Angiogenin, angiopoietin-1, angiopoietin-2, and endostatin serum levels in inflammatory bowel disease

Oikonomou, Konstantinos; Kapsoritakis, Andreas; Kapsoritaki, Anastasia I; Manolakis, Anastassios C.; Tiaka, Elisavet K.; Tsiopoulos, F.; Tsiompanidis, Ilias; Potamianos, S.

doi:10.1002/ibd.21410

Cited by 55 publications

(43 citation statements)

References 53 publications

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“…Measurements of different proangiogenic factors in human plasma and/or inflamed gut tissue have revealed significant increases in the levels of VEGF-A, platelet-derived growth factor, angiopoietin-1 and -2, and other growth factors (266,270,359). Less attention has been devoted to the changes in antiangiogenic factors in IBD.…”

Section: Vascular Responses To Chronic Inflammationmentioning

confidence: 96%

The Gastrointestinal Circulation: Physiology and Pathophysiology

Granger

Holm

Kvietys

2015

Comprehensive Physiology

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The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response.

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Section: Vascular Responses To Chronic Inflammationmentioning

confidence: 96%

The Gastrointestinal Circulation: Physiology and Pathophysiology

Granger

Holm

Kvietys

2015

Comprehensive Physiology

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“…Hypertension, a major risk factor for thrombotic events, has been characterized by low serum levels of ANG, which promotes the onset of the disease [154,155]. ANG levels are significantly higher in IBD patients than in healthy controls [118]. Moreover, ANG levels are also increased in children and adolescent patients with type 1 diabetes [156].…”

Section: Ang and Other Diseasesmentioning

confidence: 97%

“…ANG-mediated tiRNAs are also increased and abundant in chronic hepatitis B and C infection, suggesting that ANG may play roles in viral infection [117]. Moreover, ANG may have antiinflammatory activity because its protein concentrations in serum are increased during the inflammatory response or tumour necrosis factor alpha and interleukin -1β treatment [102,118,119]. The mechanisms by which ANG suppresses the inflammatory response may involve the inhibition of TBK1-mediated NF-κB nuclear translocation [120].…”

Section: Ang Participates In Immune Responsesmentioning

confidence: 99%

Three decades of research on angiogenin: a review and perspective

Sheng¹,

Xu²

2016

ABBS

181

201

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As a member of the vertebrate-specific secreted ribonucleases, angiogenin (ANG) was first isolated and identified solely by its ability to induce new blood vessel formation, and now, it has been recognized to play important roles in various physiological and pathological processes through regulating cell proliferation, survival, migration, invasion, and/or differentiation. ANG exhibits very weak ribonucleolytic activity that is critical for its biological functions, and exerts its functions through activating different signaling transduction pathways in different target cells. A series of recent studies have indicated that ANG contributes to cellular nucleic acid metabolism. Here, we comprehensively review the results of studies regarding the structure, mechanism, and function of ANG over the past three decades. Moreover, current problems and future research directions of ANG are discussed. The understanding of the function and mechanism of ANG in a wide context will help to better delineate its roles in diseases, especially in cancer and neurodegenerative diseases.

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“…30 Increased serum levels of angiogenic factors have been found in CD patients. 31,32 The majority of studies regarding CD have focused on intestinal mucosa, and conclusions of the significance of SP and NK1 receptors in the regulation of inflammation are controversial. For instance, SP and NK1 receptor levels were reported to be increased in CD mucosa in some studies 14,17,33,34 whereas other studies have shown the opposite 35 or no difference between SP levels of CD patients and controls.…”

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confidence: 99%

Distinct differences in tachykinin gene expression in ulcerative colitis, Crohn’s disease and diverticular disease: a role for hemokinin‐1?

Liu

Markus

Saghire

et al. 2011

Neurogastroenterology Motil

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Background In the intestine, the tachykinins substance P (SP) and neurokinin A (NKA) are found in neurons and have key roles in motility, secretion, and immune functions. A new tachykinin, hemokinin (HK-1), has been identified in non-neuronal cells in recent years and its role in intestinal inflammation is unclear. We aimed to examine the expression of genes encoding tachykinin peptides and receptors in colon from patients with ulcerative colitis (UC), Crohn's disease (CD), and acute diverticular disease (DD). Methods Human colon segments were dissected into mucosa and muscle, and evaluated for tachykinin and tachykinin receptor gene expression by real-time PCR. Key Results In UC mucosa, the TAC4 gene (encoding HK-1) was 10-fold more abundant than in control mucosa (P < 0.01). Similarly, TAC1 (encoding SP and NKA) and TACR1 (encoding NK1 receptor) displayed 6-fold and 12-fold upregulation, respectively, in UC mucosa, but no change occurred in UC muscle. In contrast to UC, no difference was observed for any tachykinin genes in CD mucosa. In CD muscle, expression of TAC1 (P < 0.01), TAC4 and TACR1 (both P < 0.05) were moderately upregulated. In DD, there was a decrease in TACR1 (P < 0.05), and TACR2 (encoding NK2 receptor, P < 0.0001) in muscle compared with control. Histological staining showed increased collagen fibers between muscle bundles in DD smooth muscle. Conclusions & Inferences We provide evidence for the first time that HK-1, like SP, may be involved in the pathophysiology of inflammatory bowel disease. Distinctly different expression patterns of tachykinin-related genes occur in UC, CD and DD.

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Angiogenin, angiopoietin-1, angiopoietin-2, and endostatin serum levels in inflammatory bowel disease

Abstract: Elevated serum angiogenin and angiopoietin-2 levels and lower serum angiopoietin-1 levels were shown in IBD patients, as well as a different pattern of angiogenic factor alterations related to location, treatment, smoking habits and gender.

Cited by 55 publications

References 53 publications

The Gastrointestinal Circulation: Physiology and Pathophysiology

The Gastrointestinal Circulation: Physiology and Pathophysiology

Three decades of research on angiogenin: a review and perspective

Distinct differences in tachykinin gene expression in ulcerative colitis, Crohn’s disease and diverticular disease: a role for hemokinin‐1?

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