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Differences in PVAT mRNA profiles of recipient mice transplanted with splenocytes

ABSTRACT: Differences in PVAT mRNA profiles of recipient mice transplanted with splenocytes

PROVIDER: PRJNA1011220 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25824000_1.fastq.gz	Fastqsanger.gz
	SRR25824000_2.fastq.gz	Fastqsanger.gz
	SRR25824001_1.fastq.gz	Fastqsanger.gz
	SRR25824001_2.fastq.gz	Fastqsanger.gz
	SRR25824002_1.fastq.gz	Fastqsanger.gz

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Differences in PVAT mRNA profiles of recipient mice transplanted with splenocytes

Project description:Recent investigations raise the possibility that senescent immune cells may fuel vascular damage by perivascular adipose tissue (PVAT) dysfunction, as immune cell infiltration in PVAT increases substantially in the development of vascular disease compared to the healthy state and leads to changes in PVAT-derived effector cytokine levels that comprise vascular biology.Though evidence revealed possible cross-talk among immune cells, PVAT and vasculature, it is less clear if senescent immune cells or a particular cell subset may induce PVAT dysfunction and further impair vascular biology during type 2 diabtes (T2DM). NLRP3 inflammasome plays a critical role in inflammatory response as a major component of innate immunity, it provides a molecular platform that responds to a variety of stimuli, initiating sterile inﬂammation cascade.Furthermore, there is evidence that NLRP3 inflammasome can be activated by sensing danger-associated molecular patterns (DAMPs), which in turn promotes age-related thymic demise and T cell senescence, implicating its potential role in immunosenescence. Here, we employed WT and Nlrp3 KO mice to develop T2DM, and implanted the splenocytes isolated from WT, Nlrp3 KO, WT-T2DM, Nlrp3 KO-T2DM mice that were modeled for 4 months to 3-month-old WT mice. Then, we explored the differentially expressed genes of PVAT in recipient mice implanted with splenocytes and evaluate immune infiltration of PVAT.

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Comparison between blood myeloid-derived suppressor cells (MDSCs) extracted from syngeneic kidney transplanted recipient and tolerant kidney allografted recipient induced by anti-CD28 antibody

Project description:The goal is to identify molecules involved in the accumulation of blood MDSCs in tolerant kidney allografted recipients when compared to syngeneic grafted recipients. In this study 27,088 individual rat genes expression from total mRNA of blood MDSCs from 3 tolerated allogeneic kidney transplanted recipient by anti-CD28, were compared to MDSCs from 3 syngeneic kidney transplanted recipient at day 100 post transplantation.

2011-04-13 | E-GEOD-28545 | biostudies-arrayexpress

Recipient myeloid cell subsets in transplanted allografts

Project description:Balb/c donor hearts were transplanted into C57/BL6 recipients as previously described (Corry et al, 1973). Recipient mice were treated with 250μg anti-CD40L mAb for tolerance induction on days 0, 2, and 4 as previously described (Jiang et al., 2011) or left untreated. On day 5 after transplantation graft infiltrating myeloid subsets were isolated using fluorescence activated cell sorting (FACS). Affymetrix Mouse Gene arrays were run in triplicate with the samples of interest. Raw CEL file data from Affymetrix Expression Console were background corrected, normalized, and summarized using RMA.

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Recipient myeloid cell subsets in transplanted allografts

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RNA-seq of mouse wildtype HSCs purified from recipient mice co-transplanted with wildtype or different types of lymphoid cell deficient HSCs

Project description:To investigate how HSCs functionally compensate for the B cell deficiencies of other HSCs within an organism, we co-transplanted wildtype (WT) HSCs and lineage-deficient HSCs into lethally irradiated WT recipient mice. WT HSCs were then purified from the bone marrow of recipient mice for RNA isolation and sequencing. The purpose is to determine whether there are common genes shared between compensating WT HSCs in the WT co-transplanted with uMT-/- (B6.129S2(B6)-Ighmtm1Cgn/J) and WT co-transplanted with NSG (NOD-scid IL2Rgamma null).

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Defining the lineage of thermogenic perivascular adipose tissue [Thoracic PVAT]

Project description:Brown adipose tissue can expend large amounts of energy and thus increasing its amount or activity is a promising therapeutic approach to combat metabolic disease. In humans, major deposits of brown fat cells are found intimately associated with large blood vessels, corresponding to perivascular adipose tissue (PVAT). However, the cellular origins of PVAT are poorly understood. We applied single cell transcriptomic analyses, ex vivo adipogenesis assays, and genetic fate mapping to determine the identity of perivascular adipocyte progenitors. In mice, we found that thoracic PVAT develops from a fibroblastic lineage, consisting of progenitor cells (Pdgfra+; Ly6a+; Pparg-) and preadipocytes (Pdgfra+; Ly6a+; Pparg+). Progenitor and preadipocyte cells in PVAT shared transcriptional similarity with analogous cell types in white adipose tissue, pointing towards a conserved hierarchical structure of adipose lineage cells. Interestingly, the aortic adventitia of adult animals contained a novel population of adipogenic smooth muscle cells (SMCs) (Myh11+; Pdgfra-; Pparg+) that contributed to perivascular adipocyte formation. Similarly, human PVAT contained presumptive fibroblastic and SMC-like adipocyte progenitors, as revealed by single nucleus RNAseq. Taken together, these studies define distinct populations of progenitor cells for thermogenic PVAT, providing a foundation for developing strategies to augment brown fat activity.

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Project description:Brown adipose tissue can expend large amounts of energy and thus increasing its amount or activity is a promising therapeutic approach to combat metabolic disease. In humans, major deposits of brown fat cells are found intimately associated with large blood vessels, corresponding to perivascular adipose tissue (PVAT). However, the cellular origins of PVAT are poorly understood. We applied single cell transcriptomic analyses, ex vivo adipogenesis assays, and genetic fate mapping to determine the identity of perivascular adipocyte progenitors. In mice, we found that thoracic PVAT develops from a fibroblastic lineage, consisting of progenitor cells (Pdgfra+; Ly6a+; Pparg-) and preadipocytes (Pdgfra+; Ly6a+; Pparg+). Progenitor and preadipocyte cells in PVAT shared transcriptional similarity with analogous cell types in inguinal white adipose tissue (IWAT), pointing towards a conserved hierarchical structure of adipose lineage cells. Interestingly, the aortic adventitia of adult animals contained a novel population of adipogenic smooth muscle cells (SMCs) (Myh11+; Pdgfra-; Pparg+) that contributed to perivascular adipocyte formation. Similarly, human PVAT contained presumptive fibroblastic and SMC-like adipocyte progenitors, as revealed by single nucleus RNAseq. Taken together, these studies define distinct populations of progenitor cells for thermogenic PVAT, providing a foundation for developing strategies to augment brown fat activity

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Transcriptome analysis of JAK2V617F HSPC and endogenous HSPC from irradiated and non-irradiated legs of recipient mice transplanted with JAK2V617F hematopoietic cells

Project description:using transplantation of transgenic knock-in JAK2V617F hematopoietic cells into a single irradiated leg, we show development of Polycythemia Vera (PV) from a single anatomical site in immuno-competent mice. Mutant cells colonizing the non-irradiated leg efficiently induce PV. We compared transcriptomic profiles of sorted JAK2V617F HSPC and their reciprocal endogenous WT HSPC in the non-irradiated and irradiated legs from recipient mice transplanted with JAK2V617F hematopoietic cells.

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TLR signaling in PBMCs acquired from BALB/c mice (10 days post-BMT) after being transplanted with T-cell depleted bone marrow alone (BMTCD), or in combination with TLR2,4,7-tolerant splenocytes, over their PBS-pretreated counterparts.

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2017-04-21 | GSE80574 | GEO

Blood pressure changes PVAT function and transcriptome: use of the mid-thoracic aorta coarcted rat

Project description:A mid-thoracic aorta coarcted rat was created to generate a stable pressure difference above versus below the coarctation ligature. This study determined that the PVAT around the thoracic aorta exposed to a higher pressure has a significantly reduced ability to assist stress relaxation versus that below the ligature and appears to retain the ability to be anticontractile. At the same time, the PVAT around the thoracic aorta exposed to higher pressure had a reduced adipogenic potential versus that below the ligature. Transcriptomics analyses indicated that PVAT below the coarctation showed the greatest number of DEGs with an increased profile of the synaptic neurotransmitter gene network.

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