Effect of Carbon Nanoparticle Treatment in Rice Adult plants
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ABSTRACT:
ORGANISM(S): Oryza sativa
PROVIDER: GSE200357 | GEO | 2024/07/31
REPOSITORIES: GEO
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Project description:Environmental particle inhalation and persistent herpesvirus infection are omnipresent and associated with chronic lung diseases. Previously, we showed that pulmonary exposure to soot-like carbonaceous nanoparticles (CNP) or fibre-shaped engineered double-walled carbon nanotubes (DWCNT) induced an increase of lytic virus protein expression in latently murine gammaherpesvirus 68 (MHV-68) infected mouse lungs, with a similar pattern as acute infection suggesting virus reactivation. However, the molecular mechanisms underlying herpesvirus reactivation as well as herpesvirus reactivation associated disease exacerbation caused by particle exposure remain unclear. Here, we investigated the effects of environmental relevant repeated particle exposure and herpesvirus reactivation mechanistically, and therapeutically. In the MHV-68 mouse model, we identified elevated lung inflammation and emphysema-like injury after repetitive CNP exposure. We further uncovered that CNP reactivated latent herpesvirus mainly in CD11b+ macrophages. Mechanistically, ERK1/2, JNK and p38 MAPK were rapidly activated after CNP and DWCNT exposure in persistently MHV-68 infected bone marrow-derived macrophages, followed by upregulation of viral gene expression and increased viral titer but without generating a pro-inflammatory transcriptional signature. Pharmacological inhibition of p38 activation abrogated CNP but not DWCNT triggered virus reactivation. In vivo, p38 inhibitor pretreatment of latently infected mice also attenuated CNP exposure induced MHV-68 reactivation. Our findings suggest that particle pollution is an environmental challenge to trigger herpesvirus reactivation and related chronic lung disease by activating latent herpesvirus via p38 MAPK dependent signalling. Pharmacological p38 inhibition might serve as a protective target to alleviate particle exposure related chronic lung disease exacerbations.
2023-09-29 | GSE223818 | GEO
Project description:We aimed to explore the neuroprotective efficacy of Yashtimadhu powder, prepared from the roots of Glycyrrhiza glabra L. (https://mpns.science.kew.org; http://www.ayurveda.hu/api/API-Vol-1.pdf) commonly known as licorice, a known Medhya rasayana in the Indian Ayurvedic texts against Parkinson’s disease. To test the efficacy of Yashtimadhu powder, we used rotenone to generate an in vitro PD model using retinoic acid-differentiated IMR32 cells. Yashtimadhu powder (Lot No.64) was procured from SDP Remedies and Research Centre, Mangalore, India, a GMP-certified Ayurvedic product manufacturer ((http://sdpayurveda.com/products/choorna/yastimadhu-choorna/)The Yashtimadhu neuroprotection was ascertained using cell cytotoxicity, activation of apoptotic proteins and kinases. We used Tandem mass tag (TMT)-lables to understand the differentially regulated proteins across various treatment groups, using Orbitrap Fusion Tribrid mass spectrometer. The mass spectrometry data is acquired in biological duplicates and technical triplicates. We report 4,864 proteins corresponding to 4,783 gene symbols. The proteins were filtered out based technical and biological replicate concordance, thereby reporting 3,720 proteins common among the biological replicates.
2021-09-09 | PXD019672 | Pride
Project description:Using an oral self-administration paradigm, we have seen morphine increase neural activity in the Paraventricular Nucleus of the Thalamus (PVT). Morphine binds primarily to Mu Opioid Receptors (MORs), which are highly expressed in the PVT. Translating Ribosome Affinity Purification (TRAP)-Sequencing was conducted on PVT neurons that express MORs
2022-10-04 | GSE214560 | GEO
Project description:C-type natriuretic peptide (CNP) has been recently identified as an important anabolic regulator of endochondral bone growth, but the molecular mechanism mediating these effects are not completely understood. Here we demonstrate that CNP activates the p38 MAP kinase pathway in chondrocytes and that pharmacological inhibition of p38 blocks the anabolic effects of CNP in a tibia organ culture system. We further show that CNP stimulates endochondral bone growth largely through expansion of the hypertrophic zone of the growth plate, while delaying mineralization. Both effects are reversed by p38 inhibition. We performed Affymetrix microarray analyses to identify CNP target genes in the organ culture system. These studies confirmed that hypertrophic chondrocytes are the main targets of CNP signaling in the growth plate, potentially because cGMP-dependent kinases I and II, important transducers of CNP signaling and are expressed at much higher levels in these cells than in other areas of the tibia. One of the genes most strongly induced by CNP was the Ptgs2 gene, encoding Cox2. Real-time PCR confirmed that Cox2 expression was induced by CNP in hypertrophic chondrocytes, but surprisingly in a p38-independent manner. Moreover, Cox2 inhibition â in contrast to p38 inhibition - did not block the anabolic effects of CNP. In summary, our data identify novel target genes of CNP and demonstrate that the p38 pathway is a novel, essential mediator of CNP effects on endochondral ossification, with potential implications for numerous skeletal diseases. Experiment Overall Design: Tibiae from E15.5 day old embryonic mice were isolated and cultured in minimal media in the presence of vehicle, BSA/HCl (1mM), or C-type natriuretic peptide, CNP (10-6M). On the sixth day of treatment cultured tibias were micro-dissected into the resting/proliferating, hypertrophic, and mineralized areas. Distinct zones from approximately 24 bones were pooled together, from which RNA was isolated using the Qiagen RNeasy Lipid Extraction Kit. Once the quality of total RNA from three independent trials was determined using the Agilent 2100 bioanalyzer, microarray analyses were performed at the London Regional Genomics Centre using MOE430_2.0 Affymetrix arrays. Results were analyzed using GeneSpring 7.2 software.
2008-06-13 | E-GEOD-4481 | biostudies-arrayexpress
Project description:C-type natriuretic peptide (CNP) has been recently identified as an important anabolic regulator of endochondral bone growth, but the molecular mechanism mediating these effects are not completely understood. Here we demonstrate that CNP activates the p38 MAP kinase pathway in chondrocytes and that pharmacological inhibition of p38 blocks the anabolic effects of CNP in a tibia organ culture system. We further show that CNP stimulates endochondral bone growth largely through expansion of the hypertrophic zone of the growth plate, while delaying mineralization. Both effects are reversed by p38 inhibition. We performed Affymetrix microarray analyses to identify CNP target genes in the organ culture system. These studies confirmed that hypertrophic chondrocytes are the main targets of CNP signaling in the growth plate, potentially because cGMP-dependent kinases I and II, important transducers of CNP signaling and are expressed at much higher levels in these cells than in other areas of the tibia. One of the genes most strongly induced by CNP was the Ptgs2 gene, encoding Cox2. Real-time PCR confirmed that Cox2 expression was induced by CNP in hypertrophic chondrocytes, but surprisingly in a p38-independent manner. Moreover, Cox2 inhibition – in contrast to p38 inhibition - did not block the anabolic effects of CNP. In summary, our data identify novel target genes of CNP and demonstrate that the p38 pathway is a novel, essential mediator of CNP effects on endochondral ossification, with potential implications for numerous skeletal diseases. Keywords: Growth plate zone comparison and treatment response analysis
2006-12-15 | GSE4481 | GEO
Project description:The paraventricular nucleus of the thalamus (PVT) is known to regulate various cognitive and behavioral processes. However, while functional diversity among PVT circuits has often been linked to cellular differences, the molecular identity and spatial distribution of PVT cell types remains unclear. To address this gap, here we used single nucleus RNA sequencing (snRNA-seq) and identified five molecularly distinct PVT neuronal subtypes. Additionally, multiplex fluorescent in situ hybridization of top marker genes revealed that PVT subtypes are organized by a combination of previously unidentified molecular gradients. Lastly, comparing our dataset with a recently published single-cell sequencing atlas of thalamus yielded novel insight into the PVT’s connectivity with cortex, including unexpected innervation of auditory and visual areas. This comparison also revealed that our data contains a largely non-overlapping transcriptomic map of multiple midline thalamic nuclei. Collectively, our findings uncover previously unknown features of the molecular diversity and anatomical organization of the PVT and provide a valuable resource for future investigations.
2023-03-06 | GSE208707 | GEO
Project description:RNA polymerase V (Pol V) and Pol IV are known to be specialized for RNA-directed DNA methylation (RdDM). Here, we report that Pol V, but not Pol IV, regulates hundreds of genes including JA-responsive genes and confers plant defense to Botrytis cinerea and Spodoptera exigua. About half of the Pol V-regulated genes are associated with Pol V transcripts (PVTs). We thus hypothesized that some PVTs could regulate gene expression in an RdDM-independent manner. To test this hypothesis, we studied three PVTs, PVT-ERF5a/b and PVT-ERF6, as models. PVT-ERF5a/b and PVT-ERF6 are transcribed from the upstream regions of ERF5 and ERF6 and positively regulate their transcription, thereby regulating plant defense. We further show that such regulation involves PVT-dependent H3K4me3 deposition and requires the DRD1-DMS3-RDM1 complex that mediates Pol V recruitment to the target loci. Our findings highlight an unprecedented role for PVTs in regulating gene transcription, apart from serving as scaffold RNAs to direct DNA methylation.
2024-07-23 | GSE229881 | GEO
Project description:Hepatocellular carcinoma (HCC) is a malignancy that is challenging to treat. Cancer-associated fibroblasts (CAFs) are reported to promote the malignant behavior of HCC cells via cytokines. Conophylline (CnP) has been reported to suppress activated hepatic stellate cells in liver fibrosis. We aimed to determine whether CnP is useful in suppressing tumor growth in HCC. We investigated whether CnP could suppress the HCC-promoting effect of CAFs derived from HCC tissues in vitro and in vivo. CAFs promoted the proliferation and invasion of HCC cells. CnP suppressed activated CAFs expressing α-smooth muscle actin (αSMA) and inhibited the HCC-promoting effects of CAFs. CnP significantly reduced the levels of cancer-promoting cytokines such as interleukin (IL)-6 (IL-6), IL-8, C-C Motif Chemokine Ligand 2 (CCL2), angiogenin, and osteopontin, which are secreted by CAFs. An in vivo study demonstrated that combined therapy with CnP and sorafenib against CAFs and HCC cells showed the strongest inhibition of tumor growth compared with the control and single treatment groups. Transcriptome analysis revealed that GPR68 in CAFs was strongly suppressed by CnP. The cancer-promoting effects of cytokines were eliminated by knockdown of GPR68 in CAFs. CnP inhibited the HCC-promoting effect of CAFs by suppression a number of HCC-promoting cytokines, which are secreted from CAFs expressing GPR68. Combination therapy with CnP and existing anti-cancer agents may be a promising therapeutic strategy in overcoming refractory HCC with activated CAFs.
2022-01-01 | GSE140530 | GEO
Project description:The present study tried to assess transcription level effects in the digestive gland of female mussels dietarily exposed to Ag NPs and to compare such transcription profiles in two different seasons, autumn and spring, since mussels are expected to be at a different gamete developmental stage (early and advanced gametogenic stage, respectively).
2019-01-01 | GSE124126 | GEO