These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Abnormalities of vertebral formation and Hox expression in congenital kyphoscoliotic rats.
    Author: Seki T, Shimokawa N, Iizuka H, Takagishi K, Koibuchi N.
    Journal: Mol Cell Biochem; 2008 May; 312(1-2):193-9. PubMed ID: 18327665.
    Abstract:
    Scoliosis is a condition that involves an abnormal curvature and deformity of the spinal vertebrae. The genetic background and key gene for congenital scoliosis in humans are still poorly understood. Ishibashi rats (ISR) have congenital malformation of the lumbar vertebrae leading to kyphoscoliosis similar to that seen in humans. To understand the pathogenesis of congenital scoliosis, we have studied the abnormality of vertebral formation and the associated gene expression in ISR. Almost all ISR showed kyphosis or scoliosis of the lumbar vertebrae. In ISR with severe kyphosis, some vertebral disks were missing and some vertebral bodies were fused. Of the ISR, 27% showed hemi-lumbarization of lumbar and sacral vertebrae. Homeotic transformation of the first sacral vertebra into the seventh lumbar vertebra and the resultant loss of the fourth sacral vertebra were seen in half of the ISR. We also found unilateral fusions and deformities of primary ossification centers of the lumbar vertebral column in fetal ISR. Moreover, we observed that the expression levels of Hox10 and Hox11 paralogs in lumbo-sacral transitional areas of ISR were extremely low compared with those of normal rats. These results suggest that fusion of primary ossification centers in lumbar vertebrae in the embryonic period causes scoliosis and kyphosis and that Hox genes are involved in the occurrence of homeotic transformation in lumbo-sacral vertebrae of congenital kyphoscoliotic ISR.
    [Abstract] [Full Text] [Related] [New Search]