Project description:Mesenchymal stem cells (MSCs) reportedly exist in a vascular niche occupying the outer adventitial layer. However, these cells have not been well characterized in vivo in medium- and large-sized arteries in humans, and their potential pathological role is unknown. To address this, healthy and diseased arterial tissues were obtained as surplus surgical specimens and freshly processed. We identified that CD90 marks a rare adventitial population that co-expresses MSC markers including PDGFR?, CD44, CD73, and CD105. However, unlike CD90, these additional markers were widely expressed by other cells. Human adventitial CD90+ cells fulfilled standard MSC criteria, including plastic adherence, spindle morphology, passage ability, colony formation, and differentiation into adipocytes, osteoblasts, and chondrocytes. Phenotypic and transcriptomic profiling, as well as adoptive transfer experiments, revealed a potential role in vascular disease pathogenesis, with the transcriptomic disease signature of these cells being represented in an aortic regulatory gene network that is operative in atherosclerosis.
Project description:Primary mesenchymal CD105+CD90+CD13- and CD105+CD90+CD13+ populations from human lung were isolated and characterized using bulk population mRNA sequencing to understand differences between these populations.
Project description:We described differential expression of CD90 in gp38+ fibroblasts in murine colon. We functionally characterized CD90- and CD90+ fibroblasts by co-culturing with intestinal organoids. CD90+ colon fibroblasts were able to support organoid growth while CD90- did not.
Project description:To identify candidate genes involved in enhanced tumorigenicity and metastasis of CD90+ esophageal tumor-initiating cells. The esophageal squamous carcinoma cell (ESCC) cell line KYSE-140 was sorted into CD90+ and CD90- populations by flow cytometry. Total RNA was analyzed on Affymetrix Human Genome U133 Plus GeneChip 2.0 arrays.
Project description:To explore the functional difference between CD90+CD39+ and CD90+CD39- fibroblasts in human hypertrophic scar and normal skin, the gene expresson microarray was performed on Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39+ and Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39- cells sorted from suspension disgested from three human hypertrophic scar samples; and Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39+ cells sorted from suspension disgested from three human normal skin samples
Project description:In order to find the difference between human lung tissue-derived fibroblasts and human vascular adventitial fibroblasts for enhancing tumor formation ablity of human lung adenocarcinoma cell line A549, we found that human vascular adventitial fibroblasts enhance A549 tumor formation in vivo compared to human lung tissue-derived fibroblasts. To find the responsible genes for this phenomena, we used microarray analysis to find the expression difference between lung tissue-derived fibroblasts and vascular adventitial fibroblas Cultured human lung tissue-derived fibroblasts and human vascular adventitial fibroblasts were analyzed in replicates.
Project description:Human synovial biopsies were collected from normal and osteoarthritic joints. CD90 positive cells were isolated and confirmed to have multipotent differentiation capacity. An n=2 of normal and n=2 OA lines were run on the HuGene-1_0-st-v1 array.
Project description:The tunica adventitia ensheaths arteries and veins and contains presumptive mesenchymal stem cells (MSCs) involved in vascular remodeling. We show here that a subset of human adventitial cells expresses the CD10/CALLA cell surface metalloprotease. Sorted CD10+ adventitial cells developed promptly in culture into MSCs, exhibiting higher proliferation, clonogenic and osteogenic potentials than CD10- counterparts. CD10+ adventitial cells increased expression of the cell cycle protein CCND2 via ERK1/2 and prompted NELL1 expression via NF-κB. CD10 expression was upregulated in CD10+ adventitial cells through neural secreted protein sonic hedgehog-mediated Gli1 signaling. These results suggest that CD10 expression, which marks rapidly dividing cells in other normal and malignant cell lineages, plays a role in MSC homeostasis in human tissues.