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铜缺乏猪主动脉中胶原蛋白和弹性蛋白生物合成增加的诱导作用。

Induction of increased collagen and elastin biosynthesis in copper-deficient pig aorta.

作者信息

Hill K E, Davidson J M

出版信息

Arteriosclerosis. 1986 Jan-Feb;6(1):98-104. doi: 10.1161/01.atv.6.1.98.

Abstract

Young pigs raised on a copper-deficient diet develop severe abnormalities of connective tissue due to defective cross-linking of collagen and elastin. They eventually succumb to anemia and cardiovascular damage, the latter apparently due to the defective connective tissue metabolism. We evaluated the effects of nutritional copper deficiency upon collagen and elastin synthesis using short-term explant cultures of the medial portion of four successive segments of the descending aorta from 110-day-old pigs raised on a copper-deficient diet. Collagen synthesis was evaluated by collagenase susceptibility, and elastin synthesis was quantified by immunoprecipitation with an antiporcine-elastin antiserum. In the normal developing aorta, elastin synthesis was maximal in the upper thoracic aorta, while levels of collagen synthesis were highest in the lower abdominal aorta. Both activities subsided by 110 days postpartum. Compared with controls, the copper-deficient group showed: 1) histopathologic changes confined to the luminal half of the thoracic aorta; 2) a 1.3- to 1.6-fold increase in cellularity along the entire length of the organ; 3) a 1.3- to 2.4-fold increase in relative collagen synthesis, the greatest change occurring in the thoracic portion; 4) a 3- to 4-fold increase of relative elastin synthesis in the thoracic aorta, the abdominal aorta remaining unchanged; 5) 4- to 10-fold increases in collagen production; and 6) a greater than 15-fold increase in elastin production by the tissue of the thoracic aorta.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

用缺铜饮食饲养的幼猪,由于胶原蛋白和弹性蛋白交联缺陷,会出现严重的结缔组织异常。它们最终会死于贫血和心血管损伤,后者显然是由于结缔组织代谢缺陷所致。我们使用从以缺铜饮食饲养的110日龄猪的降主动脉连续四个节段的内侧部分进行短期外植体培养,评估了营养性铜缺乏对胶原蛋白和弹性蛋白合成的影响。通过胶原酶敏感性评估胶原蛋白合成,并用抗猪弹性蛋白抗血清进行免疫沉淀来定量弹性蛋白合成。在正常发育的主动脉中,弹性蛋白合成在上胸主动脉中最高,而胶原蛋白合成水平在下腹主动脉中最高。产后110天时,这两种活性均下降。与对照组相比,缺铜组表现为:1)组织病理学变化局限于胸主动脉的管腔半侧;2)沿器官全长细胞数量增加1.3至1.6倍;3)相对胶原蛋白合成增加1.3至2.4倍,最大变化发生在胸部;4)胸主动脉中相对弹性蛋白合成增加3至4倍,腹主动脉保持不变;5)胶原蛋白产生增加4至10倍;6)胸主动脉组织的弹性蛋白产生增加超过15倍。(摘要截短于250字)

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