Ruan, J.
(Department of Clinical Laboratory, Chongqing Medical University)
,
Liu, X.G.
(Institute of Aging Research, Guangdong Medical College)
,
Zheng, H.L.
(Institute of Aging Research, Guangdong Medical College)
,
Li, J.B.
(Institute of Aging Research, Guangdong Medical College)
,
Xiong, X.D.
(Institute of Aging Research, Guangdong Medical College)
,
Zhang, C.L.
(Department of Clinical Laboratory, Chongqing Medical University)
,
Luo, C.Y.
(Institute of Laboratory Medicine, Guangdong Medical College)
,
Zhou, Z.J.
(Department of Biochemistry, Li Ka Shing Faculty of Medicine, The University of Hong Kong)
,
Shi, Q.
(Department of Clinical Laboratory, Chongqing Medical University)
,
Weng, Y.G.
(Department of Clinical Laboratory, Chongqing Medical University)
The A-type lamin deficient mouse line ($Lmna^{-/-}$) has become one of the most frequently used models for providing insights into many different aspects of A-type lamin function. To elucidate the function of Lmna in the growth and metabolism of mice, tissue growth and blood biochemistry ...
The A-type lamin deficient mouse line ($Lmna^{-/-}$) has become one of the most frequently used models for providing insights into many different aspects of A-type lamin function. To elucidate the function of Lmna in the growth and metabolism of mice, tissue growth and blood biochemistry were monitored in Lmna-deficient mice, heterozygous ($Lmna^{+/-}$) and wide-type ($Lmna^{+/+}$) backcrossed to C57BL/6 background. At 4 weeks after birth, the weight of various organs of the $Lmna^{-/-}$, $Lmna^{+/-}$ and $Lmna^{+/+}$ mice was measured. A panel of biochemical analyses consisting of 15 serological tests was examined. The results showed that Lmna deficient mice had significantly decreased body weight and increased the ratio of organ to body weight in most of tissues. Compared with $Lmna^{+/+}$ and $Lmna^{+/-}$ mice, $Lmna^{-/-}$ mice exhibited lower levels of ALP (alkaline phosphatase), Chol (cholesterol), CR (creatinine), GLU (glucose), HDL (high-density lipoprotein cholesterol) and higher levels of ALT (alanine aminotransferase) (p<0.05). $Lmna^{-/-}$ mice displayed higher AST (aspartate aminotransferase) values and lower LDL (lowdensity lipoprotein cholesterol), CK-MB (creatine kinase-MB) levels than $Lmna^{+/+}$ mice (p0.05). These changes of serological parameters may provide an experimental basis for the elucidation of Lmna gene functions.
The A-type lamin deficient mouse line ($Lmna^{-/-}$) has become one of the most frequently used models for providing insights into many different aspects of A-type lamin function. To elucidate the function of Lmna in the growth and metabolism of mice, tissue growth and blood biochemistry were monitored in Lmna-deficient mice, heterozygous ($Lmna^{+/-}$) and wide-type ($Lmna^{+/+}$) backcrossed to C57BL/6 background. At 4 weeks after birth, the weight of various organs of the $Lmna^{-/-}$, $Lmna^{+/-}$ and $Lmna^{+/+}$ mice was measured. A panel of biochemical analyses consisting of 15 serological tests was examined. The results showed that Lmna deficient mice had significantly decreased body weight and increased the ratio of organ to body weight in most of tissues. Compared with $Lmna^{+/+}$ and $Lmna^{+/-}$ mice, $Lmna^{-/-}$ mice exhibited lower levels of ALP (alkaline phosphatase), Chol (cholesterol), CR (creatinine), GLU (glucose), HDL (high-density lipoprotein cholesterol) and higher levels of ALT (alanine aminotransferase) (p<0.05). $Lmna^{-/-}$ mice displayed higher AST (aspartate aminotransferase) values and lower LDL (lowdensity lipoprotein cholesterol), CK-MB (creatine kinase-MB) levels than $Lmna^{+/+}$ mice (p0.05). These changes of serological parameters may provide an experimental basis for the elucidation of Lmna gene functions.
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문제 정의
These results will aid in the physician’s diagnosis of disease. This article explores the changes in growth and serum biochemistry in C57BL/6 mice due to homozygous or heterozygous deletion of the Lmna gene. These changes of serological parameters can implicate the affected organs of mice, and provide an experimental basis for the elucidation of Lmna gene functions.
제안 방법
Because the mice that are homozygous for the Lmna null allele began to display abnormal gait with a stiff walking posture at 3 to 4 weeks and all had died by the eighth week, we performed serological analyses of all mice at the age of 4 weeks while the animals were still in good health and were mobile. This time point was selected due to the short life-span of the homozygous mice, and it enabled us to observe changes in serum biochemistry that accompanied externally apparent phenotypic changes in Lmna-/- mice.
To explore the effect of Lmna deficiency on metabolism, we measured blood biochemical parameters of the mice on the 28th day after their birth. Ten serum samples from each group were taken for 15 analyses including glycolipid metabolism, heart function, liver function, and kidney function tests. It was found that the level of ALT (Table 1 and Figure 5C) in Lmna-/- mice was significantly higher than that of other 2 groups (p0.
데이터처리
The results are expressed as the mean+-SD, and differences between groups of mice were determined by Levene's t-test, the Satterthwaite t-test, the StudentNeuman-Keuls (SNK) test, or Dunnett’s T3 test.
이론/모형
1 Denotes variances determined using Dunnett′s T3 test; others were determined using the Student-Neuman-Keuls test.
성능/효과
In conclusion, the deletion of the Lmna gene not only affects the growth and development of C57BL/6 mice but also altered their serological biochemistry. Homozygous deletions of the Lmna gene can lead to impaired heart and liver function, as well as glucose and lipid metabolism disorders.
The wildtype mice exhibited a band of 210 bp, heterozygous mice exhibited bands at both 210 bp and 230 bp, and a single band of 230 bp was observed in homozygous Lmna deletion mice. In total, 117 mice from 13 litters were tested, among which 29 were confirmed to be wild-type, 21 were homozygous and the remainder were heterozygous. This was roughly consistent with the proportions expected based on the principle of Mendelian inheritance regularity.
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