Background: The effect of hypoxia on mesenchymal stem cells (MSCs) is an emerging topic in MSC biology. Although long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) are reported to play a critical role in regulating the biological characteristics of MSCs, their specific expression and co-expression profiles in human placenta-derived MSCs (hP-MSCs) under hypoxia and the underlying mech anisms of lncRNAs in hP-MSC biology are unknown.
Aim: To reveal the specific expression profiles of lncRNAs in hP-MSCs under hypoxia and initially explored the possible mechanism of lncRNAs on hP-MSC biology.
Methods: Here, we used a multigas incubator (92.5% N, 5% CO, and 2.5% O) to mimic the hypoxia condition and observed that hypoxic culture significantly promoted the proliferation potential of hP-MSCs. RNA sequencing technology was applied to identify the exact expression profiles of lncRNAs and mRNAs under hypoxia.
Results: We identified 289 differentially expressed lncRNAs and 240 differentially expressed mRNAs between the hypoxia and normoxia groups. Among them, the lncRNA was upregulated under hypoxia, which was also validated by reverse transcription-polymerase chain reaction. was confirmed to affect hP-MSC proliferation rates using a knockdown model. overexpression could significantly enhance the proliferation capacity of hP-MSCs, activate the PI3K/AKT pathway, and upregulate the expression of cell cycle-related proteins.
Conclusion: Our results revealed the specific expression characteristics of lncRNAs and mRNAs in hypoxia-cultured hP-MSCs and that lncRNA can promote hP-MSC proliferation through the PI3K/AKT pathway.
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http://dx.doi.org/10.4252/wjsc.v14.i9.714 | DOI Listing |
PLoS One
January 2025
Integrative Multiomics Lab, School of Bio Sciences and Technology, Vellore Institute of Technology, Vellore, Tamil Nadu, India.
Background: Rheumatoid arthritis (RA) is a degenerative autoimmune disease, often managed through symptomatic treatment. The co-occurrence of the reported extra-articular comorbidities such as inflammatory bowel disease (IBD), and dementia may complicate the pathology of the disease as well as the treatment strategies. Therefore, in our study, we aim to elucidate the key genes, and regulatory elements implicated in the progression and association of these diseases, thereby highlighting the linked potential therapeutic targets.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200083, China.
To investigate the effect of icariin (ICA) on hepatocellular carcinoma (HCC) and its autophagy/apoptosis mechanism in HCC. The anti-HCC mechanism of ICA was investigated using HCC cells treated with 20 µmol/L ICA. Cell viability and proliferation were assessed using CCK-8 and colony formation assays, respectively, while TUNEL staining evaluated anti-apoptotic effects.
View Article and Find Full Text PDFDiscov Oncol
January 2025
Department of Thyroid Surgery, The First Affiliated Hospital of Jinan University, No. 613, W. Huangpu Avenue, Tianhe District, Guangzhou, 510630, China.
Background: Accurately distinguishing lymph node metastases (LNM) from papillary thyroid carcinomas (PTC) is crucial in clinical practice. The role of the immune system in PTC-LNM has attracted increasing attention. The aim of the present study was to evaluate the differential expression of 92 immune-related proteins in the serum and identify their potential diagnostic effects in patients with PTC-LNM.
View Article and Find Full Text PDFActa Neurobiol Exp (Wars)
January 2025
Laboratory of Animal Models, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene is a critical tumor suppressor that plays an essential role in the development and functionality of the central nervous system. Located on chromosome 10 in humans and chromosome 19 in mice, PTEN encodes a protein that regulates cellular processes such as division, proliferation, growth, and survival by antagonizing the PI3K‑Akt‑mTOR signaling pathway. In neurons, PTEN dephosphorylates phosphatidylinositol‑3,4,5‑trisphosphate (PIP3) to PIP2, thereby modulating key signaling cascades involved in neurogenesis, neuronal migration, and synaptic plasticity.
View Article and Find Full Text PDFPlatelets
December 2025
Department of Pharmacology and Physiology, George Washington University, Washington, DC, USA.
Platelet-like particles (PLPs), derived from megakaryocytic cell lines MEG-01 and K-562, are widely used as a surrogate to study platelet formation and function. We demonstrate by RNA-Seq that PLPs are transcriptionally distinct from platelets. Expression of key genes in signaling pathways promoting platelet activation/aggregation, such as the PI3K/AKT, protein kinase A, phospholipase C, and α-adrenergic and GP6 receptor pathways, was missing or under-expressed in PLPs.
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