Cell apoptosis during the cloacal embryonic development in rats with anorectal malformations / 中国当代儿科杂志

<p><b>OBJECTIVE</b>In the normal embryonic development of anorectum, apoptosis plays an important role. To explore the role of apoptosis in anorectal malformations (ARM), this study investigated cell apoptosis during the cloacal embryonic development in ARM embryos.</p><p><b>METHODS</b>ARM embryos were induced by intragastric administration of ethylenethiourea (125 mg/kg) for pregnant rats on embryonic day 10 (E10). The distribution of apoptotic cells in the cloaca was ascertained by hematoxylin and eosin and TUNEL staining in the normal control embryos (n=102) and ARM embryos (n=147) on E13, E13.5, E14, E15 and E16.</p><p><b>RESULTS</b>On E13, apoptotic cells were detected in the urorectal septum of rat embryos in the control group. With the development of embryos, the number of apoptotic cells in the mesenchyme of urorectal septum gradually increased and a large number of apoptotic cells were seen in the dorsal rectal mesenchyme. On E14, apoptotic cells appeared at the terminal rectum and the dorsal cloacal membrane. On E15, the urorectal septum fused with the cloacal membrane and apoptotic cells in the urorectal septum mesenchyme continuously extended down to the fusion region. Compared with the control group, apoptotic cells in the urorectal septum, the dorsal rectal mesenchyme and the cloacal membrane of the ARM rat embryos were significantly reduced during the embryonic development. The development of the urorectal septum was delayed and it did not fuse with the cloacal membrane in ARM embryos.</p><p><b>CONCLUSIONS</b>During the embryonic development of cloaca, abnormal apoptosis in the urorectal septum, the dorsal rectal mesenchyme and the cloacal membrane may be one of the reasons for anorectal malformations. The proper regulation of cell apoptosis may be one of the key mechanisms for normal development of anorectum in the embryonic stage.</p>

Acetylation of hepatic histone H3 in rats with intrauterine growth retardation / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effects of intrauterine growth retardation (IUGR) caused by malnutrition during pregnancy on the acetylation of histone H3 and expression of histonedeacetylase1(HDAC1) in the hepar of the adult offspring and to explore the relationship between them.</p><p><b>METHODS</b>Male 8-week-old offspring from maternal protein-malnutrition dams were studied. The expression of HDAC1 mRNA in the hepar was measured by fluorescent quantization RT-PCR. The levels of hepatic nuclear HDAC1 protein and acetylation of histone H3/K9 were assessed by Western blot.</p><p><b>RESULTS</b>The hepatic HDAC1 mRNA expression in IUGR rats was reduced to 54% of that of normal control rats (t=2.042, p<0.05). A decline in nuclear expression of HDAC1 protein (438 +/- 47) was also noted when compared with normal controls (1,128 +/- 110) (t=2.179, p<0.05). In contrast, the percentage of acetylated histone H3/K9 in IUGR rats (17.3 +/- 1.6%) increased significantly compared with that of normal control rats (10.5 +/- 1.2%) (t=3.597, p<0.01). The level of acetylated histone H3/K9 was negatively correlated with the HDAC1 protein concentration (r=-0.781, p<0.01).</p><p><b>CONCLUSIONS</b>Increased hepatic acetylation of histone H3 in the IUGR offspring might be caused by decreased HDAC1 expression in nuclear protein. This may contribute to the transcription change of some genes in the hepar.</p>