gene set enrichment and promoter analyses, as well as the differential expression of pathway components identified Ras/Raf/ERK signaling as an important consequence of BMPR2 silencing. Raf family members and ERK1/2 were constitutively activated...
Source: Am J Physiol Lung Ce... - November 20, 2015 Category: Respiratory Medicine Authors: Awad KS, Elinoff JM, Wang S, Gairhe S, Ferreyra GA, Cai R, Sun J, Solomon MA, Danner RL Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research