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Recent advances in genetics of the spontaneously hypertensive rat.

Pravenec M, Kurtz TW - Curr. Hypertens. Rep. (2010)

Bottom Line: Multiple quantitative trait loci associated with hemodynamic and metabolic parameters have been mapped in the SHR.Recently, it has become possible to identify some of the specific quantitative trait gene (QTG) variants that underlie quantitative trait loci linked to complex cardiovascular and metabolic traits in SHR related strains.Recombinant inbred strains derived from SHR and Brown Norway progenitors, together with SHR congenic and transgenic strains, have proven useful for establishing the identity of several QTGs in SHR models.

View Article: PubMed Central - PubMed

Affiliation: Institute of Physiology, Academy of Sciences of the Czech Republic, Videnska 1083, Prague 4, Czech Republic. pravenec@biomed.cas.cz

ABSTRACT
The spontaneously hypertensive rat (SHR) is the most widely used animal model of essential hypertension and associated metabolic disturbances. Multiple quantitative trait loci associated with hemodynamic and metabolic parameters have been mapped in the SHR. Recently, it has become possible to identify some of the specific quantitative trait gene (QTG) variants that underlie quantitative trait loci linked to complex cardiovascular and metabolic traits in SHR related strains. Recombinant inbred strains derived from SHR and Brown Norway progenitors, together with SHR congenic and transgenic strains, have proven useful for establishing the identity of several QTGs in SHR models. It is anticipated that the combined use of linkage analyses and gene expression profiles, together with the recently available genome sequences of both the SHR and Brown Norway strains and new methods for manipulating the rat genome, will soon accelerate progress in identifying QTGs for complex traits in SHR-related strains.

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Transgenic spontaneously hypertensive rats (SHRs) derived with the Sleeping Beauty RMCE/Venus transposon vectors. F1 rats were obtained by mating the RMCE/Venus SHR line 80 with three insertional sites on chromosomes 2, 4, and 16 with the SHR progenitor. The different shades of green reflect segregation of the transgenes in F1 rats (Izsvak, Mates, Landa, Pravenec, unpublished results)
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Fig1: Transgenic spontaneously hypertensive rats (SHRs) derived with the Sleeping Beauty RMCE/Venus transposon vectors. F1 rats were obtained by mating the RMCE/Venus SHR line 80 with three insertional sites on chromosomes 2, 4, and 16 with the SHR progenitor. The different shades of green reflect segregation of the transgenes in F1 rats (Izsvak, Mates, Landa, Pravenec, unpublished results)

Mentions: Sleeping Beauty transposon vectors have proven to be useful tools for transgenesis. Recently, a highly active Sleeping Beauty transposase (SB100X) was developed and was demonstrated to be very efficient in mouse transgenesis (about 45%) [25]. SB100X also enables a rate of transgenesis of approximately 25% in the SHR [41]. Transgenic founders showed no apparent signs of mosaic transgene expression and carried a few copies of the transgene. Figure 1 shows transgenic SHRs expressing green fluorescent protein derived with the Sleeping Beauty transposon system and segregation of insertional sites in transgenic lines. Heritable and stable gene knockdown in rats has been also achieved using RNA interference with the help of lentiviral-mediated transgenesis [42].Fig. 1


Recent advances in genetics of the spontaneously hypertensive rat.

Pravenec M, Kurtz TW - Curr. Hypertens. Rep. (2010)

Transgenic spontaneously hypertensive rats (SHRs) derived with the Sleeping Beauty RMCE/Venus transposon vectors. F1 rats were obtained by mating the RMCE/Venus SHR line 80 with three insertional sites on chromosomes 2, 4, and 16 with the SHR progenitor. The different shades of green reflect segregation of the transgenes in F1 rats (Izsvak, Mates, Landa, Pravenec, unpublished results)
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2821617&req=5

Fig1: Transgenic spontaneously hypertensive rats (SHRs) derived with the Sleeping Beauty RMCE/Venus transposon vectors. F1 rats were obtained by mating the RMCE/Venus SHR line 80 with three insertional sites on chromosomes 2, 4, and 16 with the SHR progenitor. The different shades of green reflect segregation of the transgenes in F1 rats (Izsvak, Mates, Landa, Pravenec, unpublished results)
Mentions: Sleeping Beauty transposon vectors have proven to be useful tools for transgenesis. Recently, a highly active Sleeping Beauty transposase (SB100X) was developed and was demonstrated to be very efficient in mouse transgenesis (about 45%) [25]. SB100X also enables a rate of transgenesis of approximately 25% in the SHR [41]. Transgenic founders showed no apparent signs of mosaic transgene expression and carried a few copies of the transgene. Figure 1 shows transgenic SHRs expressing green fluorescent protein derived with the Sleeping Beauty transposon system and segregation of insertional sites in transgenic lines. Heritable and stable gene knockdown in rats has been also achieved using RNA interference with the help of lentiviral-mediated transgenesis [42].Fig. 1

Bottom Line: Multiple quantitative trait loci associated with hemodynamic and metabolic parameters have been mapped in the SHR.Recently, it has become possible to identify some of the specific quantitative trait gene (QTG) variants that underlie quantitative trait loci linked to complex cardiovascular and metabolic traits in SHR related strains.Recombinant inbred strains derived from SHR and Brown Norway progenitors, together with SHR congenic and transgenic strains, have proven useful for establishing the identity of several QTGs in SHR models.

View Article: PubMed Central - PubMed

Affiliation: Institute of Physiology, Academy of Sciences of the Czech Republic, Videnska 1083, Prague 4, Czech Republic. pravenec@biomed.cas.cz

ABSTRACT
The spontaneously hypertensive rat (SHR) is the most widely used animal model of essential hypertension and associated metabolic disturbances. Multiple quantitative trait loci associated with hemodynamic and metabolic parameters have been mapped in the SHR. Recently, it has become possible to identify some of the specific quantitative trait gene (QTG) variants that underlie quantitative trait loci linked to complex cardiovascular and metabolic traits in SHR related strains. Recombinant inbred strains derived from SHR and Brown Norway progenitors, together with SHR congenic and transgenic strains, have proven useful for establishing the identity of several QTGs in SHR models. It is anticipated that the combined use of linkage analyses and gene expression profiles, together with the recently available genome sequences of both the SHR and Brown Norway strains and new methods for manipulating the rat genome, will soon accelerate progress in identifying QTGs for complex traits in SHR-related strains.

Show MeSH
Related in: MedlinePlus