Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase

Shimada, Ichiroh; Matsui, Kazuhiro; Brinkmann, B.; Hohoff, Carsten; Hiraga, Kenji; Tabuchi, Yoshiaki; Takasaki, Ichiro; Kato, Ichiro; Kawaguchi, Hiroshi; Takasawa, Kumi; Iida, Reiko; Takizawa, Hisao; Matsuki, Taizo

doi:10.1007/s00414-008-0226-6

Cited by 15 publications

(12 citation statements)

References 40 publications

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“…As time after injury increased, the expression levels of sTnI mRNA gradually became stable. The findings on sTnI mRNA expression are almost identical to the results obtained by Shimada et al [27], who reported that the expression levels of TnI mRNA decreased following diffuse alveolar damage.…”

Section: Discussionsupporting

confidence: 91%

Time-dependent expression of skeletal muscle troponin I mRNA in the contused skeletal muscle of rats: a possible marker for wound age estimation

et al. 2009

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To estimate the age of skeletal muscle contusion, the expression of troponin I mRNA in contused skeletal muscle of rats was detected using real-time polymerase chain reaction (PCR). A total of 51 Sprague-Dawley male rats were divided into control and contusion groups, and another nine rats received contusion injury after death. At 0.5, 1, 6, 12, 18, 24, 30, and 36 h after contusion, the rats were killed with a lethal dose of pentobarbital. Total RNA was isolated from muscle specimens using the SV Total RNA Isolation System and reverse transcribed into first-strand cDNA. Sequence-specific primers were then used to conduct real-time PCR to analyze the expression levels of sTnI mRNA. At 0.5, 1, and 6 h after contusion, the expression levels of sTnI mRNA decreased to 78.17% (P < 0.05), 41.58% (P < 0.05), and 32.13% of that in the control group, respectively. However, there were no significant changes in the expression levels of sTnI mRNA from 6 to 36 h (P > 0.05) after contusion when normalized to RpL32 expression. The expression levels of sTnI mRNA in the normal and contused skeletal muscle of postmortem rats were about 70% of that in the control group (P < 0.05), and no significant changes in the expression levels of sTnI mRNA in the postmortem contusion group were noted among different time points after injury. This result suggests that determination of sTnI mRNA levels by real-time PCR is useful for the estimation of wound age.

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Section: Discussionsupporting

confidence: 91%

Time-dependent expression of skeletal muscle troponin I mRNA in the contused skeletal muscle of rats: a possible marker for wound age estimation

et al. 2009

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“…The clinical association of CTGF with BPD is best established by studies demonstrating increased CTGF concentrations in bronchoalveolar lavage fluid from preterm infants developing BPD (5) and increased CTGF expression in lung tissues of infants who died of BPD (6). Multiple studies have examined the potential role of CTGF in experimental BPD and demonstrated that increased CTGF expression is associated with chronic hyperoxia as well as mechanical ventilationinduced lung injury in neonatal rodents (6)(7)(8)(9)(10). Recent studies from our laboratory utilizing genetic gain-of-function and biological loss-of-function approaches have provided compelling evidence that a novel signaling network orchestrated by CTGF plays an important role in BPD pathogenesis (6,11,12).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of β-catenin signaling protects against CTGF-induced alveolar and vascular pathology in neonatal mouse lung

et al. 2016

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Background: Bronchopulmonary dysplasia (BPD) is the most common and serious chronic lung disease of premature infants. Connective tissue growth factor (CTGF) plays an important role in tissue development and remodeling. We have previously shown that targeted overexpression of CTGF in alveolar type II epithelial cells results in BPD-like pathology and activates β-catenin in neonatal mice. Methods: Utilizing this transgenic mouse model and ICG001, a specific pharmacological inhibitor of β-catenin, we tested the hypothesis that β-catenin signaling mediates the effects of CTGF in the neonatal lung. Newborn CTGF mice and control littermates received ICG001 (10 mg/kg/dose) or placebo (dimethyl sulfoxide, equal volume) by daily i.p. injection from postnatal day 5 to 15. Alveolarization, vascular development, and pulmonary hypertension (PH) were analyzed. results: Administration of ICG001 significantly downregulated expression of cyclin D1, collagen 1a1, and fibronectin, which are the known target genes of β-catenin signaling in CTGF lungs. Inhibition of β-catenin signaling improved alveolar and vascular development and decreased pulmonary vascular remodeling. More importantly, the improved vascular development and vascular remodeling led to a decrease in PH. conclusion: β-Catenin signaling mediates the autocrine and paracrine effects of CTGF in the neonatal lung. Inhibition of CTGF-β-catenin signaling may provide a novel therapy for BPD. INTRODUCTIONBronchopulmonary dysplasia (BPD) is the most common and serious chronic lung disease of premature infants (1). Over the past four decades, the incidence of this disease has significantly increased as a result of improved survival of extremely-low-birthweight infants (2). The pathology of BPD is increasingly being recognized as a developmental arrest of the immature lung caused by injurious stimuli such as mechanical ventilation, oxygen exposure, and intrauterine or postnatal infections. Larger and simplified alveoli, decreased vascular growth, and variable interstitial fibrosis are the key pathological features observed in lungs of infants who died of BPD (1). The combination of decreased vascular growth and excessive pulmonary vascular remodeling leads to pulmonary hypertension (PH) which significantly contributes to the morbidity and mortality of these infants (3). Yet, the underlying cellular and molecular mechanisms are poorly defined, and there is no effective therapy.Connective tissue growth factor (CTGF) is a matricellular protein that plays an important role in tissue development and remodeling (4). Recent studies have highlighted the potential role of CTGF in BPD development and progression. The clinical association of CTGF with BPD is best established by studies demonstrating increased CTGF concentrations in bronchoalveolar lavage fluid from preterm infants developing BPD (5) and increased CTGF expression in lung tissues of infants who died of BPD (6). Multiple studies have examined the potential role of CTGF in experimental BPD and demonstrated that increased CTG...

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“…Oxygen also causes oxidative pulmonary injury at a high concentration during artificial respiration [111]. These specific toxicities cannot be detected by morphology in acute death cases, but may be detectable by molecular biological procedures.…”

Section: Miscellaneousmentioning

confidence: 96%

Forensic molecular pathology of violent deaths

Maeda

Zhu

Ishikawa

et al. 2010

Forensic Science International

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Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase

Cited by 15 publications

References 40 publications

Time-dependent expression of skeletal muscle troponin I mRNA in the contused skeletal muscle of rats: a possible marker for wound age estimation

Time-dependent expression of skeletal muscle troponin I mRNA in the contused skeletal muscle of rats: a possible marker for wound age estimation

Inhibition of β-catenin signaling protects against CTGF-induced alveolar and vascular pathology in neonatal mouse lung

Forensic molecular pathology of violent deaths

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