Characterization of six rat strains (Rattus norvegicus) by mitochondrial DNA restriction fragment length polymorphism

Hilsdorf, Alexandre Wagner Silva; Krieger, José Eduardo

doi:10.1590/s0100-879x1999000300003

Cited by 3 publications

(3 citation statements)

References 30 publications

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“…The region of the mitochondrial genome encoding ATPase subunit 6 was analyzed, because this particular region has minimal sequence divergence, even between different rat strains (47). Islet DNA from five IUGR and control rats was PCR-amplified.…”

Section: Resultsmentioning

confidence: 99%

“…This method is based on the differential electrophoretic mobility of single-stranded DNA under nondenaturing conditions (45,46). For this study, the region encoding ATPase 6 was chosen for SSCP analysis, since there is less sequence divergence in this region (47). DNA from islets of five IUGRs and five controls at 15 weeks of age was PCR-amplified using primers to ATPase 6.…”

Section: Mtdna Analysismentioning

confidence: 99%

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Progressive Accumulation of Mitochondrial DNA Mutations and Decline in Mitochondrial Function Lead to β-Cell Failure

Simmons

Suponitsky-Kroyter

Selak

2005

Journal of Biological Chemistry

182

175

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A key adaptation enabling the fetus to survive in a limited energy environment may be the reprogramming of mitochondrial function, which can have deleterious effects. Critical questions are whether mitochondrial dysfunction progressively declines after birth, and if so, what mechanism might underlie this process. To address this, we developed a model of intrauterine growth retardation (IUGR) in the rat that leads to diabetes in adulthood. Reactive oxygen species (ROS) production and oxidative stress gradually increased in IUGR islets. ATP production was impaired and continued to deteriorate with age. The activities of complex I and III of the electron transport chain progressively declined in IUGR islets. Mitochondrial DNA point mutations accumulated with age and were associated with decreased mitochondrial DNA content and reduced expression of mitochondria-encoded genes in IUGR islets. Mitochondrial dysfunction resulted in impaired insulin secretion. These results demonstrate that IUGR induces mitochondrial dysfunction in the fetal ␤-cell, leading to increased production of ROS, which in turn damage mitochondrial DNA. A self-reinforcing cycle of progressive deterioration in mitochondrial function leads to a corresponding decline in ␤-cell function. Finally, a threshold in mitochondrial dysfunction and ROS production is reached, and diabetes ensues.Epidemiological studies have revealed strong statistical links between poor fetal growth and the subsequent development of type 2 diabetes in adulthood (1-6). These associations have led to the "fetal origins of adult disease hypothesis," which states that "to ensure fetal survival, adaptations to intrauterine deprivation result in a permanent reprogramming of key organ systems" (2). Both insulin action and insulin secretion are impaired in individuals who were growth-retarded at birth (7-12).Uteroplacental insufficiency, the most common cause of in utero growth retardation, limits the supply of critical substrates such as oxygen, glucose, and amino acids to the fetus and results in poor fetal growth (13)(14)(15). This abnormal metabolic intrauterine milieu affects development of the fetus by modifying gene expression and function of susceptible cells, such as the ␤-cell (16 -19). The molecular mechanisms responsible for permanent changes in gene expression are not known, but they are a critical element in our understanding of how factors in early development can lead to long term consequences in aging and disease.A key adaptation enabling the fetus to survive in a limited energy environment may be the reprogramming of mitochondrial function (17, 18). However, these alterations in mitochondrial function can have deleterious effects, especially in cells that have a high energy requirement, such as the ␤-cell. The ␤-cell depends upon the normal production of ATP for nutrientinduced insulin secretion (20 -27) and proliferation (28). Thus, an interruption of mitochondrial function can have profound consequences for the ␤-cell.Mitochondrial dysfunction can also lead to inc...

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Section: Resultsmentioning

confidence: 99%

Section: Mtdna Analysismentioning

confidence: 99%

Progressive Accumulation of Mitochondrial DNA Mutations and Decline in Mitochondrial Function Lead to β-Cell Failure

Simmons

Suponitsky-Kroyter

Selak

2005

Journal of Biological Chemistry

182

175

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“…uma hipertensa e não-hiperativa e a outra não-hipertensa, mas hiperativa (HENDLEY;OHLSSON, 1991). Apesar das diferenças clínicas, em termos genéticos não há divergências entre as linhagens WKY, SHR e SHR stroke prone (HILSDORF; KRIEGER, 1999).…”

Section: Ratos Espontaneamente Hipertensosunclassified

Avaliação histológica da reparação óssea em defeitos bicorticais no ângulo de mandíbula de ratos geneticamente hipertensos e de seus controles Wistar-Kyoto

Chin¹

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Arterial hypertension may affect the quality of bone repair because this disease is characterized by physiopathological vascular and bone metabolism changes. With the objective of evaluating the bone neoformation and remodeling, this study investigated the process of bone repair in spontaneously hypertensive rats (SHR) and their match controls Wistar-Kyoto (WKY). Through-in-through defects were done with trephine burs in the mandibular angle area, of 2mm diameter on the right side and 5mm diameter on the left side. The animals were divided into groups of five individuals each one and killed after 2, 3, 5, 10, 15, 30, 60 and 90 postoperative days; the mandibles were removed, fixed in 10% formalin solution, decalcified with 20% formic acid, and embedded in paraffin; the histological sections of 7 µm thickness were stained with hematoxylin and eosin. The images were captured with 40x magnification and the defect area was measured by the image processing program Image J version 1.4. The statistical analysis showed that there is no significant difference in the comparison of WKY and SHR strains (p = 0,884), independent of periods or sides; among periods, in the WKY strain (p = 0,101) and SHR one (p = 0,479), independent of sides; among periods by strains on the right side; and among strains by sides, left side with p = 0,466 and right side with p = 0,689, independent of periods. There is a significant difference between left and right side (p < 0,001), independent of strains and periods; between sides by strains, WKY and SHR, both with p < 0,001; among periods by strains on the left side, which WKY 15 days group showed an area smaller than WKY 60 days and SHR 10 days groups, and WKY 60 days group showed an area bigger than SHR 30 days and SHR 60 days groups. Despite the changes founded on the left side that could be attributed to the functional remodeling of the mandibular bone, there were no differences in the bone repair of 5mm and 2mm diameter defects between spontaneously hypertensive rats and their match controls Wistar-Kyoto.

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Marcadores moleculares e a caracterização dos recursos genéticos de peixes: desenvolvimento sustentável da aquicultura e da pesca de espécies nativas de água doce no Brasil

Hilsdorf¹

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Characterization of six rat strains (Rattus norvegicus) by mitochondrial DNA restriction fragment length polymorphism

Cited by 3 publications

References 30 publications

Progressive Accumulation of Mitochondrial DNA Mutations and Decline in Mitochondrial Function Lead to β-Cell Failure

Progressive Accumulation of Mitochondrial DNA Mutations and Decline in Mitochondrial Function Lead to β-Cell Failure

Avaliação histológica da reparação óssea em defeitos bicorticais no ângulo de mandíbula de ratos geneticamente hipertensos e de seus controles Wistar-Kyoto

Marcadores moleculares e a caracterização dos recursos genéticos de peixes: desenvolvimento sustentável da aquicultura e da pesca de espécies nativas de água doce no Brasil

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