ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
Role of hypoxia-induced transglutaminase 2 in pulmonary artery smooth muscle cell proliferation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 42 citations in OpenAlex.
- Beyond neurotransmission: the roles of serotonylation in physiological and pathological processes.Cellular & molecular biology letters · 2026Review
- Targeting transglutaminase 2 mediated exostosin glycosyltransferase 1 signaling in liver cancer stem cells with acyclic retinoid.Cell death & disease · 2023Article
- Calcium-sensing receptor in the development and treatment of pulmonary hypertension.Molecular biology reports · 2021Review
- Substrates, inhibitors, and probes of mammalian transglutaminase 2.Analytical biochemistry · 2020Review
- Increased Transglutaminase 2 Expression and Activity in Rodent Models of Obesity/Metabolic Syndrome and Aging.Frontiers in physiology · 2020Article
- Glycolysis regulated transglutaminase 2 activation in cardiopulmonary fibrogenic remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- CrossTalk proposal: The mouse SuHx model is a good model of pulmonary arterial hypertension.The Journal of physiology · 2019Article
- Role of TG2-Mediated SERCA2 Serotonylation on Hypoxic Pulmonary Vein Remodeling.Frontiers in pharmacology · 2019Article
- Serotonylation: Serotonin Signaling and Epigenetics.Frontiers in molecular neuroscience · 2019Review
- Cystatin F involvement in adenosine AScientific reports · 2018Article
- Mechanobiological Feedback in Pulmonary Vascular Disease.Frontiers in physiology · 2018Review
- Switching-Off Adora2b in Vascular Smooth Muscle Cells Halts the Development of Pulmonary Hypertension.Frontiers in physiology · 2018Article
- Transglutaminase 2 in pulmonary and cardiac tissue remodeling in experimental pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- How cells channel their stress: Interplay between Piezo1 and the cytoskeleton.Seminars in cell & developmental biology · 2017Review
- Inflammation, Autoimmunity, and Hypertension: The Essential Role of Tissue Transglutaminase.American journal of hypertension · 2017Review
- Emerging concepts in smooth muscle contributions to airway structure and function: implications for health and disease.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Update on novel targets and potential treatment avenues in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Transglutaminase is a Critical Link Between Inflammation and Hypertension.Journal of the American Heart Association · 2016Article
- Notoginsenoside Rb1 inhibits activation of ERK and p38 MAPK pathways induced by hypoxia and hypercapnia.Experimental and therapeutic medicine · 2016Article
- Effect of hypoxia on TRPV1 and TRPV4 channels in rat pulmonary arterial smooth muscle cells.Pflugers Archiv : European journal of physiology · 2016Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We previously reported that transglutaminase 2 (TG2) activity is markedly elevated in lungs of hypoxia-exposed rodent models of pulmonary hypertension (PH). Since vascular remodeling of pulmonary artery smooth muscle cells (PASMCs) is important in PH, we undertook the present study to determine whether TG2 activity is altered in PASMCs with exposure to hypoxia and whether that alteration participates in their proliferative response to hypoxia. Cultured distal bovine (b) and proximal human (h) PASMCs were exposed to hypoxia (3% O2) or normoxia (21% O2). mRNA and protein expression were determined by PCR and Western blot analyses. TG2 activity and function were visualized and determined by fluorescent labeled 5-pentylamine biotin incorporation and immunoblotting of serotonylated fibronectin. Cell proliferation was assessed by [(3)H]thymidine incorporation assay. At 24 h, both TG2 expression and activity were stimulated by hypoxia in bPASMCs. Activation of TG2 by hypoxia was blocked by inhibition of the extracellular calcium-sensing receptor or the transient receptor potential channel V4. In contrast, TG2 expression was blocked by inhibition of the transcription factor hypoxia-inducible factor-1α, supporting the presence of separate mechanisms for stimulation of activity and expression of TG2. Pulmonary arterial hypertension patient-derived hPASMCs were found to proliferate significantly more rapidly and respond to hypoxia more strongly than control-derived hPASMCs. Similar to bovine cells, hypoxia-induced proliferation of patient-derived cells was blocked by inhibition of TG2 activity. Our results suggest an important role for TG2, mediated by intracellular calcium fluxes and HIF-1α, in hypoxia-induced PASMC proliferation and possibly in vascular remodeling in PH.
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