Transcription Profiling of Platelet-Derived Growth Factor-B-Deficient Mouse Embryos Identifies RGS5 as a Novel Marker for Pericytes and Vascular Smooth Muscle Cells

Bondjers, Cecilia; Kalén, Mattias; Hellström, Mats; Scheidl, Stefan; Abramsson, Alexandra; Renner, Oliver; Lindahl, Per; Cho, Hyeseon; Kehrl, John H.; Betsholtz, Christer

doi:10.1016/s0002-9440(10)63868-0

Cited by 214 publications

(176 citation statements)

References 31 publications

(32 reference statements)

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“…23,24 However, in contrast to endosialin, RGS-5 expression is described not only for pericytes but also for cytokineactivated endothelial cells in models of atherosclerosis and during capillary tube formation. [25][26][27] Therefore, endosialin is an attractive target for the development of novel antiangiogenic therapies. Immature blood vessels are not covered by mural cells.…”

Section: Discussionmentioning

confidence: 99%

Endosialin (Tem1) Is a Marker of Tumor-Associated Myofibroblasts and Tumor Vessel-Associated Mural Cells

Christian

Winkler

Helfrich

et al. 2008

The American Journal of Pathology

145

149

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Tumor progression and metastasis are critically dependent on the tumor stroma consisting of fibrous connective tissue, newly formed blood vessels, extracellular matrix, and recruited inflammatory cells. Tumor stromal fibroblasts (activated fibroblasts or myofibroblasts) acquire a specific phenotype that differentiates them from normal resting fibroblasts. They express smooth muscle actin (SMA), and isolated myofibroblasts have higher proliferation rates than their normal counterparts.1 The importance of stromal mesenchymal interactions with adjacent epithelial cells during development is well characterized. Proliferation of mesenchymal cells is tightly controlled by soluble paracrine factors. Conversely, differentiated fibroblasts do not proliferate and acquire a quiescent phenotype.2 In contrast, the complex paracrine regulatory mechanisms between the mesenchymal tumor stroma compartment and the tumor compartment are far from being understood. Coinjection of activated fibroblasts and tumor cells has been shown to enhance the invasiveness of colon tumors.3 Tumor-associated fibroblasts affect migration and invasion of tumor cells by secreting extracellular matrix proteins, matrix metalloproteinases, and growth factors.4,5 Paracrine-acting factors affecting tumor and stromal cell interactions include fibroblast growth factors, hepatocyte growth factor, and transforming growth factor-␤. Correspondingly, elevated plasma levels of transforming growth factor-␤ have been shown to predict early metastasis.

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Section: Discussionmentioning

confidence: 99%

Endosialin (Tem1) Is a Marker of Tumor-Associated Myofibroblasts and Tumor Vessel-Associated Mural Cells

Christian

Winkler

Helfrich

et al. 2008

The American Journal of Pathology

145

149

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“…4). Rgs5 is also a marker for developing pericytes in the brain 17 , and its expression persists in adult brain vessels. We therefore investigated the role of RGS5 in the barrier function of brain capillaries during ischaemia.…”

Section: Hprt1mentioning

confidence: 99%

Vascular normalization in Rgs5-deficient tumours promotes immune destruction

Hamzah

Jugold²,

Kießling³

et al. 2008

Nature

495

425

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“…RGS5 was reported to be expressed in the heart, lung, skeletal muscle and small intestine (20). It is also reported to be expressed in pericytes and vascular smooth muscle cells (21). With regard to RGS5 and cancer, RGS5 expression has been demonstrated to be positively correlated with the degree of tumor differentiation in gastric carcinoma (22).…”

Section: Discussionmentioning

confidence: 99%

Regulator of G‑protein signaling 5 enhances portal vein invasion in hepatocellular carcinoma

et al. 2017

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Abstract. Portal vein invasion (PVI) is a major prognostic factor in hepatocellular carcinoma (HCC). The aim of the present study was to identify molecules that regulate PVI. Sections of cancerous tissue, paired noncancerous tissue and the PVI area were collected from 3 frozen HCC sections, using laser microdissection. The present study focused on 3 upregulated molecules, integrin β3 (ITGB3), secreted phosphoprotein 1 (SPP1) and regulator of G-protein signaling 5 (RGS5), and 2 molecules that were downregulated in PVI tissue compared with cancer tissue, metallothionein 1G (MT1G) and metallothionein 1H (MT1H), as determined by cDNA microarray analysis. Reverse transcription-quantitative polymerase chain reaction analysis of 32 HCC cases revealed that RGS5 mRNA levels were significantly increased and MT1 G and MT1H mRNA levels were significantly decreased in cancerous tissue compared with noncancerous tissue. However, there was no significant difference in ITGB3 and SPP1 expression. There were no significant differences between the expression of these molecules and any clinicopathologic factors, including PVI. Immunohistochemical staining for RGS5 in 60 HCC cases demonstrated that RGS5 protein levels were higher in cancerous tissue compared with paired noncancerous tissue in 63.3% of HCC cases. Furthermore, high expression of RGS5 in cancerous tissue was significantly associated with PVI and tended to be associated with intrahepatic metastasis. Confluent multinodular type was significantly more frequent in cases with high expression of RGS5 in the cancerous tissue.Therefore, RGS5 may be a useful prognostic biomarker as well as a potential target of molecular therapy to treat HCC.

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Transcription Profiling of Platelet-Derived Growth Factor-B-Deficient Mouse Embryos Identifies RGS5 as a Novel Marker for Pericytes and Vascular Smooth Muscle Cells

Cited by 214 publications

References 31 publications

Endosialin (Tem1) Is a Marker of Tumor-Associated Myofibroblasts and Tumor Vessel-Associated Mural Cells

Endosialin (Tem1) Is a Marker of Tumor-Associated Myofibroblasts and Tumor Vessel-Associated Mural Cells

Vascular normalization in Rgs5-deficient tumours promotes immune destruction

Regulator of G‑protein signaling 5 enhances portal vein invasion in hepatocellular carcinoma

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