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Chintan Gandhi - One of the best experts on this subject based on the ideXlab platform.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:BACKGROUND Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1-7. However, the effect of meconium on ACE-2 has never been studied before. OBJECTIVE To study the effect of meconium on ACE-2, and whether inhibition of proteolytic Enzymes present in the meconium reverses its effects on ACE-2. METHODS Alveolar epithelial A549 cells were exposed to F-12 medium, 2.5% meconium, meconium + a protease inhibitor cocktail (PIc) and PIc alone for 16 h. At the end of incubation, apoptosis was measured with a nuclear fragmentation assay and cell lysates were collected for ACE-2 immunoblotting and Enzyme activity. RESULTS Meconium caused a fourfold increase in apoptotic nuclei (p < 0.001). The pro-apoptotic effect of meconium can be reversed by PIc. Meconium reduced ACE-2 Enzyme activity by cleaving ACE-2 into a fragment detected at ~ 37 kDa by immunoblot. PIc prevented the degradation of ACE-2 and restored 50% of ACE-2 activity (p < 0.05). CONCLUSION These data suggest that meconium causes degradation of Lung protective ACE-2 by proteolytic Enzymes present in meconium, since the effects of meconium can be reversed by PIc.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:Background Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1–7. However, the effect of meconium on ACE-2 has never been studied before.
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degradation of the protective Lung Enzyme angiotensin converting Enzyme 2 ace 2 by human meconium a potential mechanism of meconium aspiration syndrome
Pediatrics, 2018Co-Authors: Chintan Gandhi, Ira H Gewolb, Bruce D UhalAbstract:Background: Meconium aspiration syndrome (MAS) is a significant problem in term and near-term neonates. Meconium has been shown to induce apoptotic death of alveolar epithelial cells. It is known that meconium contains pancreatic and intestine brush border Enzymes which might be responsible for acute Lung damage observed in MAS. Previous studies from our lab showed that ACE-2 is downregulated in experimental Lung fibrosis. The main function of ACE-2 is to convert the octapeptide ANG II to the heptapeptide ANG 1-7. ANG II is a …
Bruce D Uhal - One of the best experts on this subject based on the ideXlab platform.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:BACKGROUND Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1-7. However, the effect of meconium on ACE-2 has never been studied before. OBJECTIVE To study the effect of meconium on ACE-2, and whether inhibition of proteolytic Enzymes present in the meconium reverses its effects on ACE-2. METHODS Alveolar epithelial A549 cells were exposed to F-12 medium, 2.5% meconium, meconium + a protease inhibitor cocktail (PIc) and PIc alone for 16 h. At the end of incubation, apoptosis was measured with a nuclear fragmentation assay and cell lysates were collected for ACE-2 immunoblotting and Enzyme activity. RESULTS Meconium caused a fourfold increase in apoptotic nuclei (p < 0.001). The pro-apoptotic effect of meconium can be reversed by PIc. Meconium reduced ACE-2 Enzyme activity by cleaving ACE-2 into a fragment detected at ~ 37 kDa by immunoblot. PIc prevented the degradation of ACE-2 and restored 50% of ACE-2 activity (p < 0.05). CONCLUSION These data suggest that meconium causes degradation of Lung protective ACE-2 by proteolytic Enzymes present in meconium, since the effects of meconium can be reversed by PIc.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:Background Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1–7. However, the effect of meconium on ACE-2 has never been studied before.
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degradation of the protective Lung Enzyme angiotensin converting Enzyme 2 ace 2 by human meconium a potential mechanism of meconium aspiration syndrome
Pediatrics, 2018Co-Authors: Chintan Gandhi, Ira H Gewolb, Bruce D UhalAbstract:Background: Meconium aspiration syndrome (MAS) is a significant problem in term and near-term neonates. Meconium has been shown to induce apoptotic death of alveolar epithelial cells. It is known that meconium contains pancreatic and intestine brush border Enzymes which might be responsible for acute Lung damage observed in MAS. Previous studies from our lab showed that ACE-2 is downregulated in experimental Lung fibrosis. The main function of ACE-2 is to convert the octapeptide ANG II to the heptapeptide ANG 1-7. ANG II is a …
Ira H Gewolb - One of the best experts on this subject based on the ideXlab platform.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:BACKGROUND Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1-7. However, the effect of meconium on ACE-2 has never been studied before. OBJECTIVE To study the effect of meconium on ACE-2, and whether inhibition of proteolytic Enzymes present in the meconium reverses its effects on ACE-2. METHODS Alveolar epithelial A549 cells were exposed to F-12 medium, 2.5% meconium, meconium + a protease inhibitor cocktail (PIc) and PIc alone for 16 h. At the end of incubation, apoptosis was measured with a nuclear fragmentation assay and cell lysates were collected for ACE-2 immunoblotting and Enzyme activity. RESULTS Meconium caused a fourfold increase in apoptotic nuclei (p < 0.001). The pro-apoptotic effect of meconium can be reversed by PIc. Meconium reduced ACE-2 Enzyme activity by cleaving ACE-2 into a fragment detected at ~ 37 kDa by immunoblot. PIc prevented the degradation of ACE-2 and restored 50% of ACE-2 activity (p < 0.05). CONCLUSION These data suggest that meconium causes degradation of Lung protective ACE-2 by proteolytic Enzymes present in meconium, since the effects of meconium can be reversed by PIc.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:Background Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1–7. However, the effect of meconium on ACE-2 has never been studied before.
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degradation of the protective Lung Enzyme angiotensin converting Enzyme 2 ace 2 by human meconium a potential mechanism of meconium aspiration syndrome
Pediatrics, 2018Co-Authors: Chintan Gandhi, Ira H Gewolb, Bruce D UhalAbstract:Background: Meconium aspiration syndrome (MAS) is a significant problem in term and near-term neonates. Meconium has been shown to induce apoptotic death of alveolar epithelial cells. It is known that meconium contains pancreatic and intestine brush border Enzymes which might be responsible for acute Lung damage observed in MAS. Previous studies from our lab showed that ACE-2 is downregulated in experimental Lung fibrosis. The main function of ACE-2 is to convert the octapeptide ANG II to the heptapeptide ANG 1-7. ANG II is a …
Romel Holmes - One of the best experts on this subject based on the ideXlab platform.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:Background Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1–7. However, the effect of meconium on ACE-2 has never been studied before.
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degradation of Lung protective angiotensin converting Enzyme 2 by meconium in human alveolar epithelial cells a potential pathogenic mechanism in meconium aspiration syndrome
Lung, 2019Co-Authors: Chintan Gandhi, Ira H Gewolb, Romel Holmes, Bruce D UhalAbstract:BACKGROUND Pancreatic digestive Enzymes present in meconium might be responsible for meconium-induced Lung injury. The local Renin Angiotensin System plays an important role in Lung injury and inflammation. Particularly, angiotensin converting Enzyme-2 (ACE-2) has been identified as a protective Lung Enzyme against the insult. ACE-2 converts pro-apoptotic Angiotensin II to anti-apoptotic Angiotensin 1-7. However, the effect of meconium on ACE-2 has never been studied before. OBJECTIVE To study the effect of meconium on ACE-2, and whether inhibition of proteolytic Enzymes present in the meconium reverses its effects on ACE-2. METHODS Alveolar epithelial A549 cells were exposed to F-12 medium, 2.5% meconium, meconium + a protease inhibitor cocktail (PIc) and PIc alone for 16 h. At the end of incubation, apoptosis was measured with a nuclear fragmentation assay and cell lysates were collected for ACE-2 immunoblotting and Enzyme activity. RESULTS Meconium caused a fourfold increase in apoptotic nuclei (p < 0.001). The pro-apoptotic effect of meconium can be reversed by PIc. Meconium reduced ACE-2 Enzyme activity by cleaving ACE-2 into a fragment detected at ~ 37 kDa by immunoblot. PIc prevented the degradation of ACE-2 and restored 50% of ACE-2 activity (p < 0.05). CONCLUSION These data suggest that meconium causes degradation of Lung protective ACE-2 by proteolytic Enzymes present in meconium, since the effects of meconium can be reversed by PIc.
Costas Ioannides - One of the best experts on this subject based on the ideXlab platform.
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tissue differences in the modulation of rat cytochromes p450 and phase ii conjugation systems by dietary doses of phenethyl isothiocyanate
Food and Chemical Toxicology, 2008Co-Authors: Nattaya Konsue, Costas IoannidesAbstract:Abstract Rats were fed diets supplemented with phenethyl isothiocyanate (PEITC) at 0.06 (low dose, dietary intake level), 0.6 (medium dose) and 6.0 μmole/g (high dose), and xenobiotic-metabolising Enzymes were monitored in liver, Lung and kidney. At the low dose, inhibition of the hepatic O -dealkylation of ethoxy- and methoxyresorufin was noted, whereas at the high dose increases in the O -depentylation of pentoxyresorufin and O -debenzylation of benzyloxyquinoline were observed, whereas p -nitrophenol hydroxylase was inhibited. Hepatic bioactivation of 2-amino-3-methylimidazo-[4,5- f ]quinoline to mutagens was not influenced by the PEITC-treatment. In the Lung, at the high dose, ethoxyresorufin dealkylation was elevated and that of pentoxyresorufin suppressed; no significant changes were seen in the kidney. Quinone reductase was markedly elevated at all doses in liver, but the Lung Enzyme was refractive whereas in the kidney a modest rise was observed at the high dose. Hepatic glutathione S -transferase activity was stimulated by PEITC-treatment, but no effect was evident in the Lung or kidney. It is concluded that the effects of PEITC on xenobiotic-metabolising systems are dose- and tissue-dependent, with the liver being the most sensitive and the Lung generally resistant. Increased detoxication rather than cytochrome P450 inhibition is the likely mechanism of the chemopreventive activity of PEITC.
