Tissue-specific transcriptome responses in rats with early streptozotocin-induced diabetes

Knoll, Kristen; Pietrusz, Jennifer L.; Liang, Mingyu

doi:10.1152/physiolgenomics.00231.2004

Cited by 56 publications

(69 citation statements)

References 39 publications

(42 reference statements)

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“…Mononuclear cell fractions were obtained from 8 -10 wk old male SS-13 real-time PCR machine (Applied Biosystems) and analyzed as described by Knoll et al (15). Statistical analysis.…”

Section: Methodsmentioning

confidence: 99%

Bone marrow mononuclear cells induce beneficial remodeling and reduce diastolic dysfunction in the left ventricle of hypertensive SS/MCWi rats

Parker

Didier

Karcher

et al. 2012

Physiological Genomics

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Little is known about the effectiveness of BMMNC therapy in hypertensive heart disease. In the current study, we show that delivery of BMMNCs from hypertension protected SS-13 BN /MCWi donor rats, but not BMMNC from hypertension susceptible SS/MCWi donor rats, resulted in 57.2 and 83.4% reductions in perivascular and interstitial fibrosis, respectively, as well as a 60% increase in capillary-to-myocyte count in the left ventricles (LV) of hypertensive SS/MCWi recipients. These histological changes were associated with improvements in LV compliance and relaxation (103 and 46.4% improvements, respectively). Furthermore, improved diastolic function in hypertensive SS/MCWi rats receiving SS-13 BN /MCWi derived BMMNCs was associated with lower clinical indicators of heart failure, including reductions in end diastolic pressure (65%) and serum brain natriuretic peptide levels (49.9%) with no improvements observed in rats receiving SS/MCWi BMMNCs. SS/MCWi rats had a lower percentage of endothelial progenitor cells in their bone marrow relative to SS-13 BN /MCWi rats. These results suggest that administration of BMMNCs can prevent or reverse pathological remodeling in hypertensive heart disease, which contributes to ameliorating diastolic dysfunction and associated symptomology. Furthermore, the health and hypertension susceptibility of the BMMNC donor are important factors influencing therapeutic efficacy, possibly via differences in the cellular composition of bone marrow.

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“…Mononuclear cell fractions were obtained from 8 -10 wk old male SS-13 real-time PCR machine (Applied Biosystems) and analyzed as described by Knoll et al (15). Statistical analysis.…”

Section: Methodsmentioning

confidence: 99%

Bone marrow mononuclear cells induce beneficial remodeling and reduce diastolic dysfunction in the left ventricle of hypertensive SS/MCWi rats

Parker

Didier

Karcher

et al. 2012

Physiological Genomics

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“…Renal regional tissues were collected and RNA was extracted as described previously (24,25,43). Real-time PCR analysis using the Taqman chemistry was performed as described previously (21,23,27). 18S rRNA was used as an internal normalizer.…”

Section: Methodsmentioning

confidence: 99%

Renal medullary 11β-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension

Liu

Singh

Usa

et al. 2008

Physiological Genomics

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Liu Y, Singh RJ, Usa K, Netzel BC, Liang M. Renal medullary 11␤-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension. Physiol Genomics 36: 52-58, 2008. First published September 30, 2008 doi:10.1152/physiolgenomics.90283.2008.-The Dahl salt-sensitive rat is a widely used model of human salt-sensitive forms of hypertension. The kidney plays an important role in the pathogenesis of Dahl salt-sensitive hypertension, but the molecular mechanisms involved remain a subject of intensive investigation. Gene expression profiling studies suggested that 11␤-hydroxysteroid dehydrogenase type 1 might be dysregulated in the renal medulla of Dahl salt-sensitive rats. Additional analysis confirmed that renal medullary expression of 11␤-hydroxysteroid dehydrogenase type 1 was downregulated by a high-salt diet in SS-13 BN rats, a consomic rat strain with reduced blood pressure salt sensitivity, but not in Dahl salt-sensitive rats. 11␤-Hydroxysteroid dehydrogenase type 1 is known to convert inactive 11-dehydrocorticosterone to active corticosterone. The urinary corticosterone/11-dehydrocorticosterone ratio as well as urinary excretion of corticosterone was higher in Dahl salt-sensitive rats than in SS-13 BN rats. Knockdown of renal medullary 11␤-hydroxysteroid dehydrogenase type 1 with small-interfering RNA attenuated the early phase of salt-induced hypertension in Dahl salt-sensitive rats and reduced urinary excretion of corticosterone. Knockdown of 11␤-hydroxysteroid dehydrogenase type 1 did not affect blood pressure in SS-13 BN rats. Long-term attenuation of salt-induced hypertension was achieved with small hairpin RNA targeting renal medullary 11␤-hydroxysteroid dehydrogenase type 1. In summary, we have demonstrated that suppression of 11␤-hydroxysteroid dehydrogenase type 1 expression in the renal medulla attenuates salt-induced hypertension in Dahl salt-sensitive rats.

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“…The differentially expressed genes were annotated as described previously. 16,17,48,49 Real-Time PCR Real-time quantitative PCR was carried out with the same RNA used in the microarray studies using the ABI Prism 7900HT sequence detection system and SYBR Green reagents from Applied Biosystems (Foster City, CA) as described previously. 48,49 The sequences of the primers used in this study are shown in Table 3.…”

Section: Gene Expression Profilingmentioning

confidence: 99%

High Perfusion Pressure Accelerates Renal Injury in Salt-Sensitive Hypertension

Mori

Polichnowski

Glocka

et al. 2008

Journal of the American Society of Nephrology

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Renal injury in the Dahl salt-sensitive rat mimics human salt-sensitive forms of hypertension that are particularly prevalent in black individuals, but the mechanisms that lead to the development of this injury are incompletely understood. We studied the impact of renal perfusion pressure (RPP) on the development of renal injury in this model. During the development of salt-induced hypertension over 2 wk, the RPP to the left kidney was maintained at control levels (125 Ϯ 2 mmHg) by continuous servocontrol inflation of an aortic balloon implanted between the renal arteries; during the same period, the RPP to the right kidney rose to 164 Ϯ 8 mmHg. After 2 wk of a 4% salt diet, DNA microarray and real-time PCR identified genes related to fibrosis and epithelial-to-mesenchymal transition in the kidneys exposed to hypertension. The increased RPP to the right kidney accounted for differences in renal injury between the two kidneys, measured by percentage of injured cortical and juxtamedullary glomeruli, quantified proteinaceous casts, number of ED-1-positive cells per glomerular tuft area, and interstitial fibrosis. Interlobular arteriolar injury was not increased in the kidney exposed to elevated pressure but was reduced in the control kidney. We conclude that elevations of RPP contribute significantly to the fibrosis and epithelial-to-mesenchymal transition found in the early phases of hypertension in the salt-sensitive rat. Rapid development of renal injury is a prominent feature of salt-induced hypertension in the Dahl salt-sensitive (SS) rat. Within a few weeks of high salt exposure, SS rats develop substantial injuries in preglomerular vessels, glomeruli, and the tubulointerstitial compartment. [1][2][3] This prominence of renal injury in the SS rat mimics human salt-sensitive forms of hypertension that are particularly prevalent in black individuals. 4 The extent of renal injury is known to vary widely in various forms of hypertension. Rapid development of renal injury in SS rats is in sharp contrast with that observed in spontaneously hypertensive rats (SHR), another commonly used rat model of hypertension. Hypertension in the SHR of a magnitude and duration similar to that seen in SS rats results in little or no renal injury. [5][6][7][8] Moreover, although it is recognized that hypertension is a strong independent risk factor for renal failure, the effectiveness of BP control in the reduction of renal injury varies greatly between subpopulations of hypertensive patients. 9 -11 These observations have clouded the question of how much physical factors related to the elevation of renal perfusion pressure (RPP) actually contribute to renal injury in hypertension. This issue has not been easily clarified given the difficulty in sustaining a chronic increase

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Tissue-specific transcriptome responses in rats with early streptozotocin-induced diabetes

Cited by 56 publications

References 39 publications

Bone marrow mononuclear cells induce beneficial remodeling and reduce diastolic dysfunction in the left ventricle of hypertensive SS/MCWi rats

Bone marrow mononuclear cells induce beneficial remodeling and reduce diastolic dysfunction in the left ventricle of hypertensive SS/MCWi rats

Renal medullary 11β-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension

High Perfusion Pressure Accelerates Renal Injury in Salt-Sensitive Hypertension

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