ArticlePflugers Archiv : European journal of physiology2015
Heme oxygenase-1 regulates cell proliferation via carbon monoxide-mediated inhibition of T-type Ca2+ channels.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- T-Type Voltage-Gated Calcium Channels: Potential Regulators of Smooth Muscle Contractility.International journal of molecular sciences · 2024Review
- Potential Targets of Natural Products for Improving Cardiac Ischemic Injury: The Role of Nrf2 Signaling Transduction.Molecules (Basel, Switzerland) · 2024Review
- Heme: The Lord of the Iron Ring.Antioxidants (Basel, Switzerland) · 2023Review
- Downregulation of Vascular Hemeoxygenase-1 Leads to Vasculopathy in Systemic Sclerosis.Frontiers in physiology · 2022Article
- Kv1.3 voltage-gated potassium channels link cellular respiration to proliferation through a non-conducting mechanism.Cell death & disease · 2021Article
- Targeting Heme Oxygenase-1 in the Arterial Response to Injury and Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Up-regulation of heme oxygenase-1 expression and inhibition of disease-associated features by cannabidiol in vascular smooth muscle cells.Oncotarget · 2018Article
- Article
- The apolipoprotein A-I mimetic peptide, D-4F, restrains neointimal formation through heme oxygenase-1 up-regulation.Journal of cellular and molecular medicine · 2017Article
- Heme Oxygenases in Cardiovascular Health and Disease.Physiological reviews · 2016Review
- Mitochondria and carbon monoxide: cytoprotection and control of cell metabolism - a role for Ca(2+) ?The Journal of physiology · 2016Review
- Role of heme in cardiovascular physiology and disease.Journal of the American Heart Association · 2015Review
- Novel ways to regulate T-type Ca(2+) channels.Channels (Austin, Tex.) · 2015Article
- Neurointegrity and neurophysiology: astrocyte, glutamate, and carbon monoxide interactions.Medical gas researchReview
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Induction of the antioxidant enzyme heme oxygenase-1 (HO-1) affords cellular protection and suppresses proliferation of vascular smooth muscle cells (VSMCs) associated with a variety of pathological cardiovascular conditions including myocardial infarction and vascular injury. However, the underlying mechanisms are not fully understood. Over-expression of Cav3.2 T-type Ca(2+) channels in HEK293 cells raised basal [Ca(2+)]i and increased proliferation as compared with non-transfected cells. Proliferation and [Ca(2+)]i levels were reduced to levels seen in non-transfected cells either by induction of HO-1 or exposure of cells to the HO-1 product, carbon monoxide (CO) (applied as the CO releasing molecule, CORM-3). In the aortic VSMC line A7r5, proliferation was also inhibited by induction of HO-1 or by exposure of cells to CO, and patch-clamp recordings indicated that CO inhibited T-type (as well as L-type) Ca(2+) currents in these cells. Finally, in human saphenous vein smooth muscle cells, proliferation was reduced by T-type channel inhibition or by HO-1 induction or CO exposure. The effects of T-type channel blockade and HO-1 induction were non-additive. Collectively, these data indicate that HO-1 regulates proliferation via CO-mediated inhibition of T-type Ca(2+) channels. This signalling pathway provides a novel means by which proliferation of VSMCs (and other cells) may be regulated therapeutically.
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