ArticleCell death & disease2017
Protein disulfide isomerase-mediated apoptosis and proliferation of vascular smooth muscle cells induced by mechanical stress and advanced glycosylation end products result in diabetic mouse vein graft atherosclerosis.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Cascade-Activatable Nanoprobes for NIR-II Fluorescence/Photoacoustic Dual-Modal Imaging of Atherosclerotic Plaques.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Berberine suppresses mechanical stretch-induced apoptosis and proliferation in vascular smooth muscle cells via ROS/PDI/Drp1 signaling pathway.Frontiers in pharmacology · 2026Article
- Overstretch causes lipid accumulation in vascular smooth muscle cells dependent on NADPH oxidase 1.Mechanobiology in medicine · 2025Article
- Immune Regulation and Disulfidptosis in Atherosclerosis Influence Disease Progression and Therapy.Biomedicines · 2025Article
- HRD1 reduction promotes cholesterol-induced vascular smooth muscle cell phenotypic change via endoplasmic reticulum stress.Molecular and cellular biochemistry · 2024Article
- A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures.International journal of molecular sciences · 2024Review
- Disturbed flow regulates protein disulfide isomerase A1 expression via microRNA-204.Frontiers in physiology · 2024Article
- Role of glycolysis in diabetic atherosclerosis.World journal of diabetes · 2023Review
- Efficacy and underlying mechanisms of berberine against lipid metabolic diseases: a review.Frontiers in pharmacology · 2023Review
- Role of Sp1 in atherosclerosis.Molecular biology reports · 2022Review
- Expatiating the Pharmacological and Nanotechnological Aspects of the Alkaloidal Drug Berberine: Current and Future Trends.Molecules (Basel, Switzerland) · 2022Review
- Association of Loss of Occlusal Pairs of Teeth with Sarcopenia in a Chinese Population of Community-Dwelling Elderly.The journal of nutrition, health & aging · 2022Article
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- ERO1-PDI Redox Signaling in Health and Disease.Antioxidants & redox signaling · 2021Review
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- Highland Barley and Its By-Products Enriched with Phenolic Compounds for Inhibition of Pyrraline Formation by Scavenging α-Dicarbonyl Compounds.Foods (Basel, Switzerland) · 2021Article
- Extracellular vesicles derived from oesophageal cancer containing P4HB promote muscle wasting via regulating PHGDH/Bcl-2/caspase-3 pathway.Journal of extracellular vesicles · 2021Article
- Effects of Berberine on Atherosclerosis.Frontiers in pharmacology · 2021Review
- Biomechanical signal communication in vascular smooth muscle cells.Journal of cell communication and signaling · 2020Review
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein disulfide isomerase (PDI) involves cell survival and death. Whether PDI mediates mechanical stretch stress (SS) and/or advanced glycosylation end products (AGEs) -triggered simultaneous increases in proliferation and apoptosis of vascular smooth muscle cells (VSMCs) is unknown. Here, we hypothesized that different expression levels of PDI trigger completely opposite cell fates among the different VSMC subtypes. Mouse veins were grafted into carotid arteries of non-diabetic and diabetic mice for 8 weeks; the grafted veins underwent simultaneous increases in proliferation and apoptosis, which triggered vein graft arterializations in non-diabetic or atherosclerosis in diabetic mice. A higher rate of proliferation and apoptosis was seen in the diabetic group. SS and/or AGEs stimulated the quiescent cultured VSMCs, resulting in simultaneous increases in proliferation and apoptosis; they could induce increased PDI activation and expression. Both in vivo and in vitro, the proliferating VSMCs indicated weak co-expression of PDI and SM-α-actin while apoptotic or dead cells showed strong co-expression of both. Either SS or AGEs rapidly upregulated the expression of PDI, NOX1 and ROS, and their combination had synergistic effects. Inhibiting PDI simultaneously suppressed the proliferation and apoptosis of VSMCs, while inhibition of SM-α-actin with cytochalasin D led to increased apoptosis and cleaved caspases-3 but had no effect on proliferation. In conclusion, different expression levels of PDI in VSMCs induced by SS and/or AGEs triggered a simultaneous increase in proliferation and apoptosis, accelerated vein graft arterializations or atherosclerosis, leading us to propose PDI as a novel target for the treatment of vascular remodeling and diseases.
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