Product Citations: 73

Insights From Amniotic and Umbilical Cord Mesenchymal Stem Cells in Wound Healing.

In Journal of Cellular and Molecular Medicine on 1 June 2025 by Shen, N. E., Wu, Y., et al.

Skin repair is a complex physiological process that involves the coordinated actions of various cell types. This study examines the distinct roles of amniotic mesenchymal stem cells (A-MSCs) and umbilical cord mesenchymal stem cells (UC-MSCs) in skin healing using a mouse model. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses revealed significant differences in gene expression between A-MSCs and UC-MSCs. Specifically, A-MSCs exhibited upregulation of genes associated with extracellular matrix (ECM) organisation and cell migration, thereby enhancing their tissue remodelling capabilities. In contrast, UC-MSCs demonstrate increased expression of genes involved in angiogenesis and anti-inflammatory responses, highlighting their role in creating a favourable healing environment. These findings highlight the unique therapeutic potentials of A-MSCs and UC-MSCs in skin repair strategies. Although MSCs hold promise in regenerative medicine, challenges such as optimal cell selection and modulation of the inflammatory microenvironment remain to be addressed. Our research emphasises the need for continued research related to properties of MSCs to refine therapeutic approaches for effective wound healing.
© 2025 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

  • Biochemistry and Molecular biology
  • Stem Cells and Developmental Biology

CD34 serves as an intrinsic innate immune guardrail protecting stem cells from replicating retroviruses

Preprint on BioRxiv : the Preprint Server for Biology on 17 March 2025 by He, S., Haikerwal, A., et al.

Stem cells are highly resistant to viral infection compared to their differentiated progeny, and this resistance is associated with stem cell-specific restriction factors and intrinsic interferon stimulated genes (ISGs). In HIV infection, proviral DNA has been detected in certain bone marrow hematopoietic stem cells, yet widespread stem cell infection in vivo is restricted. Intriguingly, exposing bone marrow stem cells to HIV in vitro led to viral replication selectively only in the CD34 - population, but not in the CD34 + cells. The mechanism dictating this CD34-based HIV restriction remained a mystery, especially since HIV has a capacity to antagonize restriction factors and ISGs. CD34 is a common marker of hematopoietic stem and progenitor cells. Here, we report the intrinsic antiviral properties of CD34. Expression of CD34 in HIV-1 producer cells results in the loss of progeny virion infectivity. Conversely, removal of CD34 using CRISPR/Cas9 knockout or stem cell differentiation cytokines promotes HIV-1 replication in stem cells. These results suggest that in addition to restriction factors and intrinsic ISGs, CD34 serves as a host innate protection preventing retrovirus replication in stem cells. Mechanistically, CD34 does not block viral entry, integration, and release. Instead, it becomes incorporated onto progeny virions, which inactivates virus infectivity. These findings offer new insights into innate immunity in stem cells, and highlight intriguing retrovirus-host interactions in evolution.

  • Immunology and Microbiology
  • Stem Cells and Developmental Biology

KCNQ1/Kv7, a low-voltage-gated K+ channel, regulates cardiac rhythm and glucose homeostasis. While KCNQ1 mutations are associated with long-QT syndrome and type2 diabetes, its function in human pancreatic cells remains controversial. We identified a homozygous KCNQ1 mutation (R397W) in an individual with permanent neonatal diabetes melitus (PNDM) without cardiovascular symptoms. To decipher the potential mechanism(s), we introduced the mutation into human embryonic stem cells and generated islet-like organoids (SC-islets) using CRISPR-mediated homology-repair. The mutation did not affect pancreatic differentiation, but affected channel function by increasing spike frequency and Ca2+ flux, leading to insulin hypersecretion. With prolonged culturing, the mutant islets decreased their secretion and gradually deteriorated, modeling a diabetic state, which accelerated by high glucose levels. The molecular basis was the downregulated expression of voltage-activated Ca2+ channels and oxidative phosphorylation. Our study provides a better understanding of the role of KCNQ1 in regulating insulin secretion and β-cell survival in hereditary diabetes pathology.© 2024 The Authors.

While chimeric antigen receptor (CAR) T cell therapy has shown promising outcomes among patients with hematologic malignancies, it has also been associated with undesirable side-effects such as cytokine release syndrome (CRS). CRS is triggered by CAR T-cell-based activation of monocytes, which are stimulated via the CD40L-CD40R axis or via uptake of GM-CSF to secrete proinflammatory cytokines. Mouse models have been used to model CRS, but working with them is labor-intensive and they are not amenable to screening approaches. To overcome this challenge, we established two simple cell-based CRS in vitro models that entail the co-culturing of leukemic B cells with CD19-targeting CAR T cells and primary monocytes from the same donor. Upon antigen encounter, CAR T cells upregulated CD40L and released GM-CSF which in turn stimulated the monocytes to secrete IL-6. To endorse these models, we demonstrated that neutralizing antibodies or genetic disruption of the CD40L and/or CSF2 loci in CAR T cells using CRISPR-Cas technology significantly reduced IL-6 secretion by bystander monocytes without affecting the cytolytic activity of the engineered lymphocytes in vitro. Overall, our cell-based models were able to recapitulate CRS in vitro, allowing us to validate mitigation strategies based on antibodies or genome editing.

  • FC/FACS
  • Homo sapiens (Human)
  • Cell Biology
  • Immunology and Microbiology

Enzyme-free isolation of mesenchymal stem cells from decidua basalis of the human placenta.

In STAR Protocols on 15 September 2023 by Dutta Gupta, S., Sen, A., et al.

Mesenchymal stem cells (MSCs), also referred to as "medicinal signaling cells," have gained prominence as candidates for cell-based therapy and in clinical trials owing to their regenerative and therapeutic properties. Here, we present a protocol for isolating MSCs from the decidua basalis layer of human placenta using an explant culture approach. We describe steps for collecting, disinfecting, and plating placental tissue. We then detail procedures for characterizing the isolated MSCs through flow cytometry and in vitro differentiation.
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

  • Stem Cells and Developmental Biology
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