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β-Sitosterol modulates osteogenic and adipogenic balance in BMSCs to suppress osteoporosis via regulating mTOR-IMP1-Adipoq axis.

Phytomedicine

January 2025

Academy of Integrative Medicine, Dalian Medical University, Dalian, China; Department of Clinical Pharmacology, College of Pharmacy, Dalian Medical University, Dalian, China. Electronic address:

Background: Osteoporosis (OP) is a prevalent global health concern, impacting millions of individuals, especially the elderly. The etiology of senile OP is associated with the imbalance of osteogenic and adipogenic differentiation in the bone marrow mesenchymal stem cells (BMSCs). The imbalance of BMSCs differentiation fate will leading to bone loss and lipids accumulation.

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Cis-regulatory elements (CREs) control gene expression and are dynamic in their structure and function, reflecting changes in the composition of diverse effector proteins over time. However, methods for measuring the organization of effector proteins at CREs across the genome are limited, hampering efforts to connect CRE structure to their function in cell fate and disease. Here we developed PRINT, a computational method that identifies footprints of DNA-protein interactions from bulk and single-cell chromatin accessibility data across multiple scales of protein size.

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Introduction: Bone aging is linked to changes in the lineage differentiation of bone marrow stem cells (BMSCs), which show a heightened tendency to differentiate into adipocytes instead of osteoblasts. The therapeutic potential of irisin in addressing age-related diseases has garnered significant attention. More significantly, irisin has the capacity to enhance bone mass recovery and sustain overall bone health.

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Transcriptomic dynamics and cell-to-cell communication during the transition of prospermatogonia to spermatogonia revealed at single-cell resolution.

BMC Genomics

January 2025

Key Laboratory of Adaptation and Evolution of Plateau Biota, Northwest Institute of Plateau Biology, Chinese Academy of Sciences, Xining, Qinghai, 810008, China.

Background: Spermatogonia are essential for the continual production of sperm and regeneration of the entire spermatogenic lineage after injury. In mammals, spermatogonia are formed in the neonatal testis from prospermatogonia (also termed gonocytes), which are established from primordial germ cells during fetal development. Currently, the molecular regulation of the prospermatogonial to spermatogonia transition is not fully understood.

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Oligodendrocytes are generated throughout life and in neurodegenerative conditions from brain resident oligodendrocyte precursor cells (OPCs). The transition from OPC to oligodendrocyte involves a complex cascade of molecular and morphological states that position the cell to make a fate decision to integrate as a myelinating oligodendrocyte or die through apoptosis. Oligodendrocyte maturation impacts the cell death mechanisms that occur in degenerative conditions, but it is unclear if and how the cell death machinery changes as OPCs transition into oligodendrocytes.

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