Beitrag zur elektronenmikroskopischen Morphologie der menschlichen Placenta

Novel Role of Antioxidant-1 (Atox1) as a Copper-dependent Transcription Factor Involved in Cell Proliferation

“…We previously reported that Atox1 is expressed in the nucleus in the intimal lesions of atherosclerosis, which contain highly proliferating cells (19). Furthermore, higher levels of copper are located in the nuclei in highly proliferating tumors, whereas copper is located predominantly within the cytoplasm in normal tissue (13)(14)(15). In addition, nuclear accumulation of copper is strongly associated with proliferation of hepatocytes in Atp7b Ϫ/Ϫ mice, an animal model of Wilson disease (34).…”

“…Accumulating evidence suggest that copper plays a fundamental role in regulating cell growth involved in physiological repair processes such as wound healing and angiogenesis as well as in various pathophysiologies including tumor growth, atherosclerosis, and neuron degenerative diseases (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Of note, hyperproliferative lesions in cancer and atherosclerosis have higher copper levels in cell nuclei than normal tissues (13)(14)(15), while copper chelation prevents tumor growth and neointimal thickening after vascular injury (9 -12). Furthermore, Phase I and II clinical trials for the treatment of solid tumors by copper chelation showed its efficacy in disease stabilization (10,11).…”

The Villous Cytotrophoblast as an Index of Placental Ischaemia

“…It has been widely accepted that the Langhans cells of the placental villi disappear by the 30th week of pregnancy (Strachan, 1923 ;Hormann, 1948;Paine, 1957;Horn and Horalek, 1961;Clavero Nunez, 1961), except in cases of erythroblastosis foetalis (Hellman and Hertig, 1938). There is now, however, convincing evidence of the presence of such cells in the normal mature placenta, when examined both by light microscopy (Wislocki and Bennett, 1943;Sauramo, 1951;Thomsen and Blankenburg, 1956;Wigglesworth, 1962) and by electron microscopy (Wislocki and Dempsey, 1955;Vokaer, 1957;Sawasaki et al, 1957;Arnold et al, 1961). Wigglesworth (1962) further noted that there was a marked proliferation of villous Langhans cells in cases of pre-eclamptic toxaemia, and suggested that this could result from placental ischaemia.…”