Myosin VI (MVI) is the only known myosin walking towards minus end of actin filaments and is believed to play distinct role(s) than other myosins. We addressed a role of this unique motor in secretory PC12 cells, derived from rat adrenal medulla pheochromocytoma using cell lines with reduced MVI synthesis (produced by means of siRNA). Decrease of MVI expression caused severe changes in cell size and morphology, and profound defects in actin cytoskeleton organization and Golgi structure. Also, significant inhibition of cell migration as well as cell proliferation was observed. Flow cytometric analysis revealed that MVI-deficient cells were arrested in G0/G1 phase of the cell cycle but did not undergo increased senescence as compared with control cells. Also, neither polyploidy nor aneuploidy were detected. Surprisingly, no significant effect on noradrenaline secretion was observed. These data indicate that in PC12 cells MVI is involved in cell migration and proliferation but is not crucial for stimulation-dependent catecholamine release.
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http://dx.doi.org/10.1007/s10974-011-9279-0 | DOI Listing |
Antioxid Redox Signal
January 2025
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Hypoxia ischemia (HI) is a leading cause of cerebral palsy and long-term neurological sequelae in infants. Given that mitochondrial dysfunction in neurons contributes to HI brain damage, this study aimed to investigate the regulatory role of miR-9-5p in mitochondrial function following HI injury. Overexpression of miR-9-5p in HI mice or HO-exposed PC12 cells suppressed neuronal injury, associated with increased mitochondrial copy number, normalizing mitochondrial membrane potential, improved nuclear factor-erythroid factor 2-related factor 2 (Nrf2) activation, and downregulation of Keap1.
View Article and Find Full Text PDFAntioxidants (Basel)
January 2025
Department of Life and Environmental Sciences, University of Cagliari, 09042 Cagliari, Italy.
The rising global focus on healthy lifestyles and environmental sustainability has prompted interest in repurposing plant-based by-products for health benefits. With increasing life expectancy, the incidence of neurodegenerative diseases-characterized by complex, multifactorial mechanisms such as abnormal protein aggregation, mitochondrial dysfunction, oxidative stress, and inflammation-continues to grow. Medicinal plants, with their diverse bioactive compounds, offer promising therapeutic avenues for such conditions.
View Article and Find Full Text PDFHistol Histopathol
January 2025
Department of Neurology, The Affiliated People's Hospital of Jiangsu University, Zhenjiang Jiangsu, PR China.
Parkinson's disease (PD) is a limb movement disorder caused by the degeneration of brain neurons and seriously affects the quality of life of the elderly. However, the current drugs are symptomatic treatments that cannot prevent or delay the development of the disease. Targeted therapy for pathogenesis may be the direction of development in the future.
View Article and Find Full Text PDFMol Neurobiol
January 2025
School of Pharmacy, Nantong University, 19 Qixiu Road, Nantong, 226001, People's Republic of China.
Growing evidence suggests that plant compounds are emerging as a tremendous source for slowing the onset and progression of Alzheimer's disease (AD). Ursonic acid (UNA) is a naturally occurring pentacyclic triterpenoid with some hypoglycemic, anticancer, and antiinflammatory activities. However, the pharmacological effects of UNA on AD are still unknown.
View Article and Find Full Text PDFJ Ethnopharmacol
January 2025
Department of Pharmacology, Shenyang Pharmaceutical University, Shenyang, Liaoning, China; College of Pharmacy, Shenzhen Technology University, Shenzhen, Guangdong, China. Electronic address:
Ethnopharmacological Relevance: Shilong Qingxue Granule (SQG), a traditional Chinese medicine, effectively treats the secondary neurological damage and functional deficits caused by cerebral hemorrhage, though its exact mechanism remains unclear.
Aim Of The Study: This study aimed to investigate the effects of SQG and its mechanisms.
Materials And Methods: we evaluated the effects of SQG and its extracts on glutamate induced nerve damage using in vivo and in vitro models.
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