Histopathology of renal asphyxia in newborn piglets: Individual susceptibility to tubular changes

Gerosa, Clara; Iacovidou, Nicoletta; Argyri, Ioanna; Fanni, Daniela; Papalois, Apostolos; Aroni, Filippia; Faa, Gavino; Xanthos, Theodoros; Fanos, Vassilios

doi:10.5527/wjn.v4.i2.313

Cited by 6 publications

(3 citation statements)

References 18 publications

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“…Finally, the marked interindividual variability as to the extent of apoptotic cell death, previously reported by our group in kidneys [ 18 ] and hearts [ 19 ], is observed in the neurons of the brain cortex as well. This interindividual variability was observed within all 4 groups, suggesting a major role for the individual susceptibility of each animal to hypoxia/reoxygenation-related brain damage.…”

Section: Discussionsupporting

confidence: 58%

Reoxygenation of Asphyxiated Newborn Piglets: Administration of 100% Oxygen Causes Significantly Higher Apoptosis in Cortical Neurons, as Compared to 21%

Faa

Fanos

Fanni

et al. 2014

BioMed Research International

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Objective. Evaluation of neuronal changes in an animal experimental model of normocapnic hypoxia- reoxygenation. Materials and Methods. Fifty male piglets were the study subjects; normocapnic hypoxia was induced in 40 piglets and ten were sham-operated (controls). When bradycardia and/or severe hypotension occurred, reoxygenation was initiated. Animals were allocated in 4 groups according to the oxygen concentration, they were resuscitated with 18%, 21%, 40%, and 100% O2. Persisting asystole despite 10 minutes of cardiopulmonary resuscitation and return of spontaneous circulation were the endpoints of the experiment. Surviving animals were euthanized and brain cortex samples were collected, hematoxylin and eosin-stained, and examined for apoptotic bodies observing 10 consecutive high power fields. Results. Histological examination of the control group did not show any pathological change. On the contrary, apoptosis of neurons was found in 87.5% of treated animals. When specimens were examined according to the oxygen concentration used for resuscitation, we found marked intergroup variability; a higher percentage of apoptotic neurons was observed in piglets of group 4 (100% oxygen) compared to the others (P = 0.001). Conclusions. This preliminary data shows that normocapnic hypoxia and reoxygenation in Landrace/Large White piglets resulted in significant histological changes in the brain cortex. The degree of pathological changes in cortical neurons was significantly associated with the oxygen concentration used for reoxygenation, with a higher percentage of apoptotic neurons being observed in piglets reoxygenated with 100% compared to 18% O2 and to 21% O2.

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Section: Discussionsupporting

confidence: 58%

Reoxygenation of Asphyxiated Newborn Piglets: Administration of 100% Oxygen Causes Significantly Higher Apoptosis in Cortical Neurons, as Compared to 21%

Faa

Fanos

Fanni

et al. 2014

BioMed Research International

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“…In the rat burn model of our study, the H&E staining showed apparent dilatation of Bowman’s capsule in renal tissue 24 hours after severe burns, accompanied by the formation of casts in renal tubular. The expansion of Bowman’s capsule and the apparent of casts are important manifestations of kidney injury 32 33 . Additionally, both Cr and BUN were increased after severe burns, indicating that the glomerular filtration rate (GFR) decreased to less than 60% compared to normal kidney.…”

Section: Discussionmentioning

confidence: 99%

Melatonin prevents acute kidney injury in severely burned rats via the activation of SIRT1

Bai

Gao

et al. 2016

Sci Rep

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Acute kidney injury (AKI) is a common complication after severe burns. Melatonin has been reported to protect against multiple organ injuries by increasing the expression of SIRT1, a silent information regulator that regulates stress responses, inflammation, cellular senescence and apoptosis. This study aimed to investigate the protective effects of melatonin on renal tissues of burned rats and the role of SIRT1 involving the effects. Rat severely burned model was established, with or without the administration of melatonin and SIRT1 inhibitor. The renal function and histological manifestations were determined to evaluate the severity of kidney injury. The levels of acetylated-p53 (Ac-p53), acetylated-p65 (Ac-p65), NF-κB, acetylated-forkhead box O1 (Ac-FoxO1), Bcl-2 and Bax were analyzed to study the underlying mechanisms. Our results suggested that severe burns could induce acute kidney injury, which could be partially reversed by melatonin. Melatonin attenuated oxidative stress, inflammation and apoptosis accompanied by the increased expression of SIRT1. The protective effects of melatonin were abrogated by the inhibition of SIRT1. In conclusion, we demonstrate that melatonin improves severe burn-induced AKI via the activation of SIRT1 signaling.

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“…In animals that died perinatally, the lungs showed dystelectasis, most likely due to incomplete postnatal development. This may also have been the cause of the dilated tubules in kidneys of 3 of the 4 animals, since it had been shown that asphyxia in newborn piglets can lead to tubule dilation 31 . Asphyxia may have occurred in the R723G animals due to insufficient perinatal oxygen delivery.…”

Section: Resultsmentioning

confidence: 99%

Successful knock-in of Hypertrophic Cardiomyopathy-mutation R723G into the MYH7 gene mimics HCM pathology in pigs

Montag

Petersen

Flögel

et al. 2018

Sci Rep

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Familial Hypertrophic Cardiomyopathy (HCM) is the most common inherited cardiac disease. About 30% of the patients are heterozygous for mutations in the MYH7 gene encoding the ß-myosin heavy chain (MyHC). Hallmarks of HCM are cardiomyocyte disarray and hypertrophy of the left ventricle, the symptoms range from slight arrhythmias to sudden cardiac death or heart failure. To gain insight into the underlying mechanisms of the diseases’ etiology we aimed to generate genome edited pigs with an HCM-mutation. We used TALEN-mediated genome editing and successfully introduced the HCM-point mutation R723G into the MYH7 gene of porcine fibroblasts and subsequently cloned pigs that were heterozygous for the HCM-mutation R723G. No off-target effects were determined in the R723G-pigs. Surprisingly, the animals died within 24 h post partem, probably due to heart failure as indicated by a shift in the a/ß-MyHC ratio in the left ventricle. Most interestingly, the neonatal pigs displayed features of HCM, including mild myocyte disarray, malformed nuclei, and MYH7-overexpression. The finding of HCM-specific pathology in neonatal R723G-piglets suggests a very early onset of the disease and highlights the importance of novel large animal models for studying causative mechanisms and long-term progression of human cardiac diseases.

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Histopathology of renal asphyxia in newborn piglets: Individual susceptibility to tubular changes

Cited by 6 publications

References 18 publications

Reoxygenation of Asphyxiated Newborn Piglets: Administration of 100% Oxygen Causes Significantly Higher Apoptosis in Cortical Neurons, as Compared to 21%

Reoxygenation of Asphyxiated Newborn Piglets: Administration of 100% Oxygen Causes Significantly Higher Apoptosis in Cortical Neurons, as Compared to 21%

Melatonin prevents acute kidney injury in severely burned rats via the activation of SIRT1

Successful knock-in of Hypertrophic Cardiomyopathy-mutation R723G into the MYH7 gene mimics HCM pathology in pigs

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