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By providing a source of alpha-smooth muscle actin (alpha-SMA)-expressing myofibroblasts, microvascular pericytes contribute to the matrix remodeling that occurs during tissue repair. However, the extent to which pericytes may contribute to the fibroblast phenotype post-repair is unknown. In this report, we test whether pericytes isolated from human placenta can in principle become fibroblast-like. Pericytes were cultured in vitro for 11 passages. The Affymetrix mRNA expression profile of passage 2 and passage 11 pericytes was compared. The expression of type I collagen, thrombospondin and fibronectin mRNAs was induced by passaging pericytes in culture. This induction of a fibroblast phenotype was paralleled by induction of connective tissue growth factor (CTGF/CCN2) and type I collagen protein expression and the fibroblast marker ASO2. These results indicate that, in principle, pericytes have the capacity to become fibroblast-like and that pericytes may contribute to the population of fibroblasts in a healed wound.
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http://dx.doi.org/10.1007/s12079-009-0053-7 | DOI Listing |
Mol Biol Rep
September 2025
Department of Pharmacology, Govt. College of Pharmacy, Rohru, Shimla, Himachal Pradesh, 171207, India.
Alzheimer's disease (AD) is the most common, complex, and untreatable form of dementia which is characterized by severe cognitive, motor, neuropsychiatric, and behavioural impairments. These symptoms severely reduce the quality of life for patients and impose a significant burden on caregivers. The existing therapies offer only symptomatic relief without addressing the underlying silent pathological progression.
View Article and Find Full Text PDFCurr Opin Virol
September 2025
Infection Biology, Global Center for Pathogen and Human Health Research, Cleveland Clinic, Cleveland, OH 44195, USA; Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH 44195, USA. Electronic address:
Intracranial calcifications (ICCs) are a characteristic neuropathological feature of several congenital viral infections, including Zika virus (ZIKV), cytomegalovirus (CMV), and lymphocytic choriomeningitis virus (LCMV). These lesions are linked to severe neurodevelopmental outcomes, such as microcephaly, epilepsy, and cognitive deficits, yet the mechanisms underlying their formation and resolution remain unclear. ICCs are thought to arise from an imbalance in osteogenic and osteolytic signaling in the developing brain.
View Article and Find Full Text PDFbioRxiv
August 2025
Department of Pharmacology, Center for Molecular Medicine, University of Nevada, Reno School of Medicine, 1664 N Virginia St., Reno, NV 89557 USA.
Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant myopathy caused by aberrant expression of the retrogene, and it affects skeletal muscles primarily in the face, shoulder, and limbs. In healthy individuals, is expressed in early development and is subsequently silenced in most somatic tissues. The spatiotemporal pattern of DUX4 misexpression beyond the cleavage stage in FSHD is poorly understood because is not well conserved beyond primates.
View Article and Find Full Text PDFFront Mol Biosci
August 2025
Department of Nephrology, The First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Acute kidney injury is a clinical syndrome characterized by a rapid decline in renal function, driven by pathological mechanisms such as renal tubular epithelial cell injury, inflammatory responses, and microcirculatory dysfunction. In recent years, the role of angiogenesis in AKI recovery and regeneration has gained increasing attention. Angiogenesis plays a dual role in tissue repair and pathological remodeling, exhibiting complex spatiotemporal dynamics during AKI progression.
View Article and Find Full Text PDFTraumatic brain injury (TBI) frequently leads to chronic neurovascular dysfunction, yet mechanistic insights into human-specific responses have been limited by the absence of long-term, multicellular in vitro models. Here, we report a five-cell-type human neurovascular culture system, comprising endothelial cells, astrocytes, pericytes, microglia, and neurons, engineered within a 3D scaffold to study injury-induced remodeling over multiple weeks. This PENTA-culture platform recapitulates hallmark features of the neurovascular unit and enables dissection of cell-specific contributions to vascular repair and degeneration.
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