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Michal Pravenec - One of the best experts on this subject based on the ideXlab platform.

  • Genetic Analysis of Rat Chromosome 1 and the Sa Gene in Spontaneous Hypertension
    Hypertension, 2020
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Vladimir Kren, Vaclav Zidek, Jiaming Wang, Ying Yang, Nianning Qi, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in segregating populations derived from the spontaneously hypertensive rat (SHR) indicate that a blood pressure quantitative trait locus exists on rat Chromosome 1 in the vicinity of the Sa gene. On the basis of these findings and the observation of increased renal expression of the Sa gene in SHR versus normotensive rats, the Sa gene has been proposed as a candidate gene for spontaneous hypertension. In SHR congenic strains, we and others have found that replacement of a segment of SHR Chromosome 1 that contains the Sa gene with the corresponding Chromosome segment from a normotensive Brown Norway (BN) rat or Wistar-Kyoto rat can reduce blood pressure. To test whether the Sa gene is necessary for the effect of this region of Chromosome 1 on blood pressure, we studied a new SHR congenic subline that harbors a smaller segment of BN Chromosome 1 that does not include the Sa gene. Transfer of this subregion of Chromosome 1 from the BN rat onto the SHR background was associated with significant reductions in blood pressure comparable to those previously observed on transfer of a larger region of Chromosome 1 that included the Sa gene. Thus, in the SHR-BN model of hypertension, the results of these mapping studies (1) demonstrate that molecular variation in the Sa gene is not required for the effect of this region of Chromosome 1 on blood pressure and (2) should direct attention toward other candidate genes within the differential Chromosome segment of the new congenic subline.

  • genetic isolation of a Chromosome 1 region affecting susceptibility to hypertension induced renal damage in the spontaneously hypertensive rat
    Hypertension, 1999
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Karen A Griffin, Maria M Picken, Monique C Churchill, Paul C Churchill, Vladimir Kren, Vaclav Zidek, Ning Wang, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in the fawn-hooded hypertensive rat have suggested that genes influencing susceptibility to hypertension-associated renal failure may exist on rat Chromosome 1q. To investigate this possibility in a widely used model of hypertension, the spontaneously hypertensive rat (SHR), we compared susceptibility to hypertension-induced renal damage between an SHR progenitor strain and an SHR congenic strain that is genetically identical except for a defined region of Chromosome 1q. Backcross breeding with selection for the markers D1Mit3 and Igf2 on Chromosome 1 was used to create the congenic strain (designated SHR.BN- D1Mit3/Igf2 ) that carries a 22 cM segment of Chromosome 1 transferred from the normotensive Brown Norway rat onto the SHR background. Systolic blood pressure (by radiotelemetry) and urine protein excretion were measured in the SHR progenitor and congenic strains before and after the induction of accelerated hypertension by administration of DOCA-salt. At the same level of DOCA-salt hypertension, the SHR.BN- D1Mit3/Igf2 congenic strain showed significantly greater proteinuria and histologically assessed renal vascular and glomerular injury than the SHR progenitor strain. These findings demonstrate that a gene or genes that influence susceptibility to hypertension-induced renal damage have been trapped in the differential Chromosome segment of the SHR.BN- D1Mit3/Igf2 congenic strain. This congenic strain represents an important new model for the fine mapping of gene(s) on Chromosome 1 that affect susceptibility to hypertension-induced renal injury in the rat.

  • genetic isolation of a Chromosome 1 region affecting blood pressure in the spontaneously hypertensive rat
    Hypertension, 1997
    Co-Authors: Elizabeth St. Lezin, Alena Musilova, D Krenova, Vladimir Kren, Vaclav Zidek, Jiaming Wang, M Zdobinska, Ning Wang, Michal Pravenec
    Abstract:

    Abstract Recent linkage studies in the spontaneously hypertensive rat (SHR) suggest that a blood pressure regulatory gene or genes may be located on rat Chromosome 1q. To investigate this possibility, we replaced a region of Chromosome 1 in the SHR (defined by the markers D1Mit3 and Igf2 ) with the corresponding Chromosome segment from the normotensive Brown-Norway (BN) strain. In male SHR congenic rats carrying the transferred BN Chromosome segment, 24-hour average systolic and diastolic blood pressures were significantly lower than in male progenitor SHR. Polymerase chain reaction genotyping using 60 polymorphic microsatellite markers dispersed throughout the genome confirmed the congenic status of the new strain designated SHR.BN- D1Mit3/Igf2 . These findings provide direct evidence that a blood pressure regulatory gene exists on the differential segment of Chromosome 1 that is sufficient to decrease blood pressure in the SHR. The SHR.BN- D1Mit3/Igf2 congenic strain represents an important new model for fine mapping and characterization of genes on Chromosome 1 involved in the pathogenesis of spontaneous hypertension.

Elizabeth St. Lezin - One of the best experts on this subject based on the ideXlab platform.

  • Genetic Analysis of Rat Chromosome 1 and the Sa Gene in Spontaneous Hypertension
    Hypertension, 2020
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Vladimir Kren, Vaclav Zidek, Jiaming Wang, Ying Yang, Nianning Qi, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in segregating populations derived from the spontaneously hypertensive rat (SHR) indicate that a blood pressure quantitative trait locus exists on rat Chromosome 1 in the vicinity of the Sa gene. On the basis of these findings and the observation of increased renal expression of the Sa gene in SHR versus normotensive rats, the Sa gene has been proposed as a candidate gene for spontaneous hypertension. In SHR congenic strains, we and others have found that replacement of a segment of SHR Chromosome 1 that contains the Sa gene with the corresponding Chromosome segment from a normotensive Brown Norway (BN) rat or Wistar-Kyoto rat can reduce blood pressure. To test whether the Sa gene is necessary for the effect of this region of Chromosome 1 on blood pressure, we studied a new SHR congenic subline that harbors a smaller segment of BN Chromosome 1 that does not include the Sa gene. Transfer of this subregion of Chromosome 1 from the BN rat onto the SHR background was associated with significant reductions in blood pressure comparable to those previously observed on transfer of a larger region of Chromosome 1 that included the Sa gene. Thus, in the SHR-BN model of hypertension, the results of these mapping studies (1) demonstrate that molecular variation in the Sa gene is not required for the effect of this region of Chromosome 1 on blood pressure and (2) should direct attention toward other candidate genes within the differential Chromosome segment of the new congenic subline.

  • genetic isolation of a Chromosome 1 region affecting susceptibility to hypertension induced renal damage in the spontaneously hypertensive rat
    Hypertension, 1999
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Karen A Griffin, Maria M Picken, Monique C Churchill, Paul C Churchill, Vladimir Kren, Vaclav Zidek, Ning Wang, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in the fawn-hooded hypertensive rat have suggested that genes influencing susceptibility to hypertension-associated renal failure may exist on rat Chromosome 1q. To investigate this possibility in a widely used model of hypertension, the spontaneously hypertensive rat (SHR), we compared susceptibility to hypertension-induced renal damage between an SHR progenitor strain and an SHR congenic strain that is genetically identical except for a defined region of Chromosome 1q. Backcross breeding with selection for the markers D1Mit3 and Igf2 on Chromosome 1 was used to create the congenic strain (designated SHR.BN- D1Mit3/Igf2 ) that carries a 22 cM segment of Chromosome 1 transferred from the normotensive Brown Norway rat onto the SHR background. Systolic blood pressure (by radiotelemetry) and urine protein excretion were measured in the SHR progenitor and congenic strains before and after the induction of accelerated hypertension by administration of DOCA-salt. At the same level of DOCA-salt hypertension, the SHR.BN- D1Mit3/Igf2 congenic strain showed significantly greater proteinuria and histologically assessed renal vascular and glomerular injury than the SHR progenitor strain. These findings demonstrate that a gene or genes that influence susceptibility to hypertension-induced renal damage have been trapped in the differential Chromosome segment of the SHR.BN- D1Mit3/Igf2 congenic strain. This congenic strain represents an important new model for the fine mapping of gene(s) on Chromosome 1 that affect susceptibility to hypertension-induced renal injury in the rat.

  • genetic isolation of a Chromosome 1 region affecting blood pressure in the spontaneously hypertensive rat
    Hypertension, 1997
    Co-Authors: Elizabeth St. Lezin, Alena Musilova, D Krenova, Vladimir Kren, Vaclav Zidek, Jiaming Wang, M Zdobinska, Ning Wang, Michal Pravenec
    Abstract:

    Abstract Recent linkage studies in the spontaneously hypertensive rat (SHR) suggest that a blood pressure regulatory gene or genes may be located on rat Chromosome 1q. To investigate this possibility, we replaced a region of Chromosome 1 in the SHR (defined by the markers D1Mit3 and Igf2 ) with the corresponding Chromosome segment from the normotensive Brown-Norway (BN) strain. In male SHR congenic rats carrying the transferred BN Chromosome segment, 24-hour average systolic and diastolic blood pressures were significantly lower than in male progenitor SHR. Polymerase chain reaction genotyping using 60 polymorphic microsatellite markers dispersed throughout the genome confirmed the congenic status of the new strain designated SHR.BN- D1Mit3/Igf2 . These findings provide direct evidence that a blood pressure regulatory gene exists on the differential segment of Chromosome 1 that is sufficient to decrease blood pressure in the SHR. The SHR.BN- D1Mit3/Igf2 congenic strain represents an important new model for fine mapping and characterization of genes on Chromosome 1 involved in the pathogenesis of spontaneous hypertension.

Yoshiaki Nagamura - One of the best experts on this subject based on the ideXlab platform.

  • the genome sequence and structure of rice Chromosome 1
    Nature, 2002
    Co-Authors: Takuji Sasaki, Takashi Matsumoto, Kimiko Yamamoto, Katsumi Sakata, Tomoya Baba, Yuichi Katayose, Jianzhong Wu, Yoshihito Niimura, Zhukuan Cheng, Yoshiaki Nagamura
    Abstract:

    The rice species Oryza sativa is considered to be a model plant because of its small genome size, extensive genetic map, relative ease of transformation and synteny with other cereal crops1,2,3,4. Here we report the essentially complete sequence of Chromosome 1, the longest Chromosome in the rice genome. We summarize characteristics of the Chromosome structure and the biological insight gained from the sequence. The analysis of 43.3 megabases (Mb) of non-overlapping sequence reveals 6,756 protein coding genes, of which 3,161 show homology to proteins of Arabidopsis thaliana, another model plant. About 30% (2,073) of the genes have been functionally categorized. Rice Chromosome 1 is (G + C)-rich, especially in its coding regions, and is characterized by several gene families that are dispersed or arranged in tandem repeats. Comparison with a draft sequence5 indicates the importance of a high-quality finished sequence.

Vaclav Zidek - One of the best experts on this subject based on the ideXlab platform.

  • Genetic Analysis of Rat Chromosome 1 and the Sa Gene in Spontaneous Hypertension
    Hypertension, 2020
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Vladimir Kren, Vaclav Zidek, Jiaming Wang, Ying Yang, Nianning Qi, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in segregating populations derived from the spontaneously hypertensive rat (SHR) indicate that a blood pressure quantitative trait locus exists on rat Chromosome 1 in the vicinity of the Sa gene. On the basis of these findings and the observation of increased renal expression of the Sa gene in SHR versus normotensive rats, the Sa gene has been proposed as a candidate gene for spontaneous hypertension. In SHR congenic strains, we and others have found that replacement of a segment of SHR Chromosome 1 that contains the Sa gene with the corresponding Chromosome segment from a normotensive Brown Norway (BN) rat or Wistar-Kyoto rat can reduce blood pressure. To test whether the Sa gene is necessary for the effect of this region of Chromosome 1 on blood pressure, we studied a new SHR congenic subline that harbors a smaller segment of BN Chromosome 1 that does not include the Sa gene. Transfer of this subregion of Chromosome 1 from the BN rat onto the SHR background was associated with significant reductions in blood pressure comparable to those previously observed on transfer of a larger region of Chromosome 1 that included the Sa gene. Thus, in the SHR-BN model of hypertension, the results of these mapping studies (1) demonstrate that molecular variation in the Sa gene is not required for the effect of this region of Chromosome 1 on blood pressure and (2) should direct attention toward other candidate genes within the differential Chromosome segment of the new congenic subline.

  • genetic isolation of a Chromosome 1 region affecting susceptibility to hypertension induced renal damage in the spontaneously hypertensive rat
    Hypertension, 1999
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Karen A Griffin, Maria M Picken, Monique C Churchill, Paul C Churchill, Vladimir Kren, Vaclav Zidek, Ning Wang, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in the fawn-hooded hypertensive rat have suggested that genes influencing susceptibility to hypertension-associated renal failure may exist on rat Chromosome 1q. To investigate this possibility in a widely used model of hypertension, the spontaneously hypertensive rat (SHR), we compared susceptibility to hypertension-induced renal damage between an SHR progenitor strain and an SHR congenic strain that is genetically identical except for a defined region of Chromosome 1q. Backcross breeding with selection for the markers D1Mit3 and Igf2 on Chromosome 1 was used to create the congenic strain (designated SHR.BN- D1Mit3/Igf2 ) that carries a 22 cM segment of Chromosome 1 transferred from the normotensive Brown Norway rat onto the SHR background. Systolic blood pressure (by radiotelemetry) and urine protein excretion were measured in the SHR progenitor and congenic strains before and after the induction of accelerated hypertension by administration of DOCA-salt. At the same level of DOCA-salt hypertension, the SHR.BN- D1Mit3/Igf2 congenic strain showed significantly greater proteinuria and histologically assessed renal vascular and glomerular injury than the SHR progenitor strain. These findings demonstrate that a gene or genes that influence susceptibility to hypertension-induced renal damage have been trapped in the differential Chromosome segment of the SHR.BN- D1Mit3/Igf2 congenic strain. This congenic strain represents an important new model for the fine mapping of gene(s) on Chromosome 1 that affect susceptibility to hypertension-induced renal injury in the rat.

  • genetic isolation of a Chromosome 1 region affecting blood pressure in the spontaneously hypertensive rat
    Hypertension, 1997
    Co-Authors: Elizabeth St. Lezin, Alena Musilova, D Krenova, Vladimir Kren, Vaclav Zidek, Jiaming Wang, M Zdobinska, Ning Wang, Michal Pravenec
    Abstract:

    Abstract Recent linkage studies in the spontaneously hypertensive rat (SHR) suggest that a blood pressure regulatory gene or genes may be located on rat Chromosome 1q. To investigate this possibility, we replaced a region of Chromosome 1 in the SHR (defined by the markers D1Mit3 and Igf2 ) with the corresponding Chromosome segment from the normotensive Brown-Norway (BN) strain. In male SHR congenic rats carrying the transferred BN Chromosome segment, 24-hour average systolic and diastolic blood pressures were significantly lower than in male progenitor SHR. Polymerase chain reaction genotyping using 60 polymorphic microsatellite markers dispersed throughout the genome confirmed the congenic status of the new strain designated SHR.BN- D1Mit3/Igf2 . These findings provide direct evidence that a blood pressure regulatory gene exists on the differential segment of Chromosome 1 that is sufficient to decrease blood pressure in the SHR. The SHR.BN- D1Mit3/Igf2 congenic strain represents an important new model for fine mapping and characterization of genes on Chromosome 1 involved in the pathogenesis of spontaneous hypertension.

Vladimir Kren - One of the best experts on this subject based on the ideXlab platform.

  • Genetic Analysis of Rat Chromosome 1 and the Sa Gene in Spontaneous Hypertension
    Hypertension, 2020
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Vladimir Kren, Vaclav Zidek, Jiaming Wang, Ying Yang, Nianning Qi, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in segregating populations derived from the spontaneously hypertensive rat (SHR) indicate that a blood pressure quantitative trait locus exists on rat Chromosome 1 in the vicinity of the Sa gene. On the basis of these findings and the observation of increased renal expression of the Sa gene in SHR versus normotensive rats, the Sa gene has been proposed as a candidate gene for spontaneous hypertension. In SHR congenic strains, we and others have found that replacement of a segment of SHR Chromosome 1 that contains the Sa gene with the corresponding Chromosome segment from a normotensive Brown Norway (BN) rat or Wistar-Kyoto rat can reduce blood pressure. To test whether the Sa gene is necessary for the effect of this region of Chromosome 1 on blood pressure, we studied a new SHR congenic subline that harbors a smaller segment of BN Chromosome 1 that does not include the Sa gene. Transfer of this subregion of Chromosome 1 from the BN rat onto the SHR background was associated with significant reductions in blood pressure comparable to those previously observed on transfer of a larger region of Chromosome 1 that included the Sa gene. Thus, in the SHR-BN model of hypertension, the results of these mapping studies (1) demonstrate that molecular variation in the Sa gene is not required for the effect of this region of Chromosome 1 on blood pressure and (2) should direct attention toward other candidate genes within the differential Chromosome segment of the new congenic subline.

  • genetic isolation of a Chromosome 1 region affecting susceptibility to hypertension induced renal damage in the spontaneously hypertensive rat
    Hypertension, 1999
    Co-Authors: Elizabeth St. Lezin, Theodore W. Kurtz, Karen A Griffin, Maria M Picken, Monique C Churchill, Paul C Churchill, Vladimir Kren, Vaclav Zidek, Ning Wang, Michal Pravenec
    Abstract:

    Abstract —Linkage studies in the fawn-hooded hypertensive rat have suggested that genes influencing susceptibility to hypertension-associated renal failure may exist on rat Chromosome 1q. To investigate this possibility in a widely used model of hypertension, the spontaneously hypertensive rat (SHR), we compared susceptibility to hypertension-induced renal damage between an SHR progenitor strain and an SHR congenic strain that is genetically identical except for a defined region of Chromosome 1q. Backcross breeding with selection for the markers D1Mit3 and Igf2 on Chromosome 1 was used to create the congenic strain (designated SHR.BN- D1Mit3/Igf2 ) that carries a 22 cM segment of Chromosome 1 transferred from the normotensive Brown Norway rat onto the SHR background. Systolic blood pressure (by radiotelemetry) and urine protein excretion were measured in the SHR progenitor and congenic strains before and after the induction of accelerated hypertension by administration of DOCA-salt. At the same level of DOCA-salt hypertension, the SHR.BN- D1Mit3/Igf2 congenic strain showed significantly greater proteinuria and histologically assessed renal vascular and glomerular injury than the SHR progenitor strain. These findings demonstrate that a gene or genes that influence susceptibility to hypertension-induced renal damage have been trapped in the differential Chromosome segment of the SHR.BN- D1Mit3/Igf2 congenic strain. This congenic strain represents an important new model for the fine mapping of gene(s) on Chromosome 1 that affect susceptibility to hypertension-induced renal injury in the rat.

  • genetic isolation of a Chromosome 1 region affecting blood pressure in the spontaneously hypertensive rat
    Hypertension, 1997
    Co-Authors: Elizabeth St. Lezin, Alena Musilova, D Krenova, Vladimir Kren, Vaclav Zidek, Jiaming Wang, M Zdobinska, Ning Wang, Michal Pravenec
    Abstract:

    Abstract Recent linkage studies in the spontaneously hypertensive rat (SHR) suggest that a blood pressure regulatory gene or genes may be located on rat Chromosome 1q. To investigate this possibility, we replaced a region of Chromosome 1 in the SHR (defined by the markers D1Mit3 and Igf2 ) with the corresponding Chromosome segment from the normotensive Brown-Norway (BN) strain. In male SHR congenic rats carrying the transferred BN Chromosome segment, 24-hour average systolic and diastolic blood pressures were significantly lower than in male progenitor SHR. Polymerase chain reaction genotyping using 60 polymorphic microsatellite markers dispersed throughout the genome confirmed the congenic status of the new strain designated SHR.BN- D1Mit3/Igf2 . These findings provide direct evidence that a blood pressure regulatory gene exists on the differential segment of Chromosome 1 that is sufficient to decrease blood pressure in the SHR. The SHR.BN- D1Mit3/Igf2 congenic strain represents an important new model for fine mapping and characterization of genes on Chromosome 1 involved in the pathogenesis of spontaneous hypertension.