Increased functional properties of diabetic platelets might be already conditioned during thrombopoiesis in the stem cell system. This hypothesis was studied by recording the distribution characteristics of the peripheral platelet pool in 218 diabetic patients versus 51 controls. Furthermore, platelet membrane coating with the stem cell marker glycoprotein IB was analyzed in 41 diabetic subjects and compared to 23 healthy volunteers. A consistent, significant shift of the volume distribution to larger platelets was found in diabetics: Mean platelet volume (MPV) - 7.9 +/- 0.9 versus 7.2 +/- 0.8 [fl]; Megathrombocyte index (MTI) - 20.4 +/- 2.8 versus 18.1 +/- 2.5 [fl]. These deviations were present in all patient subsets, however did not correlate to parameters of glucose metabolism. Whole blood platelet count was increased in the patient group; 195.0 +/- 59.5 versus 184.0 +/- 37.5 x 10(3) plts/ul. Coating with glycoprotein IB receptors correlated significantly to platelet size in platelets of both controls and diabetics (r normal = 0.52 +/- 0.07; r diabetic = 0.46 +/- 0.1). The quantitative expression of glycoprotein IB was significantly enhanced in the diabetic group: 54,500 x 1.28 +/- 1 versus 39,100 x 1.3 +/- 1 molecules per platelet. In conclusion, these findings strongly support the assumption of diabetic stem cell dysfunction of the megakaryocytic series and progenitor cells resulting in platelets with primarily increased potency to adhere and aggregate in diabetes mellitus.

Download full-text PDF

Source
http://dx.doi.org/10.1007/BF01717328DOI Listing

Publication Analysis

Top Keywords

stem cell
12
+/- versus
12
+/-
10
diabetes mellitus
8
+/- [fl]
8
diabetic
6
platelet
6
versus
5
increased
4
increased platelet
4

Similar Publications

Background: Central nervous system (CNS) tumors lead to cancer-related mortality in children. Genetic ancestry-associated cancer prevalence and outcomes have been studied, but is limited.

Methods: We performed genetic ancestry prediction in 1,452 pediatric patients with paired normal and tumor whole genome sequencing from the Open Pediatric Cancer (OpenPedCan) project to evaluate the influence of reported race and ethnicity and ancestry-based genetic superpopulations on tumor histology, molecular subtype, survival, and treatment.

View Article and Find Full Text PDF

Aims: Bone marrow mononuclear cells (BM-MNCs) are a rich source of hematopoietic stem cells that have been widely used in experimental therapies for patients with various diseases, including fractures.Activation of angiogenesis is believed to be one of the major modes of action of BM-MNCs; however, the essential mechanism by which BM-MNCs activate angiogenesis remains elusive. This study aimed to demonstrate that BM-MNCs promote bone healing by enhancing angiogenesis through direct cell-to-cell interactions via gap junctions, in addition to a previously reported method.

View Article and Find Full Text PDF

Human Oncostatin M deficiency underlies an inherited severe bone marrow failure syndrome.

J Clin Invest

January 2025

Laboratory of Genome Dynamics in the Immune, INSERM UMR 116, Équipe Labellisée LIGUE 2023, Paris, France.

Oncostatin M (OSM) is a cytokine with the unique ability to interact with both the OSM receptor (OSMR) and the leukemia inhibitory factor receptor (LIFR). On the other hand, OSMR interacts with IL31RA to form the interleukin-31 receptor. This intricate network of cytokines and receptors makes it difficult to understand the specific function of OSM.

View Article and Find Full Text PDF

Corneal Stromal Stem Cell-Derived Extracellular Vesicles Attenuate ANGPTL7 Expression in the Human Trabecular Meshwork.

Transl Vis Sci Technol

January 2025

Department of Ophthalmology, Stein Eye Institute, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.

Purpose: Regulating intraocular pressure (IOP), mainly via the trabecular meshwork (TM), is critical in developing glaucoma. Whereas current treatments aim to lower IOP, directly targeting the dysfunctional TM tissue for therapeutic intervention has proven challenging. In our study, we utilized Dexamethasone (Dex)-treated TM cells as a model to investigate how extracellular vesicles (EVs) from immortalized corneal stromal stem cells (imCSSCs) could influence ANGPTL7 and MYOC genes expression within TM cells.

View Article and Find Full Text PDF

ANKRD11 binding to cohesin suggests a connection between KBG syndrome and Cornelia de Lange syndrome.

Proc Natl Acad Sci U S A

January 2025

Shenzhen Key Laboratory of Biomolecular Assembling and Regulation, Department of Neuroscience, School of Life Sciences, Southern University of Science and Technology, Shenzhen 518055, China.

Ankyrin Repeat Domain-containing Protein 11 () is a causative gene for KBG syndrome, a significant risk factor for Cornelia de Lange syndrome (CdLS), and a highly confident autism spectrum disorder gene. Mutations of lead to developmental abnormalities in multiple organs/tissues including the brain, craniofacial and skeletal bones, and tooth structures with unknown mechanism(s). Here, we find that ANKRD11, via a short peptide fragment in its N-terminal region, binds to the cohesin complex with a high affinity, implicating why mutation can cause CdLS.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!