The TSC-2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma
The TSC‐2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma Aims: Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous scleros...
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| Vydáno v: | Histopathology Ročník 40; číslo 5; s. 458 - 463 |
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Oxford UK
Blackwell Science Ltd
01.05.2002
Blackwell |
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| ISSN: | 0309-0167, 1365-2559 |
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| Abstract | The TSC‐2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma
Aims: Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex‐2 gene (TSC‐2) have been described in LAM cells and angiomyolipomas. The TSC‐2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression.
Methods and results: Tissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti‐tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin.
Conclusions: Our results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism. |
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| AbstractList | The TSC‐2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma
Aims: Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex‐2 gene (TSC‐2) have been described in LAM cells and angiomyolipomas. The TSC‐2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression.
Methods and results: Tissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti‐tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin.
Conclusions: Our results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism. Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex-2 gene (TSC-2) have been described in LAM cells and angiomyolipomas. The TSC-2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression.AIMSLymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex-2 gene (TSC-2) have been described in LAM cells and angiomyolipomas. The TSC-2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression.Tissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti-tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin.METHODS AND RESULTSTissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti-tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin.Our results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism.CONCLUSIONSOur results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism. Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex-2 gene (TSC-2) have been described in LAM cells and angiomyolipomas. The TSC-2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression. Tissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti-tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin. Our results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism. The TSC‐2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma Aims : Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of angiomyolipomas. Recently mutations in the tuberous sclerosis complex‐2 gene (TSC‐2) have been described in LAM cells and angiomyolipomas. The TSC‐2 protein tuberin is a tumour suppressor and its loss may result in cellular proliferation. We used immunohistochemistry to test the hypothesis that uncontrolled cellular proliferation in lymphangioleiomyomatosis is the result of reduced tuberin protein expression. Methods and results : Tissue from normal lung, normal kidney, lymphangioleiomyomatosis and angiomyolipomas was immunostained with three separate anti‐tuberin antibodies. Tuberin staining in normal tissues was similar to that previously described. Surprisingly, tuberin was strongly expressed in the LAM cells of all cases of lymphangioleiomyomatosis and angiomyolipoma at a greater level than in normal smooth muscle cells. The perivascular cells of angiomyolipomas, however, did not stain for tuberin. Conclusions : Our results suggest that a loss of tuberin protein in LAM cells is not the cause of the cellular proliferation seen in lymphangioleiomyomatosis. Lymphangioleiomyomatosis may result either from the expression of a mutant tuberin with abnormal function, as a result of mutations in functionally related proteins, or from more than one mechanism. |
| Author | Knox, A J Tattersfield, A E Ronan, J Clelland, C A Johnson, S R |
| Author_xml | – sequence: 1 givenname: S R surname: Johnson fullname: Johnson, S R organization: Division of Therapeutics, University of Nottingham, UK – sequence: 2 givenname: C A surname: Clelland fullname: Clelland, C A organization: Department of Histopathology, City Hospital, Nottingham, UK – sequence: 3 givenname: J surname: Ronan fullname: Ronan, J organization: Department of Histopathology, City Hospital, Nottingham, UK – sequence: 4 givenname: A E surname: Tattersfield fullname: Tattersfield, A E organization: Division of Respiratory Medicine, University of Nottingham, UK – sequence: 5 givenname: A J surname: Knox fullname: Knox, A J organization: Division of Respiratory Medicine, University of Nottingham, UK |
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| Cites_doi | 10.1086/301804 10.1136/thx.54.3.254 10.1073/pnas.97.11.6085 10.1074/jbc.272.46.29301 10.1038/ng0294-193 10.1152/ajplung.1999.277.6.L1109 10.1164/ajrccm.164.8.2104095 10.1165/ajrcmb.21.3.3693 |
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| Keywords | Kidney disease Diffuse Human Immunohistochemistry Lung disease Lymphangiomatosis Urinary system disease Respiratory disease Leiomyomata Gene expression Carcinogenesis Bronchopulmonary Kidney Pathology Gene Tuberin Bronchus disease Benign neoplasm Angiomyolipoma Mutation Bourneville syndrome Tumor suppressor gene |
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| References | Henske EP, Wessner LL, Golden J et al. Loss of tuberin in both subependymal giant cell astrocytomas and angiomyolipomas supports a two hit model for the pathogenesis of tuberous sclerosis tumours. Am. J. Pathol. 1997; 151 ; 1639-1647. Green AJ, Smith M, Yates JRW. Loss of heterozygosity on chromosome 16p13.3 in hamartomas from tuberous sclerosis patients. Nature Genet. 1994; 6 ; 193-196. Johnson SR, Knox AJ. Autocrine production of matrix metalloproteinase-2 is required for human airway smooth muscle proliferation. Am. J. Physiol. (Lung Cell Mol. Physiol.) 1999; 277 ; L1109-L1117. Soucek T, Pusch O, Wienecke R et al. Role of the tuberous sclerosis gene-2 product in cell cycle control. J. Biol. Chem. 1997; 272 ; 29301-29308. Smolarek TA, Wessner LL, McCormack FX et al. Evidence that lymphangioleiomyomatosis is caused by TSC2 mutations: chromosome 16p13 loss of heterozygosity in angiomyolipomas and lymph nodes from women with lymphangiomyomatosis Am. J. Hum. Genet. 1998; 62 ; 810810. Yu J, Astrinidis A, Henske EP. Chromosome 16 loss of heterozygosity in tuberous sclerosis and sporadic lymphangiomyomatosis. Am. J. Respir. Crit. Care Med. 2001; 164 ; 1537-1540. Johnson SR. Lymphangioleiomyomatosis: clinical features, management and basic mechanisms Thorax 1999; 54 ; 254-264. Wienecke R, Maize JC Jr, Shoarinejad F et al. Co-localization of the TSC2 product tuberin with its target Rap1 in the Golgi apparatus. Oncogene 1996; 13 ; 913-923. Valensi QJ. Pulmonary lymphangiomyoma, a probable forme fruste of tuberous sclerosis. Am. Rev. Respir. Dis. 1973; 108 ; 1411-1415. Plank TL, Logginidou H, Klein-Szanto A, Henske EP. The expression of hamartin, the product of the TSC1 gene, in normal human tissues and in TSC1- and TSC2-linked angiomyolipomas. Mod. Pathol. 1999; 12 ; 539-545. Matsumoto Y, Horiba K, Usuki J et al. Markers of cell proliferation and expression of melanosomal antigen in lymphangioleiomyomatosis. Am. J. Respir. Cell Mol. Biol. 1999; 21 ; 327-336. Carsillo T, Astrinidis A, Henske EP. Mutations in the tuberous sclerosis complex gene TSC2 are a cause of sporadic pulmonary lymphangioleiomyomatosis. Proc. Natl Acad. Sci. USA 2000; 97 ; 6085-6090. 1999; 12 1999; 54 1999; 21 2001; 164 1999; 277 1973; 108 1998; 62 1996; 13 1997; 151 1997; 272 1994; 6 2000; 97 Wienecke R (e_1_2_6_8_2) 1996; 13 Plank TL (e_1_2_6_11_2) 1999; 12 e_1_2_6_7_2 Henske EP (e_1_2_6_9_2) 1997; 151 Valensi QJ (e_1_2_6_3_2) 1973; 108 e_1_2_6_4_2 e_1_2_6_6_2 e_1_2_6_5_2 e_1_2_6_12_2 e_1_2_6_13_2 e_1_2_6_2_2 e_1_2_6_10_2 |
| References_xml | – reference: Yu J, Astrinidis A, Henske EP. Chromosome 16 loss of heterozygosity in tuberous sclerosis and sporadic lymphangiomyomatosis. Am. J. Respir. Crit. Care Med. 2001; 164 ; 1537-1540. – reference: Plank TL, Logginidou H, Klein-Szanto A, Henske EP. The expression of hamartin, the product of the TSC1 gene, in normal human tissues and in TSC1- and TSC2-linked angiomyolipomas. Mod. Pathol. 1999; 12 ; 539-545. – reference: Henske EP, Wessner LL, Golden J et al. Loss of tuberin in both subependymal giant cell astrocytomas and angiomyolipomas supports a two hit model for the pathogenesis of tuberous sclerosis tumours. Am. J. Pathol. 1997; 151 ; 1639-1647. – reference: Valensi QJ. Pulmonary lymphangiomyoma, a probable forme fruste of tuberous sclerosis. Am. Rev. Respir. Dis. 1973; 108 ; 1411-1415. – reference: Carsillo T, Astrinidis A, Henske EP. Mutations in the tuberous sclerosis complex gene TSC2 are a cause of sporadic pulmonary lymphangioleiomyomatosis. Proc. Natl Acad. Sci. USA 2000; 97 ; 6085-6090. – reference: Johnson SR, Knox AJ. Autocrine production of matrix metalloproteinase-2 is required for human airway smooth muscle proliferation. Am. J. Physiol. (Lung Cell Mol. Physiol.) 1999; 277 ; L1109-L1117. – reference: Green AJ, Smith M, Yates JRW. Loss of heterozygosity on chromosome 16p13.3 in hamartomas from tuberous sclerosis patients. Nature Genet. 1994; 6 ; 193-196. – reference: Soucek T, Pusch O, Wienecke R et al. Role of the tuberous sclerosis gene-2 product in cell cycle control. J. Biol. Chem. 1997; 272 ; 29301-29308. – reference: Wienecke R, Maize JC Jr, Shoarinejad F et al. Co-localization of the TSC2 product tuberin with its target Rap1 in the Golgi apparatus. Oncogene 1996; 13 ; 913-923. – reference: Smolarek TA, Wessner LL, McCormack FX et al. Evidence that lymphangioleiomyomatosis is caused by TSC2 mutations: chromosome 16p13 loss of heterozygosity in angiomyolipomas and lymph nodes from women with lymphangiomyomatosis Am. J. Hum. Genet. 1998; 62 ; 810810. – reference: Matsumoto Y, Horiba K, Usuki J et al. Markers of cell proliferation and expression of melanosomal antigen in lymphangioleiomyomatosis. Am. J. Respir. Cell Mol. Biol. 1999; 21 ; 327-336. – reference: Johnson SR. Lymphangioleiomyomatosis: clinical features, management and basic mechanisms Thorax 1999; 54 ; 254-264. – volume: 97 start-page: 6085 year: 2000 end-page: 6090 article-title: Mutations in the tuberous sclerosis complex gene TSC2 are a cause of sporadic pulmonary lymphangioleiomyomatosis publication-title: Proc. Natl Acad. Sci. USA – volume: 62 start-page: 810 year: 1998 end-page: 810 article-title: Evidence that lymphangioleiomyomatosis is caused by TSC2 mutations: chromosome 16p13 loss of heterozygosity in angiomyolipomas and lymph nodes from women with lymphangiomyomatosis publication-title: Am. J. Hum. Genet. – volume: 108 start-page: 1411 year: 1973 end-page: 1415 article-title: Pulmonary lymphangiomyoma, a probable forme fruste of tuberous sclerosis publication-title: Am. Rev. Respir. Dis. – volume: 21 start-page: 327 year: 1999 end-page: 336 article-title: Markers of cell proliferation and expression of melanosomal antigen in lymphangioleiomyomatosis publication-title: Am. J. Respir. Cell Mol. Biol. – volume: 164 start-page: 1537 year: 2001 end-page: 1540 article-title: Chromosome 16 loss of heterozygosity in tuberous sclerosis and sporadic lymphangiomyomatosis publication-title: Am. J. Respir. Crit. Care Med. – volume: 277 start-page: L1109 year: 1999 end-page: L1117 article-title: Autocrine production of matrix metalloproteinase‐2 is required for human airway smooth muscle proliferation publication-title: Am. J. Physiol. (Lung Cell Mol. Physiol.) – volume: 272 start-page: 29301 year: 1997 end-page: 29308 article-title: Role of the tuberous sclerosis gene‐2 product in cell cycle control publication-title: J. Biol. Chem. – volume: 54 start-page: 254 year: 1999 end-page: 264 article-title: Lymphangioleiomyomatosis: clinical features, management and basic mechanisms publication-title: Thorax – volume: 13 start-page: 913 year: 1996 end-page: 923 article-title: Co‐localization of the TSC2 product tuberin with its target Rap1 in the Golgi apparatus publication-title: Oncogene – volume: 151 start-page: 1639 year: 1997 end-page: 1647 article-title: Loss of tuberin in both subependymal giant cell astrocytomas and angiomyolipomas supports a two hit model for the pathogenesis of tuberous sclerosis tumours publication-title: Am. J. Pathol. – volume: 12 start-page: 539 year: 1999 end-page: 545 article-title: The expression of hamartin, the product of the TSC1 gene, in normal human tissues and in TSC1‐ and TSC2‐linked angiomyolipomas publication-title: Mod. Pathol. – volume: 6 start-page: 193 year: 1994 end-page: 196 article-title: Loss of heterozygosity on chromosome 16p13.3 in hamartomas from tuberous sclerosis patients publication-title: Nature Genet. – ident: e_1_2_6_5_2 doi: 10.1086/301804 – ident: e_1_2_6_2_2 doi: 10.1136/thx.54.3.254 – volume: 12 start-page: 539 year: 1999 ident: e_1_2_6_11_2 article-title: The expression of hamartin, the product of the TSC1 gene, in normal human tissues and in TSC1‐ and TSC2‐linked angiomyolipomas publication-title: Mod. Pathol. – volume: 151 start-page: 1639 year: 1997 ident: e_1_2_6_9_2 article-title: Loss of tuberin in both subependymal giant cell astrocytomas and angiomyolipomas supports a two hit model for the pathogenesis of tuberous sclerosis tumours publication-title: Am. J. Pathol. – volume: 108 start-page: 1411 year: 1973 ident: e_1_2_6_3_2 article-title: Pulmonary lymphangiomyoma, a probable forme fruste of tuberous sclerosis publication-title: Am. Rev. Respir. Dis. – ident: e_1_2_6_6_2 doi: 10.1073/pnas.97.11.6085 – ident: e_1_2_6_10_2 doi: 10.1074/jbc.272.46.29301 – volume: 13 start-page: 913 year: 1996 ident: e_1_2_6_8_2 article-title: Co‐localization of the TSC2 product tuberin with its target Rap1 in the Golgi apparatus publication-title: Oncogene – ident: e_1_2_6_4_2 doi: 10.1038/ng0294-193 – ident: e_1_2_6_7_2 doi: 10.1152/ajplung.1999.277.6.L1109 – ident: e_1_2_6_13_2 doi: 10.1164/ajrccm.164.8.2104095 – ident: e_1_2_6_12_2 doi: 10.1165/ajrcmb.21.3.3693 |
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| Snippet | The TSC‐2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma
Aims: Lymphangioleiomyomatosis is categorized by proliferation of... The TSC‐2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma Aims : Lymphangioleiomyomatosis is categorized by proliferation of... Lymphangioleiomyomatosis is categorized by proliferation of abnormal smooth muscle cells (LAM cells) in the lungs and lymphatics and the presence of... |
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| SubjectTerms | Adult Aged angiomyolipoma Angiomyolipoma - metabolism Angiomyolipoma - pathology Biological and medical sciences Female Humans Immunohistochemistry Kidney Neoplasms - metabolism Kidney Neoplasms - pathology Kidneys Lung Neoplasms - metabolism Lung Neoplasms - pathology lymphangioleiomyomatosis Lymphangioleiomyomatosis - metabolism Lymphangioleiomyomatosis - pathology Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Pneumology Repressor Proteins - biosynthesis tuberin tuberous sclerosis Tuberous Sclerosis Complex 2 Protein Tumor Suppressor Proteins Tumors of the respiratory system and mediastinum Tumors of the urinary system tumour suppressor |
| Title | The TSC-2 product tuberin is expressed in lymphangioleiomyomatosis and angiomyolipoma |
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