早老症分子機轉之研究
Date Issued
2001
Date
2001
Author(s)
胡務亮
DOI
892320B002229
Abstract
Aging is a mysterious process results from multiple
factors, and studies of the causes of aging are often
obscured by the complexity of this phenomenon.
Therefore, it is suggested that progeria, which presents
a less complicated etiology and phenotype may allow
research to focus on a regulation site involved in
development and aging. Hutchinson-Gilford progeria
syndrome (progeria) is a rare disease characterized by
selected features of premature aging. Presentations
include a general failure of the child to thrive, and
features of an aged appearance of the skin, alopecia,
decreased subcutaneous fat, prominent scalp veins,
thin limbs, and osteolysis. The formation of
atherosclerotic plaques result in the death of the
majority of progeria patients in the second decade of
life. The etiology of progeria is still unknown. Some
other progeroid syndromes have been found to be
associated with defects in either DNA repair or
replication. For example, the Werner syndrome WRN
gene is a DNA helicase. These diseases usually
demonstrate clear UV sensitivity or tumor formation.
Previous studies on progeria showed many
non-specific changes. In order to make a breakthrough
the molecular basis of progeria, we plan to do
differential display study. We have had cultured skin
fibroblasts from domestic patients with progeria. We
have extract RNA from skin fibroblasts from both
normal controls and progeria patients. The passage
numbers are from 10 to 12. Ordinarily the progeria
cells survive not much beyond 20 generations, but
normal cells usually survive more than 30 generations.
We label the RNA with non-isotope method. The
labeled probes were used to hybridize micro-array
filter paper. The results showed that the differences
between the two kinds of cells were quite large, and
the background noise was high. We tried several times,
but we still can not get readable result to further
analysis. We hope in the future, modern micro-array
techniques could be applied to this project, that both
hybridization, signal development and reading will be
automatic. Then we will have chance to overcome
current obstacles.
Subjects
Progeria
Hutchinson-Gilford syndrome
differential display
Publisher
臺北市：國立臺灣大學醫學院小兒科
Type
report
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