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ABSTRACT: NOD2 contributes to Parvimonas micra-induced bone resorption in diabetic rats with experimental periodontitis

PROVIDER: PRJNA1099929 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28674176_1.fastq.gz	Fastqsanger.gz
	SRR28674176_2.fastq.gz	Fastqsanger.gz
	SRR28674177_1.fastq.gz	Fastqsanger.gz
	SRR28674177_2.fastq.gz	Fastqsanger.gz
	SRR28674178_1.fastq.gz	Fastqsanger.gz

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Project description:Parvimonas micra

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Parvimonas micra

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Comparison of mRNA expression levels in peri-implantitis and periodontitis within the same host environment

Project description:Purpose: The aim of this study was to explore whether differences exist and to what an extent of the immune-mediated inflammatory reactions between periodontitis and peri-implantitis at the transcriptional level in the same susceptible host. Methods: Ligature-induced experimental peri-implantitis and periodontitis in the same mice were established. Gingival tissues of healthy, periodontitis and peri-implantitis sites from the same oral cavity were collected and used for RNA-sequencing. Differentially expressed genes (DEGs) were screened between periodontitis/peri-implantitis sites and healthy sites. The enrichment analysis of DEGs were analyzed. Comprehensive immune landscape was annotated by seq-ImmuCC. Results: The results showed that 137 and 353 up-regulated DEGs as well as and 670 and 174 down-regulated DEGs were specifically expressed periodontitis/peri-implantitis group compared to the healthy control group, respectively. The pathways of complement and coagulation cascade and osteoclast differentiation were dominating in the peri-implantitis sites. Moreover, peri-implantitis sites exhibited elevated macrophage proportions and relatively enriched macrophage activation and bone loss compared with periodontitis. Conclusions: Results indicated that peri-implantitis and periodontitis exhibited significantly distinct transcriptional signatures. Additionally, the study suggests that the interplay between macrophages and bone resorption are comparatively more active in peri-implantitis compared with periodontitis. These biological processes may be factors contributing to the pathogenesis of peri-implantitis being distinct from that of periodontitis.

2022-06-06 | GSE186882 | GEO

Parvimonas micra strain:JM503A

Project description:Parvimonas micra strain:JM503A Genome sequencing

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Parvimonas micra strain:KCOM 1037

Project description:Genome sequencing of Parvimonas micra KCOM 1037

| PRJNA485032 | ENA

Parvimonas micra A293

Project description:Parvimonas micra A293 Genome sequencing and assembly

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Project description:Parvimonas micra in colorectal cancer patients (CRC)

| PRJNA857572 | ENA

High-throughput sequencing analysis of BMMs and BMMs-derived osteoclasts

Project description:Long noncoding RNAs (lncRNAs) have emerged as integral regulators of physiology and disease, but specific roles of lncRNAs in bone resorption remain largely unknown. Here, RNA-seq analysis indicated that lncRNA Nron was a candidate funtional regulators of bone resorption. Our further experimental analysis showed that Nron regulates bone resorption in mice. We further identified a functional motif of Nron. Consequently, delivery of Nron functional motif specifically in osteoclasts reversed bone loss without obvious side-effects in vivo. Together, our study indicate that Nron is a key bone resorption suppressor and reveal Nron functional motif might be a potential therapeutic strategy to combat excessive bone absorption in osteoporosis.

2019-07-19 | GSE134457 | GEO

Parvimonas micra strain:KCOM 1535 (=ChDC B708)

Project description:Parvimonas micra strain:KCOM 1535 (=ChDC B708) Genome sequencing

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Glomerular Haematopoietic Prostaglandin D Synthase‐Prostaglandin D2 Axis Contributes to the Periodontitis‐Related Exacerbation of Diabetic Nephropathy in KK‐Ay Mice

Project description:Diabetic nephropathy (DN) is the leading cause of dialysis and is associated with cardiovascular diseases. To prevent the progression of DN, not only glycemic control but also intervention to exacerbating factors such as chronic inflammation and infection. Recent clinical studies have shown the possible association between chronic kidney disease including DN, and periodontitis. However, the causal relationship that periodontitis could contribute to the progression of DN and its molecular mechanisms has not been understood. In the present study, we investigated ligature-induced experimental periodontitis that might exacerbate glomerular pathology in a DN model KK-Ay mice and the underlying molecular mechanisms. KK-Ay mice with experimental periodontitis showed significantly increased urinary albumin to creatinine ratio, and glomerular pathologies such as glomerular size, mesangial expansion area, fibrotic area, and number of CD68-positive leukocytes compared to those without ligatures. RNA-sequencing in the glomeruli revealed that hematopoietic prostaglandin d2 synthase (Hpgds) was the possible factor bridging periodontitis with the progression of DN. We also found that Hpgds expression was significantly upregulated by hyperglycemia and inflammatory stimuli in mesangial cells. Prostaglandin D2 enhanced hyperglycemia-induced collagen expression in mesangial cells and downregulated the tight junction in renal endothelial cells. Lastly, oral administration with an HPGDS inhibitor HQL-79 successfully prevented the progression of DN in KK-Ay mice by experimental periodontitis. Taken together, experimental periodontitis might contribute to the progression of DN via acceleration of glomerular pathology by upregulation of HPGDS in mesangial cells.

2025-05-03 | GSE261386 | GEO

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