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Pre-clinical and clinical studies revealed that mesenchymal stromal cell (MSC) transplants elicit tissue repair. Conditioning MSC prior to transplantation may boost their ability to support repair. We investigated macrophage-derived inflammation as a means to condition MSC by comprehensively analyzing their transcriptome and secretome. Conditioning MSC with macrophage-derived inflammation resulted in 3208 differentially expressed genes, which were annotated with significantly enriched GO terms for 1085 biological processes, 85 cellular components, and 79 molecular functions. Inflammation-mediated conditioning increased the secretion of growth factors that are key for tissue repair, including vascular endothelial growth factor, hepatocyte growth factor, nerve growth factor and glial-derived neurotrophic factor. Furthermore, we found that inflammation-mediated conditioning induces transcriptomic changes that challenge the viability and mobility of MSC. Our data support the notion that macrophage-derived inflammation stimulates MSC to augment their paracrine repair-supporting activity. The results suggest that inflammatory pre-conditioning enhances the therapeutic potential of MSC transplants.
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http://dx.doi.org/10.3390/ijms22020781 | DOI Listing |
Arch Med Res
September 2025
Department and Graduate Institute of Microbiology and Immunology, National Defense Medical Center, Taipei, Taiwan. Electronic address:
Background: Atherosclerosis, a leading cause of cardiovascular disease (CVD) mortality worldwide, is characterized by dysregulated lipid metabolism and unresolved inflammation. Macrophage-derived foam cell formation and apoptosis contribute to plaque formation and vulnerability. Elevated serum galectin-3 (Gal-3) levels are associated with increased CVD risk, and Gal-3 in plaques is strongly associated with macrophages.
View Article and Find Full Text PDFMater Today Bio
October 2025
Department of Vascular Surgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, China.
Atherosclerosis (AS) is a chronic inflammatory disease driven by endothelial dysfunction, vascular smooth muscle cell proliferation, and insufficient resolution of inflammation. Nitric oxide (NO) plays a crucial role in vascular homeostasis by promoting endothelial cell proliferation, maintaining endothelial integrity, suppressing smooth muscle cell hyperplasia, and exerting potent anti-inflammatory effects. However, clinical application of NO is hindered by its short half-life, lack of targeting, and uncontrolled release.
View Article and Find Full Text PDFJ Invest Dermatol
September 2025
Department of Surgery, University of California San Diego, La Jolla, CA, United States; Department of Dermatology, University of California San Diego, La Jolla, CA, United States. Electronic address:
Normal cutaneous wound healing is a multicellular process that involves the release of small extracellular vesicles (sEVs) that coordinate intercellular communication by delivery of sEV payloads to recipient cells. We have recently shown how the pro-reparative activity of inflammatory cell sEVs, especially macrophage and neutrophil-derived sEVs, in the wound bed is dysregulated in impaired wound healing. Here we show that loss of Rab27A, a small GTPase that has a regulatory function in sEV secretion, reduces the release of neutrophil and macrophage-derived sEVs.
View Article and Find Full Text PDFMol Metab
September 2025
Department of Medicine, Division of Endocrinology & Metabolism, University of California San Diego; La Jolla, California, USA. Electronic address:
Obesity is intricately linked to various metabolic diseases; however, some individuals maintain metabolic health despite being classified as obese. A critical factor underlying this paradox is the expansion of white adipose tissue (WAT), which can occur through two mechanisms: hypertrophy (the enlargement of existing fat cells) and hyperplasia (the formation of new fat cells from adipocyte precursor cells, or APCs). Hyperplasia is regarded as a healthier mode of WAT expansion, as it tends to reduce inflammation and protect against insulin resistance.
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Haihe Laboratory of Cell Ecosystem, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center fo
Persistent overactivation of the renal sympathetic nervous system drives kidney inflammation and fibrosis. Macrophages contribute to fibrogenesis by secreting various pro-fibrogenic mediators. However, whether the sympathetic nervous system regulates renal fibrosis by modulating macrophage-fibroblast interaction remains unclear.
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