Collins James F
Department of Pediatrics and Nutritional Sciences, Steele Children's Research Center, University of Arizona, Tucson, Arizona, USA.
Biol Res. 2006;39(1):25-37.
Previous studies revealed novel genetic changes in the duodenal mucosa of iron-deprived rats during postnatal development. These observations are now extended to compare the genetic response to iron deficiency in the duodenum versus jejunum of 12-wk-old rats. cRNA samples were prepared from the duodenal and jejunal mucosa of three groups each of control and iron-deficient rats and hybridized with RAE 230A and 230B gene chips (Affymetrix). Stringent data reduction strategies were employed. Results showed that several genes were similarly induced in both gut segments, including DMT1, Dcytb, transferrin receptor 1, heme oxygenase 1, metallothionein, the Menkes copper ATPase (ATP7A), tripartitie motif protein 27, and the sodium-dependent vitamin C transporter. However, a subset of genes showed regulation in only one or the other gut segment. In duodenum only, gastrokine 1, trefoil factor 1 and claudin 2 were induced by iron-deficiency. Other genes previously identified were only regulated in the duodenum. Overall, these studies demonstrate similarities and distinct differences in the genetic response to iron deprivation in the duodenum versus jejunum and provide evidence that more distal gut segments also may play a role in increasing iron absorption in iron-deficiency anemia.
先前的研究揭示了出生后发育期间缺铁大鼠十二指肠黏膜中的新基因变化。现在将这些观察结果进行扩展,以比较12周龄大鼠十二指肠与空肠对缺铁的基因反应。从每组三只对照大鼠和缺铁大鼠的十二指肠和空肠黏膜中制备cRNA样本,并与RAE 230A和230B基因芯片(Affymetrix)杂交。采用了严格的数据缩减策略。结果显示,在两个肠道段中均有几个基因被类似地诱导,包括二价金属离子转运体1(DMT1)、十二指肠细胞色素b(Dcytb)、转铁蛋白受体1、血红素加氧酶1、金属硫蛋白、门克斯铜ATP酶(ATP7A)、三联基序蛋白27和钠依赖性维生素C转运体。然而,一部分基因仅在一个或另一个肠道段中显示出调控。仅在十二指肠中,缺铁诱导了胃动素1、三叶因子1和紧密连接蛋白2。先前鉴定的其他基因仅在十二指肠中受到调控。总体而言,这些研究证明了十二指肠与空肠对缺铁的基因反应中的相似性和明显差异,并提供了证据表明更远端的肠道段在缺铁性贫血中增加铁吸收方面也可能发挥作用。