Genes controlling proliferation and differentiation of astrocytes are likely to play an important role in the pathogenesis of astrocytic gliomas and could serve as therapeutic targets. mRNA differential display analysis identified two genes, viz. BAALC and RAMP3, whose expression is altered in primary astrocytes treated with differentiation inducers. BAALC, which has been reported to be expressed in neural progenitor cells, was found to be up regulated in both normal and malignant astrocytes on inhibition of proliferation. RAMP3 functions as a modulator of the receptor for adrenomedullin (AM). AM has been suggested to act as autocrine/paracrine growth factor for gliomas. Our studies show RAMP3 down regulation on staurosporine treatment of astrocytes, suggesting protein kinase C inhibition as a possible strategy for inhibiting AM activity and thereby growth of glioma cells.
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http://dx.doi.org/10.1016/j.cellbi.2005.10.022 | DOI Listing |
Mol Neurobiol
January 2025
Guizhou Key Laboratory of Brain Science, Zunyi Medical University, Xinpu New District Campus No. 1 Street, Zunyi, 563000, China.
Previous studies have shown that astrocyte activation in the anterior cingulate cortex (ACC), accompanied by upregulation of the astrocyte marker S100 calcium binding protein B (S100B), contributes to comorbid anxiety in chronic inflammatory pain (CIP), but the exact downstream mechanism is still being explored. The receptor for advanced glycation end-products (RAGE) plays an important role in chronic pain and psychosis by recognizing ligands, including S100B. Therefore, we speculate that RAGE may be involved in astrocyte regulation of the comorbidity between CIP and anxiety by recognizing S100B.
View Article and Find Full Text PDFToxicon
January 2025
National Council of Research (CNR), Institute of Biochemistry and Cell Biology, 00015 Monterotondo (RM), Italy.
Botulinum neurotoxin type A (BoNT/A) has expanded its therapeutic uses beyond neuromuscular disorders to include treatments for various pain syndromes and neurological conditions. Originally recognized for blocking acetylcholine release at neuromuscular junctions, BoNT/A's effects extend to both peripheral and central nervous systems. Its ability to undergo retrograde transport allows BoNT/A to modulate synaptic transmission and reduce pain centrally, influencing neurotransmitter systems beyond muscle control.
View Article and Find Full Text PDFPhytomedicine
January 2025
Department of Pharmacy, Xijing Hospital, Fourth Military Medical University, Changle West Street 15, Xi'an, Shaanxi, 710032, China. Electronic address:
Background: The pathogenesis of neuropathic pain is complex and lacks effective clinical treatment strategies. Medical plants and herbal extracts from traditional Chinese medicine with multi-target comprehensive effects have attracted great attention from scientists.
Purpose: To investigate the pharmacological active components and mechanism underlying the anti-neuralgia effect of classic analgesic formulas Duhuo Jisheng Mixture (DJM).
Inflamm Res
January 2025
Department of Ultrasound, The Second Xiangya Hospital of Central South University, Changsha, 410011, China.
Background: Hyperoxia-induced brain injury is a severe neurological complication that is often accompanied by adverse long-term prognosis. The pathogenesis of hyperoxia-induced brain injury is highly complex, with neuroinflammation playing a crucial role. The activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, which plays a pivotal role in regulating and amplifying the inflammatory response, is the pathological core of hyperoxia-induced brain injury.
View Article and Find Full Text PDFPharmaceuticals (Basel)
January 2025
Department of Basic Sciences, Ponce Research Institute, Ponce Health Sciences University, Ponce, PR 00716, USA.
Background/objectives: Cocaine use disorder is an intersecting issue in populations with HIV-1, further exacerbating the clinical course of the disease and contributing to neurotoxicity and neuroinflammation. Cocaine and HIV neurotoxins play roles in neuronal damage during neuroHIV progression by disrupting glutamate homeostasis in the brain. Even with combined antiretroviral therapy (cART), HIV-1 Nef, an early viral protein expressed in approximately 1% of infected astrocytes, remains a key neurotoxin.
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