Publications by authors named "A Mutirangura"
Objectives: Long interspersed nuclear element-1 (LINE-1) and Alu elements are major targets of methylation, an epigenetic mechanism that is associated with several biological processes. Alterations of methylation of LINE-1 and Alu have been reported in cancers, diseases, and ageing. However, these alterations have not been studied in osteogenic differentiation of dental pulp stem cells (DPSCs), which are a promising source of tissue regeneration.
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- Non-syndromic cleft lip with or without palate (NSCL/P) is a common birth defect, potentially influenced by abnormal DNA methylation in pregnant mothers.
- The study involved 39 NSCL/P patients and 33 mothers, analyzing Alu methylation and cellular aging markers in blood and tissue samples.
- Findings showed specific patterns of Alu methylation changes in patients with cleft lip and palate, indicating the mother's methylation status may contribute to the severity of the child's cleft condition.
Article Synopsis
- Dry eye disease (DED) is a complex condition linked to aging that disrupts tear film stability, highlighting a need for better research models of the lacrimal gland (LG) to develop new treatments.
- * The authors created two types of LG organoids using a magnetic 3D bioprinting technique that mimics both functional and aging states of the gland, allowing for the study of LG behaviors and cellular responses.
- * They discovered that a novel gene therapy, HMGB1-Box A, could protect LG organoids from age-related cellular damage and dysfunction, demonstrating potential for future treatments of DED.
Introduction: Human dental pulp stem cells (DPSCs) are pivotal in tissue engineering and cell-based therapies due to their significant differentiation potential and accessibility. A major challenge in in vitro cell expansion is their replicative senescence, which impacts their regeneration and differentiation capabilities. While genetic factors influence these processes, epigenetic regulations such as Alu methylation also play crucial roles.
View Article and Find Full Text PDFBackground/aim: Disability and mortality rates for renal failure are still increasing. DNA damage and oxidative stress intoxication from body metabolism, high blood glucose, or the environment cause significant kidney damage. Recently, we reported that Box A of HMGB1 (Box A) acts as molecular scissors, producing DNA gaps that prevent DNA damage in kidney cell lines and ultimately reverse aging phenotypes in aging rat models.
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