Dysregulated ACE/Ang II/Ang1-7 signaling provokes cardiovascular and inflammatory sequelae of endotoxemia in weaning preeclamptic rats

Abuiessa, Salwa A.; Helmy, Mai M.; El‐Gowelli, Hanan M.; El‐Gowilly, Sahar M.; El‐Mas, Mahmoud M.

doi:10.1016/j.ejphar.2022.175344

Cited by 7 publications

(2 citation statements)

References 74 publications

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“…Consistent with reported clinical and experimental studies of exacerbated renal damage and morbidity and mortality in PE dams 29 , 30 , the present study demonstrated distinct functional and structural manifestations of renal injury in the L-NAME rodent model of PE. Opposite changes in urine protein (increases) and CrCl (decreases), positive hallmarks of renal damage 31 , 32 , were demonstrated in PE dams at GD20 compared with respective control rats and remained manifest till weaning (3 weeks post-labor). The excessive proteinuria has been attributed to the L-NAME-induced renal vascular wall thickening and elevated glomerular pressure 33 .…”

Section: Discussionmentioning

confidence: 97%

The suppression of MAPK/NOX/MMP signaling prompts renoprotection conferred by prenatal naproxen in weaning preeclamptic rats

Abdelhady,

Ali,

Yacout

et al. 2023

Sci Rep

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Although nonsteroidal antiinflammatory drugs (NSAIDs) are frequently used for fever and pain during pregnancy, their possible interaction with perinatal renal injury induced by preeclampsia (PE) has not been addressed. Here, studies were undertaken in the N(gamma)-nitro-l-arginine methyl ester (l-NAME) PE model to assess the influence of gestational NSAIDs on renal damage in weaning dams. PE-evoked increments and decrements in urine protein and creatinine clearance, respectively, were intensified by celecoxib and weakened by diclofenac or naproxen. Naproxen also improved renal cloudy swelling, necrosis, and reduced glomerular area evoked by PE. The concomitant rises in renal expression of markers of oxidative stress (NOX2/4), extracellular matrix metaloproteinase deposition (MMP9), and prostanoids (PGE2, PGF2α, TXA2) were all more effectively reduced by naproxen compared with celecoxib or diclofenac. Western blotting showed tripled expression of mitogen-activated protein kinases (MAPKs; p-p38, p-JNK1, p-ERK1, p-ERK2) in PE kidneys that was overturned by all NSAIDs, with naproxen producing the largest drop in p-ERK2 expression. The PE-provoked elevation in renal expression of autophagic marker LC3 was reduced by naproxen and diclofenac, but not celecoxib. The data suggests superior effect for naproxen over other NSAIDs in rectifying preeclamptic renal injury and predisposing inflammatory, oxidative, autophagic, and fibrotic signals.

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Section: Discussionmentioning

confidence: 97%

The suppression of MAPK/NOX/MMP signaling prompts renoprotection conferred by prenatal naproxen in weaning preeclamptic rats

Abdelhady,

Ali,

Yacout

et al. 2023

Sci Rep

Self Cite

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“…The results suggested that TAA caused the increase of Ang II content in the left ventricular myocardial tissue of rats, indicating that there might be a correlation between Ang II content and TAA. Ang II is the key vasoactive substance in the renin-Ang system, and it maintains the stability of cardiovascular functions [24] . Ang IImediated vascular inflammatory reactions could link the interaction between hypertension and other cardiovascular diseases and are involved in the progression of cardiovascular diseases through multiple mechanisms.…”

Section: Detection Of Protein Levels By Western Blotmentioning

confidence: 99%

Effect of Angiotensin II-Mediated Janus Kinase/Signal Transducers and Activators of Transcription Pathways on Thoracic Aortic Smooth Muscle Cells

Zhang,

Lu,

Yan

2024

IJPS

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At present, the effect of angiotensin II on the biological behavior of smooth muscle cells of thoracic aortic aneurysm is not clear. In this study, thoracic aortic aneurysm rat model (thoracic aortic aneurysm model group) was prepared by applying calcium chloride to blood vessels, and normal rats were taken as a sham operation group (sham group), with 10 rats in each group. The changes of angiotensin II content in plasma and left ventricular myocardial tissue were detected. Normal rat thoracic aortic smooth muscle cells were extracted and divided into the control group, angiotensin II group (1 μg/ml angiotensin II), and angiotensin II+angiotensin receptor blocker group (1×10 -6 mol/l candesartan+1 μg/ml angiotensin II). The cholecystokinin cell counting kit-8, flow cytometry, Transwell chamber, scratch healing, and Western blot experiments were used to detect cell proliferation, apoptosis, invasion, migration, and the expression changes of Janus kinase/signal transducers and activators of transcription pathway-related proteins. The results showed that angiotensin II content in left ventricular myocardium of thoracic aortic aneurysm group was higher than that of Sham group (p<0.01). Compared with the control group, angiotensin II group showed increased cell proliferative activity, number of invaded cells, mobility, and expression levels of Ras-related C3 botulinum toxin substrate 1, phosphorylated-Janus kinase 2, phosphorylated-signal transducers and activators of transcription 1, and phosphorylated-signal transducers and activators of transcription 3 proteins, and decreased apoptosis rate (p<0.05). Compared with the angiotensin II group, the cell proliferative activity, the number of invaded cells, and mobility as well as the expression levels of Ras-related C3 botulinum toxin substrate 1, phosphorylated-Janus kinase 2, phosphorylated-signal transducers and activators of transcription 1, and phosphorylatedsignal transducers and activators of transcription 3 proteins in the angiotensin II+angiotensin receptor blocker group were decreased, and the apoptosis rate was increased (p<0.05). These results indicated that angiotensin II could induce the proliferation, invasion, and migration of thoracic aortic aneurysm smooth muscle cells, and promote apoptosis.

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Gestationally administered RAS modulators reprogram endotoxic cardiovascular and inflammatory profiles in adult male offspring of preeclamptic rats

Abuiessa,

Helmy,

El-Gowelli

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Dysregulated ACE/Ang II/Ang1-7 signaling provokes cardiovascular and inflammatory sequelae of endotoxemia in weaning preeclamptic rats

Cited by 7 publications

References 74 publications

The suppression of MAPK/NOX/MMP signaling prompts renoprotection conferred by prenatal naproxen in weaning preeclamptic rats

The suppression of MAPK/NOX/MMP signaling prompts renoprotection conferred by prenatal naproxen in weaning preeclamptic rats

Effect of Angiotensin II-Mediated Janus Kinase/Signal Transducers and Activators of Transcription Pathways on Thoracic Aortic Smooth Muscle Cells

Gestationally administered RAS modulators reprogram endotoxic cardiovascular and inflammatory profiles in adult male offspring of preeclamptic rats

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