Mechanisms of normal and tumor-derived angiogenesis

Papetti, Michael; Herman, Ira M.

doi:10.1152/ajpcell.00389.2001

Cited by 674 publications

(625 citation statements)

References 237 publications

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“…Normal vessels are dependent on pericyte coverage to maintain their function, although tumour vessels are able to exist without them. 3 The degree of pericyte coverage varies among different tumour types, with prostate cancer taking an intermediate position with a pericyte coverage of about 30%. 17 The finding of a lower degree of pericyte coverage in LNCaP-19 was not unexpected, because that correlates with an ongoing angiogenesis and thereby with the high MVD previously detected in LNCaP-19 compared to LNCaP.…”

Section: Discussionmentioning

confidence: 99%

“…2 These changes in vessel morphology are a result of the angiogenic stimulation from the tumour cells, which is not as well orchestrated as in the development of normal tissues. 3 In prostate cancer, increased angiogenesis, detected as increased microvessel density (MVD), has been correlated both to Gleason grade, prostate-specific antigen relapse and time to progression, 4,5 as well as metastatic potential. 6 Angiogenesis has been demonstrated to be increased in androgen-independent prostate cancer in experimental animal models and in humans, 7,8 making these late stage cancers suitable targets for specific antiangiogenic strategies.…”

Section: Introductionmentioning

confidence: 99%

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Pericyte coverage decreases invasion of tumour cells into blood vessels in prostate cancer xenografts

Welén

Jennbacken

Tešan

et al. 2008

Prostate Cancer Prostatic Dis

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Androgen-independent prostate cancer is an aggressive disease with high angiogenic and metastatic potential. Increased microvessel density and altered invasion properties have previously been described in LNCaP-19, an androgen-independent subline to LNCaP. To characterize the differences in angiogenesis and invasion, the vessels of these tumour xenografts were investigated with immunohistochemistry, and the influence of tumour cells on endothelial cell migration, proliferation and tube formation was studied in vitro. The blood vessels of LNCaP were found to be stabilized by pericytes more frequently than vessels in LNCaP-19. Further, tumour cell invasion was decreased in pericyte-covered blood vessels in both the tumour types. LNCaP-19 displayed an increased potential to induce endothelial cell migration in vitro. In conclusion, pericyte coverage seems to be important for the invasion of tumour cells into blood vessels. Further, LNCaP-19 has lower pericyte coverage and an increased potential to induce endothelial cell migration, which reflects its high microvessel density.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pericyte coverage decreases invasion of tumour cells into blood vessels in prostate cancer xenografts

Welén

Jennbacken

Tešan

et al. 2008

Prostate Cancer Prostatic Dis

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“…VEGF-A is the only bona fide endothelial cell growth factor; moreover, its presence is essential for initiation of the angiogenic program (76,77). VEGF-A exhibits predominantly pro-angiogenic activity in AT (78).…”

Section: Angiogenesis a Rate-limiting Step For At Expansion And Remomentioning

confidence: 99%

Adipose tissue remodeling and obesity

Sun¹,

Kusminski²,

Scherer³

2011

J. Clin. Invest.

1,496

1,314

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To fulfill its role as the major energy-storing tissue, adipose has several unique properties that cannot be seen in any other organ, including an almost unlimited capacity to expand in a non-transformed state. As such, the tissue requires potent mechanisms to remodel, acutely and chronically. Adipocytes can rapidly reach the diffusional limit of oxygen during growth; hypoxia is therefore an early determinant that limits healthy expansion. Proper expansion requires a highly coordinated response among many different cell types, including endothelial precursor cells, immune cells, and preadipocytes. There are therefore remarkable similarities between adipose expansion and growth of solid tumors, a phenomenon that presents both an opportunity and a challenge, since pharmacological interventions supporting healthy adipose tissue adaptation can also facilitate tumor growth. IntroductionAdipose tissue (AT) can respond rapidly and dynamically to alterations in nutrient deprivation and excess through adipocyte hypertrophy and hyperplasia, thereby fulfilling its major role in wholebody energy homeostasis. AT remodeling is an ongoing process that is pathologically accelerated in the obese state, and thus, features such as reduced angiogenic remodeling, ECM overproduction, a heightened state of immune cell infiltration and subsequent proinflammatory responses prevail in many obese fat-pads (1). However, not all AT expansion is necessarily associated with pathological changes. The concept of the "metabolically healthy obese" state (2) suggests that some individuals can preserve systemic insulin sensitivity on the basis of "healthy" AT expansion, bypassing all of the aforementioned pathological consequences associated with obesity (3), thereby also avoiding the obesity-associated lipotoxic side effects. Many physiologically relevant processes important for human AT remodeling can be studied in rodent models, with the added advantage that processes related to AT expansion and reduction can occur at an extremely rapid rate. A 24-hour fast in a mouse is associated with a dramatic loss of AT mass and an acute remodeling process that involves rapid infiltration of macrophages; moreover, merely 24 to 48 hours of exposure to a high-fat diet (HFD) can cause a prompt increase in adipocyte size (4). AT is therefore an ideal model system to study rapid alterations in tissue expansion and reduction, as it adapts to a differential nutrient supply. Here, we will focus on key aspects of the intricate dynamics of AT remodeling and subsequent inflammatory consequences that arise from obesity.

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“…In humans, adipose tissue TNF- mRNA correlates with body mass index, percentage of body fat and hyperinsulinaemia (Katsuki et al, 1998). TNF- promotes endothelial cell tube formation in vitro and inhibits endothelial cell proliferation (Papetti et al, 2002). A functional role of TNF- in adipogenesis and insulin resistance has been studied in the genetically obese and diabetic ob/ob mice (Uysal et al, 1997).…”

Section: Growth Factors and Cytokinesmentioning

confidence: 99%