ArticleDiabetes2010
Transient inhibition of transforming growth factor-beta1 in human diabetic CD34+ cells enhances vascular reparative functions.
Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Resilient Calvarial Bone Marrow Supports Retinal Repair in Type 2 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Precision Medicine for Diabetic Retinopathy: Integrating Genetics, Biomarkers, Lifestyle, and AI.Genes · 2025Review
- The role of telomerase reverse transcriptase in the mitochondrial protective functions of Angiotensin-(1-7) in diabetic CD34Biochemical pharmacology · 2024Article
- Aldose Reductase as a Key Target in the Prevention and Treatment of Diabetic Retinopathy: A Comprehensive Review.Biomedicines · 2024Review
- Stem cells and diabetic retinopathy: From models to treatment.Molecular biology reports · 2023Review
- Transforming growth factor-β1/Thrombospondin-1/CD47 axis mediates dysfunction in CD34European journal of pharmacology · 2022Article
- Effect of intravitreal ranibizumab on fibrovascular membranes in patients with proliferative diabetic retinopathy.International journal of ophthalmology · 2022Article
- Transforming growth factor-β1 signalling triggers vascular endothelial growth factor resistance and monocyte dysfunction in type 2 diabetes mellitus.Journal of cellular and molecular medicine · 2021Article
- Concise review: current trends on applications of stem cells in diabetic nephropathy.Cell death & disease · 2020Review
- Adult Stem Cell Therapeutics in Diabetic Retinopathy.International journal of molecular sciences · 2019Review
- Hematopoietic stem/progenitor involvement in retinal microvascular repair during diabetes: Implications for bone marrow rejuvenation.Vision research · 2017Review
- Advances in bone marrow stem cell therapy for retinal dysfunction.Progress in retinal and eye research · 2017Review
- Stem cell therapies in the treatment of diabetic retinopathy and keratopathy.Experimental biology and medicine (Maywood, N.J.) · 2016Review
- Editorial: Cell-Based Therapies for Diabetic Microvascular Complications.Frontiers in endocrinology · 2015Article
- Growth factors/chemokines in diabetic vitreous and aqueous alter the function of bone marrow-derived progenitor (CD34⁺) cells in humans.American journal of physiology. Endocrinology and metabolism · 2014Article
- Article
- Poly-ADP-ribose-polymerase inhibition ameliorates hind limb ischemia reperfusion injury in a murine model of type 2 diabetes.Annals of surgery · 2013Article
- Circulating mononuclear progenitor cells: differential roles for subpopulations in repair of retinal vascular injury.Investigative ophthalmology & visual science · 2013Article
- Article
- Long-term type 1 diabetes influences haematopoietic stem cells by reducing vascular repair potential and increasing inflammatory monocyte generation in a murine model.Diabetologia · 2013Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
objectivePeripheral blood CD34(+) cells from diabetic patients demonstrate reduced vascular reparative function due to decreased proliferation and diminished migratory prowess, largely resulting from decreased nitric oxide (NO) bioavailability. The level of TGF-beta, a key factor that modulates stem cell quiescence, is increased in the serum of type 2 diabetic patients. We asked whether transient TGF-beta1 inhibition in CD34(+) cells would improve their reparative ability. RESEARCH DESIGN AND
methodsTo inhibit TGF-beta1 protein expression, CD34(+) cells were treated ex vivo with antisense phosphorodiamidate morpholino oligomers (TGF-beta1-PMOs) and analyzed for cell surface CXCR4 expression, cell survival in the absence of added growth factors, SDF-1-induced migration, NO release, and in vivo retinal vascular reparative ability.
resultsTGF-beta1-PMO treatment of diabetic CD34(+) cells resulted in increased expression of CXCR4, enhanced survival in the absence of growth factors, and increased migration and NO release as compared with cells treated with control PMO. Using a retinal ischemia reperfusion injury model in mice, we observed that recruitment of diabetic CD34(+) cells to injured acellular retinal capillaries was greater after TGF-beta1-PMO treatment compared with control PMO-treated cells.
conclusionsTransient inhibition of TGF-beta1 may represent a promising therapeutic strategy for restoring the reparative capacity of dysfunctional diabetic CD34(+) cells.
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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.