ArticleThe Journal of biological chemistry2014
Heparin prevents intracellular hyaluronan synthesis and autophagy responses in hyperglycemic dividing mesangial cells and activates synthesis of an extensive extracellular monocyte-adhesive hyaluronan matrix after completing cell division.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Enoxaparin preserves cellular morphology and modulates mitophagy-associated Parkin-LC3 in acute ischemic rat myocardium.Revista da Associacao Medica Brasileira (1992) · 2025Article
- Multifaceted Heparin: Diverse Applications beyond Anticoagulant Therapy.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The Mechanism of Hyperglycemia-Induced Renal Cell Injury in Diabetic Nephropathy Disease: An Update.Life (Basel, Switzerland) · 2023Review
- Heparin binding proteins on monocyte cell surfaces regulates pre-inflammatory responses in diabetes.Journal of allergy and infectious diseases · 2023Article
- Non-reducing End of Heparin Tri-saccharide is a Scavenger Tool to Detoxify the Glucose Toxicity in Diabetes.Journal of cellular immunology · 2023Article
- Modulation of hyaluronan signaling as a therapeutic target in human disease.Pharmacology & therapeutics · 2022Review
- Article
- Heparin inhibits proinflammatory and promotes anti-inflammatory macrophage polarization under hyperglycemic stress.The Journal of biological chemistry · 2020Article
- Heparin affects cytosolic glucose responses of hyperglycemic dividing mesangial cells.The Journal of biological chemistry · 2019Article
- Cardiac fibroblast activation and hyaluronan synthesis in response to hyperglycemia and diet-induced insulin resistance.Scientific reports · 2019Article
- The journey of hyaluronan research in theThe Journal of biological chemistry · 2019Review
- Endothelial Glycocalyx as a Shield Against Diabetic Vascular Complications: Involvement of Hyaluronan and Hyaluronidases.Arteriosclerosis, thrombosis, and vascular biology · 2018Review
- Molecular Functions of Glycoconjugates in Autophagy.Journal of molecular biology · 2016Review
- myo-Inositol Oxygenase Overexpression Accentuates Generation of Reactive Oxygen Species and Exacerbates Cellular Injury following High Glucose Ambience: A NEW MECHANISM RELEVANT TO THE PATHOGENESIS OF DIABETIC NEPHROPATHY.The Journal of biological chemistry · 2016Article
- The Responses of Hyperglycemic Dividing Mesangial Cells to Heparin Are Mediated by the Non-reducing Terminal Trisaccharide.The Journal of biological chemistry · 2015Article
- Heparin interaction with a receptor on hyperglycemic dividing cells prevents intracellular hyaluronan synthesis and autophagy responses in models of type 1 diabetes.Matrix biology : journal of the International Society for Matrix Biology · 2015Review
- Regulation of synthesis and roles of hyaluronan in peritoneal dialysis.BioMed research international · 2015Review
- Hyperglycemia diverts dividing stem cells to pathological adipogenesis.Stem cell research & therapy · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Growth-arrested rat mesangial cells (RMCs) at a G0/G1 interphase stimulated to divide in hyperglycemic medium initiate intracellular hyaluronan synthesis that induces autophagy/cyclin D3-induced formation of a monocyte-adhesive extracellular hyaluronan matrix after completing cell division. This study shows that heparin inhibits the intracellular hyaluronan synthesis and autophagy responses, but at the end of cell division it induces synthesis of a much larger extracellular monocyte-adhesive hyaluronan matrix. Heparin bound to RMC surfaces by 1 h, internalizes into the Golgi/endoplasmic reticulum region by 2 h, and was nearly gone by 4 h. Treatment by heparin for only the first 4 h was sufficient for its function. Streptozotocin diabetic rats treated daily with heparin showed similar results. Glomeruli in sections of diabetic kidneys showed extensive accumulation of autophagic RMCs, increased hyaluronan matrix, and influx of macrophages over 6 weeks. Hyaluronan staining in the glomeruli of heparin-treated diabetic rats was very high at week 1 and decreased to near control level by 6 weeks without any RMC autophagy. However, the influx of macrophages by 6 weeks was as pronounced as in diabetic glomeruli. The results are as follows: 1) heparin blocks synthesis of hyaluronan in intracellular compartments, which prevents the autophagy and cyclin D3 responses thereby allowing RMCs to complete cell division and sustain function; 2) interaction of heparin with RMCs in early G1 phase is sufficient to induce signaling pathway(s) for its functions; and 3) influxed macrophages effectively remove the hyaluronan matrix without inducing pro-fibrotic responses that lead to nephropathy and proteinurea in diabetic kidneys.
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