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Interleukin-12 sustained release system promotes hematopoietic recovery after radiation injury

ABSTRACT: Interleukin-12 sustained release system promotes hematopoietic recovery after radiation injury

PROVIDER: PRJNA1112312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29052605_1.fastq.gz	Fastqsanger.gz
	SRR29052605_2.fastq.gz	Fastqsanger.gz
	SRR29052606_1.fastq.gz	Fastqsanger.gz
	SRR29052606_2.fastq.gz	Fastqsanger.gz
	SRR29052607_1.fastq.gz	Fastqsanger.gz

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Interleukin-12 sustained release system promotes hematopoietic recovery after radiation injury

Project description:The continuous production of all mature blood cell lineages is maintained by Hematopoietic stem cells (HSCs), but they are highly susceptible to damage by ionizing radiation (IR) that induces death. Therefore, devising the therapeutic strategies that can mitigate hematopoietic toxicity caused by IR would benefit acute radiation syndrome (ARS) victims and radiation therapy patients. Here, we prepared an injectable hydrogel based on RGD-alginate and Laponite by a simple mixing method to release IL-12 (RGD-Alg/Laponite@IL-12) slowly and locally. The localization administration of RGD-Alg/Laponite@IL-12 substantially increased the survival and promoted the hematopoietic recovery of mice following sublethal-dose irradiation. These results suggested that local intra-bone marrow injection of RGD-Alg/Laponite@IL-12 hydrogel can effectively stimulate IL12R-PI3K/AKT signaling axis, which promotes proliferation and hematopoietic growth factors (HGFs) secretion of bone marrow mesenchymal stem/stromal cells (BM-MSCs). This signaling axis facilitates hematopoietic microenvironment repair and plays a pivotal role in hematopoietic reconstitution. In conclusion, our study attempted a biomaterial-sustained release of IL-12 for the treatment of irradiated hematopoietic injury and provided a new therapeutic strategy for hematopoietic acute radiation syndrome (H-ARS).

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Interleukin 13 Signaling to Macrophages Promotes Functional Recovery after Myocardial Infarction

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An in situ depot for the sustained release of a TLR7/8 agonist in combination with a TGFβ inhibitor promotes anti-tumor immune responses

Project description:The study aims to identify intratumoral TCRb CD3R diversity, number and overlap between tumors from mice carrying bilateral CT26 tumors with a treatment group being injected in one tumor (Tumor_R) with a sustained release technology providing sustained release of R848 and RepSox (CarboCell TLR:TGFb, termed CC) and not injected in the contralateral tumor (Tumor_L) compared to untreated control mice (termed UT). The Mice bearing bilateral CT26 tumors received three unilateral (Tumor_R) CarboCell TLR:TGFb injections. Tumors were harvested one week after CarboCell treatment (31 days after inoculation). Untreated tumors were harvested 17 days after inoculation. Genomic DNA was extracted and purified from tumors using the DNeasy Blood & Tissue Kit (QIAGEN) according to the manufacturer's instructions. RNA-free genomic DNA was obtained by adding 4 μl RNase A (100 mg/ml, QIAGEN). Immunosequencing of TCRβ CDR3 regions was performed using the survey ImmunoSeq Assay (Adaptive Biotechnologies, Seattle, WA). Analysis were performed to identify the shared nucleotide sequences between the treated and untreated tumors. The sample overlap was also analysed to determine the extent to which rearrangements are shared between samples using the sample overlap tool to generate a Morisita Index. The tool will compute the specified overlap measure between injected and uninfected tumor on CarboCell TLR:TGFb mice and controls.

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2024-01-29 | GSE253243 | GEO

UV radiation-induced DNA damage

Project description:DNA damage caused by UV radiation initiates cellular recovery mechanisms, which involve activation of DNA damage response pathways, cell cycle arrest and apoptosis. To assess cellular transcriptional responses to UVC-induced DNA damage we compared time course responses of human skin fibroblasts to low and high doses of UVC radiation known to induce a transient cellular replicative arrest or apoptosis, respectively. UVC radiation elicited >3-fold changes in 460 out of 12,000 transcripts and 89% of these represented downregulated transcripts. Only 5% of the regulated genes were common to both low and high doses of radiation. Cells inflicted with a low dose of UVC exhibited transcription profiles demonstrating transient regulation followed by recovery, whereas the responses were persistent after the high dose. A detailed clustering analysis and functional classification of the targets implied regulation of biologically divergent responses and suggested involvement of transcriptional and translational machinery, inflammatory, anti-proliferative and anti-angiogenic responses. The data support the notion that UVC radiation induces prominent, dose-dependent downregulation of transcription. However, the data strongly suggest that transcriptional repression is also target gene selective. Furthermore, the results demonstrate that dose-dependent induction of cell cycle arrest and apoptosis by UVC radiation are transcriptionally highly distinct responses. Keywords: other

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Exogenous Interleukin-10 versus Glucocorticoids: Effect on Gene Expression and Pro-inflammatory Cytokine Release in Polymorphonuclear Leukocytes and Monocytes of the Newborn

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