Endothelial/Pericyte Interactions

Armulik, Annika; Abramsson, Alexandra; Betsholtz, Christer

doi:10.1161/01.res.0000182903.16652.d7

Cited by 1,788 publications

(1,714 citation statements)

References 134 publications

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“…27 Interestingly, in TPA-treated skin tissues, ␣-SMA ϩ cells are mainly located around the blood vessels in the skin ( Figure 1C and see Supplemental Figure S2, http://ajp.amjpathol.org) and these cells are likely to be vascular smooth muscle cells or pericytes around the vascular walls. 28 We double-stained the skin tissue with ␣-SMA and FSP1 and found that there were seldom ␣-SMA and FSP1 double positive cells in the TPA-treated skin ( Figure 1B), which is similar with the former discovery in the tumor, 29 indicating that TPA mainly simulated the proliferation of a unique population of FSP1 ϩ fibroblasts that are regarded as the most important class of fibroblasts present in many tissues. 20,30 FSP1 usually serves as a sensitive and specific marker for fibroblasts.…”

Section: Discussionsupporting

confidence: 72%

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Zhang

Chen

Xiao

et al. 2011

The American Journal of Pathology

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Cancer development is often associated with increased fibroblast proliferation and extensive fibrosis; however, the role of fibroblasts during carcinogenesis remains largely unknown. Using the 7,12-dimethylbenz-(a)anthracene and 12-O-tetradecanoylphorbol-13-acetateinduced two-stage skin carcinogenesis model, we demonstrated here that there was a massive accumulation and proliferation of fibroblasts in the skin shortly after application of carcinogen. Selective abatement of these cells during the promotion stage drastically decreased incidence and progression of papillomas. This correlated well with reduced macrophage infiltration and impaired cytokine storm in the affected skin. 12-O-tetradecanoylphorbol-13-acetate stimulated skin fibroblasts, secreting high levels of monocyte chemotactic protein-1, and neutralization of this chemokine eliminated almost completely the fibroblast-induced chemotaxis of macrophages. These results strongly suggest that fibroblasts promote skin tumor development by producing monocyte chemotactic protein-1 and maintaining chronic inflammation.

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Section: Discussionsupporting

confidence: 72%

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Zhang

Chen

Xiao

et al. 2011

The American Journal of Pathology

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“…2,3,6,9,10,12e16 Such broad adaptability is proposed to enable pericytes and resident fibroblasts to repeatedly adjust to support growing, injured, or regenerating vascular or airway structures. 2,6,13 Figure 1 Tissue architecture and mesenchymal lineages in the lung. A: Electron microscopy photomicrographs of normal mouse lung showing fibroblast processes abutting epithelium and pericyte processes attached to endothelium and within a loose capillary basement membrane.…”

Section: Characteristics Of Lung Pericytes and Resident Fibroblastsmentioning

confidence: 99%

Lung Pericytes and Resident Fibroblasts

Barron

Gharib

Duffield

2016

The American Journal of Pathology

109

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Pericytes, resident fibroblasts, and mesenchymal stem cells are poorly described cell populations. They have recently been characterized in much greater detail in rodent lungs and have been shown to play important roles in development, homeostasis, response to injury and pathogens, as well as recovery from damage. These closely related mesenchymal cell populations form extensive connections to the lung's internal structure, as well as its internal and external surfaces. They generate and remodel extracellular matrix, coregulate the vasculature, help maintain and restore the epithelium, and act as sentries for the immune system. In this review, we revisit these functions in light of significant advances in characterizing and tracking lung fibroblast populations in rodents. Lineage tracing experiments have mapped the heritage, identified functions that discriminate lung pericytes from resident fibroblasts, identified a subset of mesenchymal stem cells, and shown these populations to be the predominant progenitors of pathological fibroblasts and myofibroblasts in lung diseases. These findings point to the importance of resident lung mesenchymal populations as therapeutic targets in acute lung injury as well as fibrotic and degenerative diseases. Far from being passive and quiescent, pericytes and resident fibroblasts are busily sensing and responding, through diverse mechanisms, to changes in lung health and function. (Am J Pathol 2016 http://dx

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“…Reciprocal communication between endothelial cells and pericytes also involve angiopoietin-Tie2 signaling that is required for vessel stabilization (Armulik et al, 2005). Paracrine signaling between pericytes and endothelial cells is suggested by the general expression of the Tie2 receptor on endothelial (Sato et al, 1995) cells, whilst its ligand Ang1 is mainly expressed on juxtaposed perivascular pericytes (Sundberg et al, 2002).…”

Section: Pericyte/vsm-endothelial Cell Interactions In the Tumor Micrmentioning

confidence: 99%

The brain tumor microenvironment

Charles

Holland

Gilbertson

et al. 2011

Glia

693

327

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High-grade brain tumors are heterogeneous with respect to the composition of bona fide tumor cells and with respect to a range of intermingling parenchymal cells. Glioblastomas harbor multiple cell types, some with increased tumorigenicity and stem cell-like capacity. The stem-like cells may be the cells of origin for tumor relapse. However, the tumor-associated parenchymal cells such as vascular cells, microglia, peripheral immune cells, and neural precursor cells also play a vital role in controlling the course of pathology. In this review, we describe the multiple interactions of bulk glioma cells and glioma stem cells with parenchymal cell populations and highlight the pathological impact as well as signaling pathways known for these types of cell-cell communication. The tumor-vasculature not only nourishes glioblastomas, but also provides a specialized niche for these stem-like cells. In addition, microglial cells, which can contribute up to 30% of a brain tumor mass, play a role in glioblastoma cell invasion. Moreover, non-neoplastic astrocytes can be converted into a reactive phenotype by the glioma microenvironment and can then secrete a number of factors which influences tumor biology. The young brain may have the capacity to inhibit gliomagenesis by the endogenous neural precursor cells, which secrete tumor suppressive factors. The factors, pathways, and interactions described in this review provide a new prospective on the cell biology of primary brain tumors, which may ultimately generate new treatment modalities. However, our picture of the multiple interactions between parenchymal and tumor cells is still incomplete. V

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Endothelial/Pericyte Interactions

Cited by 1,788 publications

References 134 publications

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

FSP1+ Fibroblasts Promote Skin Carcinogenesis by Maintaining MCP-1-Mediated Macrophage Infiltration and Chronic Inflammation

Lung Pericytes and Resident Fibroblasts

The brain tumor microenvironment

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