ArticlePloS one2012
Endothelin-1 augments Na⁺/H⁺ exchange activity in murine pulmonary arterial smooth muscle cells via Rho kinase.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Dexamethasone disrupts intracellular pH homeostasis to delay coronavirus infectious bronchitis virus cell entry via sodium hydrogen exchanger 3 activation.Journal of virology · 2025Article
- Unleashing the Potential of Nrf2: A Novel Therapeutic Target for Pulmonary Vascular Remodeling.Antioxidants (Basel, Switzerland) · 2023Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Hypotension in hereditary cardiomyopathy.Pflugers Archiv : European journal of physiology · 2022Article
- The antihyperlipidemic drug potassium piperonate impairs the migration and tumorigenesis of breast cancer cellsFrontiers in oncology · 2022Article
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- Cellular Pathways Promoting Pulmonary Vascular Remodeling by Hypoxia.Physiology (Bethesda, Md.) · 2020Review
- Rho kinase and NaPhysiological reports · 2018Article
- LASS2 inhibits growth and invasion of bladder cancer by regulating ATPase activity.Oncology letters · 2017Article
- Pulmonary vascular and ventricular dysfunction in the susceptible patient (2015 Grover Conference series).Pulmonary circulation · 2016Review
- High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.American journal of physiology. Renal physiology · 2016Article
- Effects and mechanism of acid rain on plant chloroplast ATP synthase.Environmental science and pollution research international · 2016Article
- Lung Circulation.Comprehensive Physiology · 2016Review
- Role of Rho kinase and Na+/H+ exchange in hypoxia-induced pulmonary arterial smooth muscle cell proliferation and migration.Physiological reports · 2016Article
- The Na+/H+ exchanger contributes to increased smooth muscle proliferation and migration in a rat model of pulmonary arterial hypertension.Physiological reports · 2016Article
- Effects and mechanism of Xin Mai Jia in a rabbit model of atherosclerosis.Experimental and therapeutic medicine · 2015Article
- Na(+)/H(+) exchange and hypoxic pulmonary hypertension.Pulmonary circulation · 2015Review
- Response of plasma membrane H+-ATPase in rice (Oryza sativa) seedlings to simulated acid rain.Environmental science and pollution research international · 2015Article
- Article
- Targeting the mevalonate cascade as a new therapeutic approach in heart disease, cancer and pulmonary disease.Pharmacology & therapeutics · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Excessive production of endothelin-1 (ET-1), a potent vasoconstrictor, occurs with several forms of pulmonary hypertension. In addition to modulating vasomotor tone, ET-1 can potentiate pulmonary arterial smooth muscle cell (PASMC) growth and migration, both of which contribute to the vascular remodeling that occurs during the development of pulmonary hypertension. It is well established that changes in cell proliferation and migration in PASMCs are associated with alkalinization of intracellular pH (pH(i)), typically due to activation of Na(+)/H(+) exchange (NHE). In the systemic vasculature, ET-1 increases pH(i), Na(+)/H(+) exchange activity and stimulates cell growth via a mechanism dependent on protein kinase C (PKC). These results, coupled with data describing elevated levels of ET-1 in hypertensive animals/humans, suggest that ET-1 may play an important role in modulating pH(i) and smooth muscle growth in the lung; however, the effect of ET-1 on basal pH(i) and NHE activity has yet to be examined in PASMCs. Thus, we used fluorescent microscopy in transiently (3-5 days) cultured rat PASMCs and the pH-sensitive dye, BCECF-AM, to measure changes in basal pH(i) and NHE activity induced by increasing concentrations of ET-1 (10(-10) to 10(-8) M). We found that application of exogenous ET-1 increased pH(i) and NHE activity in PASMCs and that the ET-1-induced augmentation of NHE was prevented in PASMCs pretreated with an inhibitor of Rho kinase, but not inhibitors of PKC. Moreover, direct activation of PKC had no effect on pH(i) or NHE activity in PASMCs. Our results indicate that ET-1 can modulate pH homeostasis in PASMCs via a signaling pathway that includes Rho kinase and that, in contrast to systemic vascular smooth muscle, activation of PKC does not appear to be an important regulator of PASMC pH(i).
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Registered trials
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