特发性高钙尿症VDR基因单核苷酸多态性及其表达调控研究
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摘要
第一部分遗传性高钙尿大鼠维生素D受体基因SNP与特发性高钙尿症的相关性研究
目的建立具有人类特发性高钙尿相似特点并且能够稳定遗传的高钙尿大鼠模型，探讨GHS大鼠维生素D受体基因单核苷酸多态性(SNP)与特发性高钙尿症之间有无相关性。
方法将80只SD大鼠分别单独置于鼠代谢笼，收集连续两次24小时尿并测定尿钙，有最大尿钙值的3只雄鼠和雌鼠被选择繁殖后代，以后同此法选择3～4只雄鼠和4～6只雌鼠继续繁殖。然后提取42例GHS大鼠及24例正常对照大鼠全血标本中基因组DNA，应用聚合酶链反应结合DNA测序方法检测并分析了VDR基因5’-调控区的多态性位点单核苷酸多态性分布。
结果在实验组中，80％(12／15)的雄鼠和56％(9／16)的雌鼠24h尿钙排泄明显高于对照组(2.98+1.16)和(2.54+1.04)mg／d，无论性别实验组大鼠的尿钙排泄明显高于对照组(P＜0.05)，检测血中钙，磷两组均无明显区别，1，25(OH)_2D_3水平不高(P＞0.05)。GHS大鼠VDR基因5’-调控区共发现6个多态位点，将这些多态位点基因型变化与正常组比较，其中两个位点存在明显统计学差异。
结论本研究成功地建立的大鼠实验性遗传性高钙尿症模型。遗传高钙尿鼠模型具有和人类该疾病相似的遗传背景，是研究IH在尿结石形成中的作用机制的一种很好的模型。研究还提示GHS大鼠VDR基因5’-调控区的单核苷酸多态性在GHS大鼠特发性高钙尿的发生中可能起到重要作用。
第二部分
论文一大鼠VDR组织特异性启动子荧光素酶报告基因载体的构建
目的为进行VDR基因启动子的活性分析，构建含大鼠VDR基因启动子的荧光素酶报告基因重组表达质粒。
方法以大鼠VDR基因组DNA为模板，通过PCR方法扩增转录起始位点上游DNA序列。PCR产物定向克隆到含荧光素酶报告基因的载体pGL3-Basic中，并经限制性内切酶消化鉴定。
结果通过酶切鉴定和基因测序，证明成功地构建了含大鼠VDR基因启动子的荧光素酶报告基因的载体pGL3-GHS-Luc和pGL3-N-Luc。两种质粒仅仅存在两处单核苷酸的差异。
结论成功构建了含大鼠VDR启动子片段的报告基因载体，为分析VDR基因启动子的活性以及VDR基因的转录调控机制奠定了基础。
论文二大鼠VDR基因多态性对荧光素酶报告基因表达水平的影响
目的研究VDR基因5’端启动子序列对荧光素酶在Hela细胞中表达的影响，评价VDR基因启动子对下游基因的转录调节。
方法将构建的不同大鼠VDR启动子荧光素酶表达载体pGL3-GHS-luc、pGL3-N-luc及空载pGL3-Basic经lipofectin转染Hela细胞，G418抗性筛选得到含各不同质粒的稳定阳性细胞克隆，检测报告基因荧光素酶表达。
结果所构建的报告基因均能在Hela细胞中表达，pGL3-GHS载体转染的Hela细胞荧光素酶表达水平高于pGL3-N载体。
结论VDR基因5’-调控区SNP在转录调控水平存在差异，这些差异可能对特发性高钙尿症的发生机制存在一定的影响。
第三部分大鼠VDR基因5’端非编码区启动子报告基因载体的构建和分析
目的克隆大鼠VDR基因基因启动子，构建含VDR基因启动子不同片段的报告基因载体，在Hela细胞中分析各种载体中VDR启动子活性。
方法PCR、报告基因载体构建、瞬时转染和报告基因检测。
结果通过PCR方法获得VDR启动子的3个不同片段，将它们克隆到萤火虫荧光素酶报告基因载体pGL3-Basic中，构建出3种含VDR启动子不同片段的报告基因载体，将这些报告基因载体瞬时转染至Hela细胞，载体中的启动子具有不同的活性。
结论成功构建了含大鼠VDR启动子片段的报告基因载体，为以后研究VDR基因表达调控的分子机制提供了实验工具。
Objective To establish a colony of geneticlly hypercalciuria rats model which can stablely descending and explore the pathogenetic role in intestinal calcium hyperabsorption with the rats model, and obtain more information concerning single nucleotide polymorphism (SNP) of Vitamin D receptor gene of GHS rats in Idiopathic hypercalciuria.
Methods 40 male and 40 female adult Sprague-Dawley rats were screned for hypercalciuria. The rats were placed in individual metabolic cages. Two successsve 24h urine collections were then obtained to measure the urine calcium excretion. The three male and three female rats used to breed the next generation. A similar protocol was used to select the two to three hypercalciuric males and three to four hypercalciuric females for inbreeding of subsequent generations. Then 42 GHS rats and 24 normal control rats took part in this study. Genomic DNA was extracted from peripheral leukocytes isolated from EDTA anticoagulated blood by standard method with phenol and chloroform. All the gene from 5' -regulation region of VDR were amplified by PCR. After purified, the PCR products were sequenced.
Results Urine calcium excretion in 12/15 males and 9/16 females were significantly above the mean of the controls. The content of serum calcium, phosphorus and l,25(OH)_2D_3 were similar(P>0.05). Six polymorphism sites were found in GHS rats. There were significant differences in two of SNPs between GHS rats and normal controls.
Conclusion Genetic hypercalciuric rats model were established succesfully and they are similar to human idopathic hypercalciuria , which may be familial and is thought to be genetic in origin. So the model is suitable for the study on the mechanism of idiopathic hypercalciuria. These findings suggest that the single nucleotide polymorphism in 5'-regulation region of the VDR gene may play a significant role in mechanism of Idiopathic hypercalciuria. Objective To evaluate VDR gene promoter on gene transcription, we construct
luciferase reporter plasmid pGL3-GHS-Luc and pGL3-N-Luc.
Methods The VDR DNA of GHS rats and normal control rats were used as templates
in the polymerase chain reaction to amplify their upstream regions from the
transcription initiation sites. The PCR products were directly cloned into
the luciferase reporter vector pGL3 - Basic. pGL3-GHS-Luc and pGL3-N-Luc were
confirmed by constriction analyses.
Results Restriction enzymes digestion and nucleotide sequencing confirmed
that the recombinant plasmids were correct without base mutation and deletion.
There were only two differents of single nucleotide between pGL3-GHS-Luc and
pGL3-N-Luc.
Conclusion Rat VDR promoter luciferase reporter gene plasmids were
successfully constructed. The construction of VDR recombinant plasmid lay a
foundation of the analysis of promoter activities and make an important basis
for studying transcrip tional regulation mechanisms of VDR gene. Objective To study the impact of VDR 5' flanking promotor of rats on the
expression of luciferase in Hela cell, and evaluate in vitro regulation of VDR
promoter on gene transcription.
Methods pGL3-GIS、 pGL3-N and pGL3-Basic were transfected into Hela cells by
lipofectin and selected by G418 respectivly, after amplifiction of the
positive cell clones, expression of luciferase was detected and
quantitatively analysised by digital image system.
Results Reporter gene plasmids under the direction of the VDR 5' flanking
promotor can be expressed in Hela cells. They had different luciferase
activities, and the expression of pGL3-GHS was significantly higher than of
pGL3-N.
Conclusion These findings suggest that the single nucleotide polymorphism
in 5'-regulation region of the VDR gene may play a significant role in
mechanism of Idiopathic hypercalciuria. Objective To clone the promoter of VDR gene and construct luciferase reporter
gene vectors containing different VDR promoter fragments, and to analyze the
promoter activity of various constructions using Hela cells.
Methods PCR, construct luciferase reporter gene vectors, transient
transfection and luciferase assay were used.
Results Three different fragments of VDR promoter of rat were gotten. Then
they were cloned into pGL3-Basic luciferase expression vector. These three
VDR promoter luciferase reporter gene vectors had different luciferase
activity after transfection into Hela cells respectively.
Conclusion Rat VDR promoter luciferase reporter gene plasmids were
successfully constructed, which will provide a useful tool for study of the
molecular mechanism of VDR expression in future.
目的建立具有人类特发性高钙尿相似特点并且能够稳定遗传的高钙尿大鼠模型，探讨GHS大鼠维生素D受体基因单核苷酸多态性(SNP)与特发性高钙尿症之间有无相关性。
方法将80只SD大鼠分别单独置于鼠代谢笼，收集连续两次24小时尿并测定尿钙，有最大尿钙值的3只雄鼠和雌鼠被选择繁殖后代，以后同此法选择3～4只雄鼠和4～6只雌鼠继续繁殖。然后提取42例GHS大鼠及24例正常对照大鼠全血标本中基因组DNA，应用聚合酶链反应结合DNA测序方法检测并分析了VDR基因5’-调控区的多态性位点单核苷酸多态性分布。
结果在实验组中，80％(12／15)的雄鼠和56％(9／16)的雌鼠24h尿钙排泄明显高于对照组(2.98+1.16)和(2.54+1.04)mg／d，无论性别实验组大鼠的尿钙排泄明显高于对照组(P＜0.05)，检测血中钙，磷两组均无明显区别，1，25(OH)_2D_3水平不高(P＞0.05)。GHS大鼠VDR基因5’-调控区共发现6个多态位点，将这些多态位点基因型变化与正常组比较，其中两个位点存在明显统计学差异。
结论本研究成功地建立的大鼠实验性遗传性高钙尿症模型。遗传高钙尿鼠模型具有和人类该疾病相似的遗传背景，是研究IH在尿结石形成中的作用机制的一种很好的模型。研究还提示GHS大鼠VDR基因5’-调控区的单核苷酸多态性在GHS大鼠特发性高钙尿的发生中可能起到重要作用。
第二部分
论文一大鼠VDR组织特异性启动子荧光素酶报告基因载体的构建
目的为进行VDR基因启动子的活性分析，构建含大鼠VDR基因启动子的荧光素酶报告基因重组表达质粒。
方法以大鼠VDR基因组DNA为模板，通过PCR方法扩增转录起始位点上游DNA序列。PCR产物定向克隆到含荧光素酶报告基因的载体pGL3-Basic中，并经限制性内切酶消化鉴定。
结果通过酶切鉴定和基因测序，证明成功地构建了含大鼠VDR基因启动子的荧光素酶报告基因的载体pGL3-GHS-Luc和pGL3-N-Luc。两种质粒仅仅存在两处单核苷酸的差异。
结论成功构建了含大鼠VDR启动子片段的报告基因载体，为分析VDR基因启动子的活性以及VDR基因的转录调控机制奠定了基础。
论文二大鼠VDR基因多态性对荧光素酶报告基因表达水平的影响
目的研究VDR基因5’端启动子序列对荧光素酶在Hela细胞中表达的影响，评价VDR基因启动子对下游基因的转录调节。
方法将构建的不同大鼠VDR启动子荧光素酶表达载体pGL3-GHS-luc、pGL3-N-luc及空载pGL3-Basic经lipofectin转染Hela细胞，G418抗性筛选得到含各不同质粒的稳定阳性细胞克隆，检测报告基因荧光素酶表达。
结果所构建的报告基因均能在Hela细胞中表达，pGL3-GHS载体转染的Hela细胞荧光素酶表达水平高于pGL3-N载体。
结论VDR基因5’-调控区SNP在转录调控水平存在差异，这些差异可能对特发性高钙尿症的发生机制存在一定的影响。
第三部分大鼠VDR基因5’端非编码区启动子报告基因载体的构建和分析
目的克隆大鼠VDR基因基因启动子，构建含VDR基因启动子不同片段的报告基因载体，在Hela细胞中分析各种载体中VDR启动子活性。
方法PCR、报告基因载体构建、瞬时转染和报告基因检测。
结果通过PCR方法获得VDR启动子的3个不同片段，将它们克隆到萤火虫荧光素酶报告基因载体pGL3-Basic中，构建出3种含VDR启动子不同片段的报告基因载体，将这些报告基因载体瞬时转染至Hela细胞，载体中的启动子具有不同的活性。
结论成功构建了含大鼠VDR启动子片段的报告基因载体，为以后研究VDR基因表达调控的分子机制提供了实验工具。
Objective To establish a colony of geneticlly hypercalciuria rats model which can stablely descending and explore the pathogenetic role in intestinal calcium hyperabsorption with the rats model, and obtain more information concerning single nucleotide polymorphism (SNP) of Vitamin D receptor gene of GHS rats in Idiopathic hypercalciuria.
Methods 40 male and 40 female adult Sprague-Dawley rats were screned for hypercalciuria. The rats were placed in individual metabolic cages. Two successsve 24h urine collections were then obtained to measure the urine calcium excretion. The three male and three female rats used to breed the next generation. A similar protocol was used to select the two to three hypercalciuric males and three to four hypercalciuric females for inbreeding of subsequent generations. Then 42 GHS rats and 24 normal control rats took part in this study. Genomic DNA was extracted from peripheral leukocytes isolated from EDTA anticoagulated blood by standard method with phenol and chloroform. All the gene from 5' -regulation region of VDR were amplified by PCR. After purified, the PCR products were sequenced.
Results Urine calcium excretion in 12/15 males and 9/16 females were significantly above the mean of the controls. The content of serum calcium, phosphorus and l,25(OH)_2D_3 were similar(P>0.05). Six polymorphism sites were found in GHS rats. There were significant differences in two of SNPs between GHS rats and normal controls.
Conclusion Genetic hypercalciuric rats model were established succesfully and they are similar to human idopathic hypercalciuria , which may be familial and is thought to be genetic in origin. So the model is suitable for the study on the mechanism of idiopathic hypercalciuria. These findings suggest that the single nucleotide polymorphism in 5'-regulation region of the VDR gene may play a significant role in mechanism of Idiopathic hypercalciuria. Objective To evaluate VDR gene promoter on gene transcription, we construct
luciferase reporter plasmid pGL3-GHS-Luc and pGL3-N-Luc.
Methods The VDR DNA of GHS rats and normal control rats were used as templates
in the polymerase chain reaction to amplify their upstream regions from the
transcription initiation sites. The PCR products were directly cloned into
the luciferase reporter vector pGL3 - Basic. pGL3-GHS-Luc and pGL3-N-Luc were
confirmed by constriction analyses.
Results Restriction enzymes digestion and nucleotide sequencing confirmed
that the recombinant plasmids were correct without base mutation and deletion.
There were only two differents of single nucleotide between pGL3-GHS-Luc and
pGL3-N-Luc.
Conclusion Rat VDR promoter luciferase reporter gene plasmids were
successfully constructed. The construction of VDR recombinant plasmid lay a
foundation of the analysis of promoter activities and make an important basis
for studying transcrip tional regulation mechanisms of VDR gene. Objective To study the impact of VDR 5' flanking promotor of rats on the
expression of luciferase in Hela cell, and evaluate in vitro regulation of VDR
promoter on gene transcription.
Methods pGL3-GIS、 pGL3-N and pGL3-Basic were transfected into Hela cells by
lipofectin and selected by G418 respectivly, after amplifiction of the
positive cell clones, expression of luciferase was detected and
quantitatively analysised by digital image system.
Results Reporter gene plasmids under the direction of the VDR 5' flanking
promotor can be expressed in Hela cells. They had different luciferase
activities, and the expression of pGL3-GHS was significantly higher than of
pGL3-N.
Conclusion These findings suggest that the single nucleotide polymorphism
in 5'-regulation region of the VDR gene may play a significant role in
mechanism of Idiopathic hypercalciuria. Objective To clone the promoter of VDR gene and construct luciferase reporter
gene vectors containing different VDR promoter fragments, and to analyze the
promoter activity of various constructions using Hela cells.
Methods PCR, construct luciferase reporter gene vectors, transient
transfection and luciferase assay were used.
Results Three different fragments of VDR promoter of rat were gotten. Then
they were cloned into pGL3-Basic luciferase expression vector. These three
VDR promoter luciferase reporter gene vectors had different luciferase
activity after transfection into Hela cells respectively.
Conclusion Rat VDR promoter luciferase reporter gene plasmids were
successfully constructed, which will provide a useful tool for study of the
molecular mechanism of VDR expression in future.
引文
1.Coe FL, Parks JH, Moore Es. Familial idiopathic hypercalciuria. N Engl J Med. 1979,300:337-340
2. Tasca A, Cacciola A, Ferrarese P, et al. Bone alterations in patients with idiopathic hypercalciuria and calcium nephrolithiasis. Urology. 2002, 59(6): 865-869
3. Aladjem M, Barr J, lahat E, et al. Renal and absorptive hypercalciuria:a metabolic disturbance with varying and interchanging modes of expression. Pediatrics. 1996, 97: 216-219
4. Bushinsky DA, Favus MJ. Mechanism of hypercalciuria in genetic hypercalciuric rats. Inherited defect in intestinal calcium transport.J Clin Invest. 1988, 82(5): 1585-1591.
5. Stapleton FB. Idiopathic hypercalciura assocaton with isolated hematuria and risk of urolithiasis in children. Kidney Int, 1990, 37: 807-811
6. IidaK, Shinki T, Yamaguchi A, et al. A possible role of vitamin D receptors in regulating vitamin D activation in the kidney. Proc Natl Acad Sci USA. 1995, 20, 92(13): 6112-6116.
7. Deluca HF, ZieroldC. Mechanisms and Functions of Vitamin D. Nutr Rev. 1998, 56(2): S4-10.
8. Ogata E. The potential use of vitamin D analogs in the treatment of cancer. Calcif Tissue Int. 1997, 60(1): 130-133.
9. Furuya Y, Akakura K, Masai M, et al. Vitamin D receptor gene polymorphism in Japanese patients with prostate cancer. Endocr J. 1999, 46(3): 467-470
10. Wagner KD, Wagner N, Sukhatme VP, et al. Activation of vitamin D receptor by the Wilms' tumor gene product mediates apoptosis of renal cells. J Am Soc Nephrol. 2001, 12(6): 1188-1196.
11. Xiao Qing Li , Tembe V , Bushisky DA , t al . Increased intestinal vitamin D receptor in genetic hypercalciuric rats. A cause of intestinal calcium hyperabsorption. J Clin Invest, 1993, 91: 661-667
12. Zerwekh JE, Hughes MR, Reed BY, et al. Evidence for normal vitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria. J Clin Endocrinol Metab, 1995, 80(10): 2960-2965
13. Scott P, Ouimet D, Valiquette L, et al . Suggestive evidence for a susceptibility gene near the vitamin D receptor locus in idiopathic calcium stone formation. J Am Soc Nephrol, 1999, 10 (5) : 1007-1013
14. Nishijima S, Sugaya K, Naito A, et al. Association of vitamin D receptor gene polymorphism with urolithiasis. J Urol. 2002, 167(5): 2188-2191.
1. Aladjem M, Barr J, lahat E, et al. Renal and absorptive hypercalciuria: a metabolic disturbance with varying and interchanging modes of expression. Pediatrics, 1996, 97: 216-219
2. Stapleton FB. Idiopathic hypercalciura assocaton with isolated hematuria and risk of urolithiasis in children. Kidney Int, 1990, 37: 807-811
3. Iida K, Shinki T, Yamaguchi A, et al. A possible role of vitamin D receptors in regulating vitamin D activation in the kidney. Proc Natl Acad Sci USA. 1995, 20; 92(13): 6112-6116.
4. Deluca HF, Zierold C. Mechanisms and Functions of Vitamin D. Nutr Rev. 1998, 56(2): S4-10.
5. Ogata E. The potential use of vitamin D analogs in the treatment of cancer. Calcif Tissue Int. 1997, 60(1): 130-133.
6. Furuya Y, Akakura K, Masai M, et al. Vitamin D receptor gene polymorphism in Japanese patients with prostate cancer. Endocr J. 1999, 46(3): 467-470
7. Wagner KD, Wagner N, Sukhatme VP, et al. Activation of vitamin D receptor by the Wilms' tumor gene product mediates apoptosis of renal cells. J Am Soc Nephrol. 2001, 12(6): 1188-1196.
8. Xiao Qing Li , Tembe V , Bushisky DA , t al . Increased intestinal vitamin D receptor in genetic hypercalciuric rats. A cause of intestinal calcium hyperabsorption. J Clin Invest, 1993, 91: 661-667
9. Zerwekh JE, Hughes MR, Reed BY, et al. Evidence for normal vitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria. J Clin Endocrinol Metab, 1995, 80(10): 2960-2965
10.Scott P, Ouimet D, Valiquette L, et al . Suggestive evidence for a susceptibility gene near the vitamin D receptor locus in idiopathic calcium stone formation. J Am Soc Nephrol, 1999, 10 (5): 1007-1013
11.Nishijima S, Sugaya K, Naito A, et al. Association of vitamin D receptor gene polymorphism with urolithiasis. J Urol. 2002, 167(5): 2188-2191
1. Stapleton FB. Idiopathic hypercalciura assocaton with isolated hematuria and risk of urolithiasis in children. Kidney Int, 1990,37: 807-811
2. Coe FL, Parks JH, Moore Es. Familial idiopathic hypercalciuria. N Engl J Med, 1979,300: 337-340
3. Nishijima S, Sugaya K, Naito A, et al. Association of vitamin D receptor gene polymorphism with urolithiasis. J Urol. 2002,167(5): 2188-2191
4. Elizabeth A. C. Sellers, Atul Sharma, et al. Adaptation of Inuit children to a low-calcium diet. CMAJ . 2003,168 (9): 1141-1143
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7. Miyamoto K, Kesterson RA , Yamamoto H, et al. Structural organization of human vitamin D receptor chromosomal gene and its promoter. Mol Endocrinol, 1997, 11: 1165-1179
8. Wang SG, Liu JH, Hu SQ,et al. Association of Vitamin D receptor gene polymorphisms with Calcium Oxalate Calculus Disease. Journal of Huazhong University of Science and Technology[Med Sci]. 2003, 23(1):38-41
9. Chen WC, Chen HY, Hsu CD, et al. No association of vitamin D receptor gene BsmI polymorphisms with calcium oxalate stone formation. Mol Urol. 2001, 5(1) :7-10.
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1. Heilberg IP , Teixeira SH , Martini LA , et al. Vitamin D receptor gene polymorphism and bone mineral density in hypercalciuric calcium-stone- forming patients. Nephron, 2002; 90(1):51-57
2. Nishijima S, Sugaya K, Naito A, et al. Association of vitamin D receptor gene polymorphism with urolithiasis. J Urol. 2002,167(5) :2188-2191
3. Yao J, Kathpalia P, Bushinsky DA, et al. Hyperresponsiveness of vitamin D receptor gene expression to 1, 25-dihydroxyvitamin D_3. A new characteristic of genetic hypercalciuric stone-forming rats. J Clin Invest. 1998, 101(10): 2223-2232.
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