ArticleFree radical biology & medicine2012
NAD(P)H oxidase-dependent intracellular and extracellular O2•- production in coronary arterial myocytes from CD38 knockout mice.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Review
- Review
- Lysosome Function in Cardiovascular Diseases.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021Review
- Lysosomal TRPML1 Channel: Implications in Cardiovascular and Kidney Diseases.Advances in experimental medicine and biology · 2021Article
- Downregulation of Lysosomal Acid Ceramidase Mediates HMGB1-Induced Migration and Proliferation of Mouse Coronary Arterial Myocytes.Frontiers in cell and developmental biology · 2020Article
- Contribution of cathepsin B-dependent Nlrp3 inflammasome activation to nicotine-induced endothelial barrier dysfunction.European journal of pharmacology · 2019Article
- Contribution of transcription factor EB to adipoRon-induced inhibition of arterial smooth muscle cell proliferation and migration.American journal of physiology. Cell physiology · 2019Article
- Activation of TFEB ameliorates dedifferentiation of arterial smooth muscle cells and neointima formation in mice with high-fat diet.Cell death & disease · 2019Article
- Inhibitory effects of growth differentiation factor 11 on autophagy deficiency-induced dedifferentiation of arterial smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2019Article
- Protective Role of Autophagy in Nlrp3 Inflammasome Activation and Medial Thickening of Mouse Coronary Arteries.The American journal of pathology · 2018Article
- Contribution of p62/SQSTM1 to PDGF-BB-induced myofibroblast-like phenotypic transition in vascular smooth muscle cells lacking Smpd1 gene.Cell death & disease · 2018Article
- Improvement of vascular dysfunction by argirein through inhibiting endothelial cell apoptosis associated with ET-1/Nox4 signal pathway in diabetic rats.Scientific reports · 2018Article
- Implication of CD38 gene in autophagic degradation of collagen I in mouse coronary arterial myocytes.Frontiers in bioscience (Landmark edition) · 2017Article
- Contribution of p62 to Phenotype Transition of Coronary Arterial Myocytes with Defective Autophagy.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017Article
- Regulation of dynein-mediated autophagosomes trafficking by ASM in CASMCs.Frontiers in bioscience (Landmark edition) · 2016Article
- Contribution of Nrf2 to Atherogenic Phenotype Switching of Coronary Arterial Smooth Muscle Cells Lacking CD38 Gene.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015Article
- Enhancement of dynein-mediated autophagosome trafficking and autophagy maturation by ROS in mouse coronary arterial myocytes.Journal of cellular and molecular medicine · 2014Article
- Control of autophagy maturation by acid sphingomyelinase in mouse coronary arterial smooth muscle cells: protective role in atherosclerosis.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Defective autophagosome trafficking contributes to impaired autophagic flux in coronary arterial myocytes lacking CD38 gene.Cardiovascular research · 2014Article
- Roles and mechanisms of the CD38/cyclic adenosine diphosphate ribose/Ca(2+) signaling pathway.World journal of biological chemistry · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Activation of NAD(P)H oxidase has been reported to produce superoxide (O(2)(•-)) extracellularly as an autocrine/paracrine regulator or intracellularly as a signaling messenger in a variety of mammalian cells. However, it remains unknown how the activity of NAD(P)H oxidase is regulated in arterial myocytes. Recently, CD38-associated ADP-ribosylcyclase has been reported to use an NAD(P)H oxidase product, NAD(+) or NADP(+), to produce cyclic ADP-ribose (cADPR) or nicotinic acid adenine dinucleotide phosphate, which mediates intracellular Ca(2+) signaling. This study was designed to test a hypothesis that the CD38/cADPR pathway as a downstream event exerts feedback regulatory action on the NAD(P)H oxidase activity in production of extra- or intracellular O(2)(•-) in mouse coronary arterial myocytes (CAMs). By fluorescence microscopic imaging, we simultaneously monitored extra- and intracellular O(2)(•-) production in wild-type (CD38(+/+)) and CD38 knockout (CD38(-/-)) CAMs in response to oxotremorine (OXO), a muscarinic type 1 receptor agonist. It was found that CD38 deficiency prevented OXO-induced intracellular but not extracellular O(2)(•-) production in CAMs. Consistently, the OXO-induced intracellular O(2)(•-) production was markedly inhibited by CD38 shRNA or the CD38 inhibitor nicotinamide in CD38(+/+) CAMs. Further, Nox4 siRNA inhibited OXO-induced intracellular but not extracellular O(2)(•-) production, whereas Nox1 siRNA attenuated both intracellular and extracellular O(2)(•-) production in CD38(+/+) CAMs. Direct delivery of exogenous cADPR into CAMs markedly elevated intracellular Ca(2+) and O(2)(•-) production in CD38(-/-) CAMs. Functionally, CD38 deficiency or Nox1 siRNA and Nox4 siRNA prevented OXO-induced contraction in isolated perfused coronary arteries in CD38 WT mice. These results provide direct evidence that the CD38/cADPR pathway is an important controller of Nox4-mediated intracellular O(2)(•-) production and that CD38-dependent intracellular O(2)(•-) production is augmented in an autocrine manner by CD38-independent Nox1-derived extracellular O(2)(•-) production in CAMs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.