La prolactine et son fragment 16 kDa dans les tissus de mammifères

Lkhider, Mustapha; Seddiki, Touria; Ollivier-Bousquet, Michèle

doi:10.1051/medsci/201026121049

Cited by 7 publications

(2 citation statements)

References 40 publications

(56 reference statements)

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“…Recent results suggest tissue enzymes play an important role in the production of this form of PRL in several tissues including the retina, myocardium, and mammary glands. The cleavage leading to the production of 16 kDa PRL may occur extracellularly in the interstitial medium and therefore in the vicinity of blood capillaries [36]. …”

Section: Discussionmentioning

confidence: 99%

Correlations of Vascular Architecture and Angiogenesis with Pituitary Adenoma Histotype

Takano

Akutsu

Hara

et al. 2014

International Journal of Endocrinology

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Vascular endothelial growth factor (VEGF) is a potent angiogenic factor in solid tumors. However, its role in angiogenesis in pituitary adenoma is controversial. Angiogenesis in solid tumors including pituitary adenoma is commonly evaluated by microvascular density (MVD). Here, we evaluated MVD and the role of VEGF in vascular architecture in 51 pituitary adenomas (24 nonfunctioning, 13 prolactin-secreting, 10 growth hormone-secreting, 3 adrenocorticotropic hormone-secreting, and 1 thyroid-stimulating hormone-secreting). Paraffin sections were stained with CD34 and VEGF. MVD and vascular architecture parameters (vessel area, diameter, perimeter, and roundness) were evaluated in CD34-stained sections. Immunohistochemistry showed 27/51 tumors (53%) were VEGF-positive. There were no significant differences in MVD, any vascular parameter, or adenoma volume between VEGF-positive and VEGF-negative tumors. VEGF mRNA expression was significantly higher in VEGF-positive tumors. There were no significant correlations between VEGF mRNA expression and MVD or vascular parameters. However, vessel diameter and perimeter were significantly larger in prolactin-secreting than nonfunctioning and growth hormone-secreting macroadenomas. The difference in vessel diameter was observed among both VEGF-positive and all adenomas (micro- and macroadenoma). Thus, VEGF may have limited roles in the development of vascular architecture and tumor angiogenesis in pituitary adenomas, but the differences in vessel architecture by histotype (i.e., larger vessel diameter and perimeter in prolactin-secreting adenomas) suggest the hormonal regulation of vessel architecture rather than angiogenesis

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Section: Discussionmentioning

confidence: 99%

Correlations of Vascular Architecture and Angiogenesis with Pituitary Adenoma Histotype

Takano

Akutsu

Hara

et al. 2014

International Journal of Endocrinology

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“…The intact 199 amino acid, 23 kD human PRL molecule is proangiogenic [51,[60][61][62][63][64][65][66]. However, shorter 16 kD fragments of PRL family members potently inhibit angiogenesis and are therefore termed angioinhibins [49,51,60,66,67].…”

Section: Proangiogenic Activities Of Plf and Prlmentioning

confidence: 99%

A Positive Feedback Loop Between Prolactin and Stat5 Promotes Angiogenesis

Yang

Friedl

2014

Advances in Experimental Medicine and Biology

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The signal transduction events that orchestrate cellular activities required for angiogenesis remain incompletely understood. We and others recently described that proangiogenic mediators such as fibroblast growth factors can activate members of the signal transducers and activators of transcription (STAT) family. STAT5 activation is necessary and sufficient to induce migration, invasion and tube formation of endothelial cells. STAT5 effects on endothelial cells require the secretion of the prolactin (PRL) family member proliferin-1 (PLF1) in mice and PRL in humans. In human endothelial cells, PRL activates the PRL receptor (PRLR) resulting in MAPK and STAT5 activation, thus closing a positive feedback loop. In vivo, endothelial cell-derived PRL is expected to combine with PRL of tumor cell and pituitary origin to raise the concentration of this polypeptide hormone in the tumor microenvironment. Thus, PRL may stimulate tumor angiogenesis via autocrine, paracrine, and endocrine pathways. The disruption of tumor angiogenesis by interfering with PRL signaling may offer an attractive target for therapeutic intervention.

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État de l’art sur la prolactine

Chabbert-Buffet

2013

Acquis Et Limites en Sénologie / Assets and Limits in Breast Diseases

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La prolactine et son fragment 16 kDa dans les tissus de mammifères

Cited by 7 publications

References 40 publications

Correlations of Vascular Architecture and Angiogenesis with Pituitary Adenoma Histotype

Correlations of Vascular Architecture and Angiogenesis with Pituitary Adenoma Histotype

A Positive Feedback Loop Between Prolactin and Stat5 Promotes Angiogenesis

État de l’art sur la prolactine

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