Cannabis Use and Cannabidiol Modulate HIV-Induced Alterations in TREM2 Expression: Implications for Age-Related Neuropathogenesis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE285294 | GEO | 2025/11/07
REPOSITORIES: GEO
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Project description:Previous studies have shown that cannabis use in people living with HIV-1 is associated with a lower viral load, lower circulating CD16+ monocytes, and high CD4+ T-cell count, suggesting a potential therapeutic application. HIV-1 infected U1 monocytes and primary macrophages were used to assess the effects of CBD in HIV-1 infection. Our data suggests that CBD treatment results in a significant reduction in the number of EVs released from infected cells. Additional findings suggest that this may be mediated by a reduction in viral transcription and autophagy activation. To see the effect of CBD in autophagy activation, U1 and U1 Monocyte Derived Macrophages cells were cultured and lysed. D-Biotin or Biotinylated CBD pull-down from the lysates was performed using Streptavidin-Sepharose beads, which were washed with TNE50 / TNE300 (high salt) + 0.1% NP40 buffers. The complexes were analyzed by mass spectrometry. Reactome enrichment analysis was used to assess the CBD pull-down of HIV-1 infected monocytes (U1) and HIV-1 infected MDM proteins for involvement of the autophagy pathway.
2022-04-04 | PXD027263 | Pride
Project description:In the current study, we aimed at exploring the effects of the major non-psychotropic phytocannabinoid of Cannabis sativa, (-)-cannabidiol (CBD), on human sebaceous gland functions. We found that CBD behaved as a highly effective anti-acne agent, targeting all the three key, sebocyte-specific steps of the pathogenesis (i.e. without compromising viability or basal sebaceous lipid production, CBD normalized pro-acne agents-induced excessive lipid synthesis, reduced proliferation and exerted anti-inflammatory actions). The goal of the present microarray analyses was to identify signaling pathways and target genes being involved in mediating the above beneficial effects of CBD. Microarray analyses were performed by using three independent sets of control (vehicle-treated) and CBD-treated (10 M-NM-<M, 24-hr) human, immortalized SZ95 sebocytes. The first two sets of the samples were analyzed by two-color microarrays (M-bM-^@M-^\rep1M-bM-^@M-^] and M-bM-^@M-^\rep2M-bM-^@M-^]). Later on, the RNA from the second sample set was used for the M-bM-^@M-^\rep2-1M-bM-^@M-^] hybridization (techical repeat). Finally, we analyzed the third (biological) sample set by using one-color microarray (M-bM-^@M-^\rep3M-bM-^@M-^]).
2014-07-29 | E-GEOD-57571 | biostudies-arrayexpress
Project description:In the current study, we aimed at exploring the effects of the major non-psychotropic phytocannabinoid of Cannabis sativa, (-)-cannabidiol (CBD), on human sebaceous gland functions. We found that CBD behaved as a highly effective anti-acne agent, targeting all the three key, sebocyte-specific steps of the pathogenesis (i.e. without compromising viability or basal sebaceous lipid production, CBD normalized pro-acne agents-induced excessive lipid synthesis, reduced proliferation and exerted anti-inflammatory actions). The goal of the present microarray analyses was to identify signaling pathways and target genes being involved in mediating the above beneficial effects of CBD.
2014-07-29 | GSE57571 | GEO
Project description:Cannabidiol (CBD), a phytochemical derived from Cannabis sativa L., has been demonstrated to exhibit promising anti-tumor properties in multiple cancer types. However, the effects of CBD on Hepatocellular carcinoma cells (HCC) remains unknown. We have shown that CBD effectively suppresses HCC cell growth in vivo and in vitro, and induced HCC cell pyroptosis in a caspase-3/GSDME-dependent manner. We further demonstrated that accumulation of Integrative Stress Response (ISR) and mitochondrial stress may contribute to the initiation of pyroptotic signaling by CBD. Simultaneously, CBD can repress aerobic glycolysis through modulation of the ATF4-IGFBP1-Akt axis, due to the depletion of ATP and crucial intermediate metabolites. Collectively, these observations indicate that CBD could be considered as a potential compound for HCC therapy.
2021-07-14 | GSE179661 | GEO
Project description:Cannabis sativa high CBD and highTHC chemovars
| PRJNA884159 | ENA
Project description:Epitranscriptomic modifications [N6-methyladenosine (m6A)] regulate various diseases, including cancer and inflammation. Despite their functional relevance in neural development and differentiation, the role of m6A modifications in HIV neuropathogenesis is unknown. Using anti-N6-methyladenosine (m6A) antibody-immunoprecipitation and microarray profiling, we identified m6A modifications in miRNAs in basal ganglia (BG) of uninfected (VEH) and SIV-infected Rhesus macaques (RMs) on combination anti-retroviral therapy (cART) and either VEH-treated (VEH/SIV/cART), or THC:CBD-treated (THC:CBD/SIV/cART). HIV/SIV infection promoted an overall hypomethylated miRNA m6A profile. While THC:CBD did not significantly impact the overall hypomethylated m6A profile, specific miRNAs predicted to target proinflammatory genes showed marked m6A hypomethylation compared to VEH-treated RMs. Additionally, specific BG m6A-modified miRNAs were detected in BG-derived extracellular vesicles. Mechanistically, the DRACH motif in the miR-194-5p seed region was significantly m6A hypomethylated in THC:CBD/SIV/cART RMs. Unlike wild-type, in-vitro transfected m6A-modified miR-194-5p mimics failed to downregulate STAT1 protein expression. Further, compared to VEH/SIV/cART RMs, THC:CBD significantly reduced m6A methylation of 44 miRNAs directly involved in regulating CNS network genes. Our findings indicate that m6A epitranscriptomic marks in the seed nucleotides can impair miRNA function and that cannabinoids may preserve it by reducing m6A methylation levels, thus, providing a mechanistic explanation underlying their anti-neuroinflammatory effects in HIV/SIV infection.
2025-06-15 | GSE296015 | GEO
Project description:Canabidiol (CBD), derived from Cannabis sativa plant exhibits beneficial in alleviating a number of of oral and dental pathoses This study aimed to explore the impact of CBD on several traits of human dental pulp stem cell (hDPSC) such as their proliferation, apoptosis, migration, and odonto/osteogenic differentiation. hDPSCs were harvested from human dental pulp tissues. The cells were treated with 1.25, 2.5, 5, 10, 25, and 50 μg/mL CBD. Cell response in terms of cell proliferation, colony-forming unit, cell cycle progression, cell migration, apoptosis, and odonto/osteogenic differentiation of hDPSCs were assessed in normal and P. gingivalis lipopolysaccharide (LPS)-induced `inflammatory` milieus. RNA sequencing and proteomic analysis were performed to predict target pathways impacted by CBD. In a normal physiological growth milieu, exposure to 5 μg/mL CBD attenuated hDPSCs proliferation and reduced the number of colony-forming units. On the contrary, in LPS-exposed hDPSCs, a dose of 1.25 μg/mL CBD restored proliferation and odonto/osteogenic differentiation. Proteomic analysis demonstrated that several proteins involved in cell proliferation and differentiation were upregulated following CBD exposure, including CCL8, CDC42, and KFL5. RNA sequencing data indicated that CBD upregulated Notch signaling pathway. In an inhibitory experiment, DAPT, a Notch inhibitor, reduced the effect of CBD-rescued LPS-attenuated mineralization in hDPSCs, suggesting that CBD potentially mediates Notch activation to exert its effect on odonto/osteogenic differentiation of hDPSCs. CBD recovers the proliferation and survival of hDPSCs following exposure to LPS. Additionally,we report here, for the first time, that CBD-mediated Notch activation effectively restores the odonto/osteogenic differentiation ability of hDPSCs. These results while uncovers and underscore the potential role of CBD as a therapeutic option to enhance dentin regeneration.
2025-08-31 | GSE271641 | GEO
Project description:Increased availability of cannabis and cannabinoid-containing products necessitates the need for understanding how exposure to these compounds can affect development. Using cannabinoid receptor-null zebrafish (cnr1-/- and cnr2-/-), we conducted experiments to assess the roles of these receptors in ∆9-tetrahydrocannabinol (THC) and cannabidiol (CBD) developmental and behavioral toxicity. THC increased mortality and deformities (pericardial and yolk sac edemas, a reduction in size) in cnr1-/- and cnr2-/- fish. Conversely, CBD-induced malformations and mortality were significantly reduced in the cnr1-/- and cnr2-/- larvae. THC and CBD exposure caused significantly decreased larval behavior (96 hpf), however, decreased distance travelled was protected in the cnr1-/- and cnr2-/- fish, suggesting these receptors are responsible for mediating behavioral toxicity. Transcriptomic profiling in cnr+/+ embryos developmentally exposed to 4 μM THC or 0.5 μM CBD revealed that a significant portion of differentially expressed genes were targets of PPARγ, a predicted upstream regulator. In Cnr-positive embryos, co-exposure to the PPARγ inhibitor GW9662 and THC or CBD, there was increased toxicity compared to exposure with THC or CBD alone. Co-treatment in the cnr2-/- fish with GW9662 did not alter the CBD-induced decrease in activity. However, co-treatment with GW9662 did remove the protective effect observed in cnr1-/- fish treated to CBD alone. Collectively, these results indicate that PPARγ, Cnr1, and Cnr2 all play crucial roles in the developmental toxicity of THC and CBD.
2021-01-01 | GSE164128 | GEO
Project description:Cannabidiol (CBD), a cannabinoid from the cannabis plant, is widely used in sports for recovery, pain management, and sleep improvement, yet its effects on muscle are not well understood. This study aimed to determine the transcriptional response of murine skeletal muscle myotubes to broad-spectrum CBD and synthetic CBD (sCBD), hypothesizing significant changes in metabolism, myogenesis, and inflammation, with unique gene expression profiles for broad-spectrum CBD due to its additional compounds. Differentiated C2C12 myotubes were treated with 10 µM CBD, sCBD, or vehicle control (DMSO) for 24 hours before RNA extraction. Poly-A tail enriched mRNA libraries were constructed and sequenced using 2x50 bp paired-end sequencing. CBD and sCBD treatment induced 4489 and 1979 differentially expressed genes (DEGs; p <0.001, FDR step-up <0.05), respectively, with common upregulation of 857 genes and common downregulation of 648 genes. Common upregulated DEGs were associated with “response to unfolded protein”, “cell redox homeostasis”, “endoplasmic reticulum stress”, “oxidative stress” and “cellular response to hypoxia”. Common downregulated DEGs were linked to “sarcomere organization”, “skeletal muscle tissue development”, “regulation of muscle contraction”, “skeletal muscle contraction” and “muscle contraction”. CBD treatment induced 1342 unique upregulated DEGs and 1137 unique downregulated DEGs, compared to 154 and 152 unique up- and downregulated DEGs in sCBD. The transcriptional data indicate that CBD may induce mild cellular stress, activating pathways associated with altered redox balance, unfolded protein response, and endoplasmic reticulum stress. We hypothesize that CBD interacts with muscle and may elicit a ‘mitohormetic’ effect that warrants further investigation.
2024-09-25 | GSE272113 | GEO
Project description:Despite the growing prevalence of autism, no pharmacological interventions have been approved for core symptoms. The endocannabinoid system (ECS) has recently gained interest as a potential target for treating autism. Cannabidiol (CBD), a compound found in the Cannabis plant (C. Sativa), is a potential autism treatment due to its tolerability and promising early results in fragile X syndrome patients. Here, we aimed to evaluate the efficacy of CBD in treating social deficits and restrictive/repetitive behaviours in two monogenetic models of autism, Shank3 and Fmr1 knock-out (KO) mice. Male and female mice were tested in the 3-chamber social apparatus or for self-grooming and open field test (baseline or pre-treatment), followed by 5 daily treatments of vehicle or CBD (s.c., 5mg/kg for males, 50mg/kg for females) and tested again after the last injection (post-treatment). At baseline and following vehicle treatment, male and female Shank3 and Fmr1 KO mice exhibited deficits in social novelty, which were restored to control levels following CBD administration. Meanwhile, self-grooming (increased in male and female Shank3 KO mice) and open-field exploration (decreased locomotion in Shank3 KO mice) were not affected by CBD. Females had hippocampal CBD levels ~11.6 times higher than males (concordant with the dosing) and presented elevated levels of anandamide (AEA) in the CBD-treated groups. Transcriptomic analysis of the hippocampus revealed a lack of overlap in the CBD differentially expressed genes (DEGs) among the different strains and between sexes. These results suggest sex- and strain-specific mechanisms for CBD and support its therapeutic effects for syndromic autism.
2025-08-31 | GSE295664 | GEO