scholarly journals Hypoxia in�utero increases the risk of pulmonary hypertension in rat offspring and is associated with vasopressin type‑2 receptor upregulation

2020 ◽  
Author(s):  
Hao Ding ◽  
Yuchuan Luo ◽  
Ke Hu ◽  
Huaying Huang ◽  
Pei Liu ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
In Utero ◽  
Rat Offspring ◽  
Receptor Upregulation

scholarly journals EXPRESS: Pulmonary Hypertension Associated With Neurofibromatosis Type 2

2021 ◽  
pp. 204589402110295
Author(s):  
Hirohisa Taniguchi ◽  
Tomoya Takashima ◽  
Ly Tu ◽  
Raphaël Thuillet ◽  
Asuka Furukawa ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Neurofibromatosis Type ◽  
Pulmonary Vascular Remodeling ◽  
Life Threatening ◽  
History Of ◽  
Pulmonary Arterial ◽  
First Time

Although precapillary pulmonary hypertension (PH) is a rare but severe complication of patients with neurofibromatosis type 1 (NF1), its association with NF2 remains unknown. Herein, we report a case of a 44-year-old woman who was initially diagnosed with idiopathic pulmonary arterial hypertension (IPAH) and treated with PAH-specific combination therapy. However, a careful assessment for a relevant family history of the disease and genetic testing reveal that this patient had a mutation in the NF2 gene. Using immunofluorescence and Western blotting, we demonstrated a decrease in endothelial NF2 protein in lungs from IPAH patients compared to control lungs, suggesting a potential role of NF2 in PAH development. To our knowledge, this is the first time that precapillary PH has been described in a patient with NF2. The altered endothelial NF2 expression pattern in PAH lungs should stimulate work to better understand how NF2 is contributing to the pulmonary vascular remodeling associated to these severe life-threatening conditions.

scholarly journals Alcohol Exposure in Utero Increases Susceptibility to Prostate Tumorigenesis in Rat Offspring

2013 ◽  
Vol 37 (11) ◽  
pp. 1901-1909 ◽  
Author(s):  
Sengottuvelan Murugan ◽  
Changqing Zhang ◽  
Sepideh Mojtahedzadeh ◽  
Dipak K. Sarkar
Keyword(s):  
Alcohol Exposure ◽  
In Utero ◽  
Prostate Tumorigenesis ◽  
Rat Offspring

In utero exposure of high-dose di-n-butyl phthalate resulted in opposite effects on testicular cell apoptosis in late embryonic and pubertal male rat offspring

2017 ◽  
Vol 36 (12) ◽  
pp. 1236-1247 ◽  
Author(s):  
H Shen ◽  
K Liao ◽  
H-F Wu ◽  
H-C Lu ◽  
Y Li ◽  
...  
Keyword(s):  
Western Blot ◽  
Cell Apoptosis ◽  
In Utero ◽  
Male Rat ◽  
In Utero Exposure ◽  
High Dose ◽  
Testicular Cell ◽  
Rat Testis ◽  
Rat Offspring ◽  
Butyl Phthalate

Objective: To investigate the effects of in utero exposure to high-dose di- n-butyl phthalate (DBP) on testicular cell apoptosis in late embryonic and pubertal male rat offspring. Methods: Twenty pregnant Sprague-Dawley (SD) rats were divided into two groups. During gestation day (GD) 12 to GD 19, control group was given 1 ml day−1 of olive oil and experimental group was given DBP 500 mg kg−1 day−1 by gavage. On GD 19.5 and postnatal day (PND) 45, the testes were removed. Morphological analysis of the testes was observed by transmission electron microscopy and hematoxylin and eosin (H&E) staining. Testicular cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). The expression of Bcl-2, Bax, and p53 was presented by immunohistochemistry (IHC) and western blot. Data of the two groups was compared using independent samples t-test and Mann–Whitney test by SPSS 20.0. Results: H&E staining showed that spermatogenetic cells were significantly decreased in DBP exposed pubertal rat testis. The apoptosis index of testes in DBP-treated group was significantly lower on GD 19.5 but higher on PND 45 than that of the controls ( p < 0.01). IHC and western blot revealed significantly increased expression of Bcl-2 in GD 19.5 rat testis and Bax and p53 in PND 45 rat testis after DBP exposure, compared with the control ( p < 0.05). Conclusion: In utero exposure of high-dose DBP resulted in opposite effects on testicular cell apoptosis in late embryonic and pubertal rat offspring. The overexpression of Bcl-2, Bax, and p53 might be related to the occurrence of abnormal apoptosis and finally produce male infertility.

scholarly journals Hypoxia-induced pulmonary hypertension in type 2 diabetic mice

2017 ◽  
Vol 7 (1) ◽  
pp. 175-185 ◽  
Author(s):  
Minglin Pan ◽  
Ying Han ◽  
Rui Si ◽  
Rui Guo ◽  
Ankit Desai ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Diabetic Mice ◽  
Type 2 Diabetic

scholarly journals Preliminary assessment of correlation between T-lymphocyte responses and control of porcine reproductive and respiratory syndrome virus (PRRSV) in piglets born after in-utero infection of a type 2 PRRSV

2018 ◽  
Vol 58 (1) ◽  
pp. 9-16
Author(s):  
Sang-Ho Cha ◽  
Carey Bandaranayaka-Mudiyanselage ◽  
Chandima B. Bandaranayaka-Mudiyanselage ◽  
Dharani Ajiththos ◽  
Kyoung-Jin Yoon ◽  
...  
Keyword(s):  
T Lymphocyte ◽  
In Utero ◽  
Respiratory Syndrome Virus ◽  
Preliminary Assessment ◽  
Lymphocyte Responses ◽  
And Control

Abstract 14372: Identification of the Genes That Are Involved in Severe Pulmonary Hypertension in Type 2 Diabetic Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Qiuyu Zheng ◽  
Atsumi Tsuji-Hosokawa ◽  
Jody T Cabrera ◽  
Jian Wang ◽  
Ayako Makino
Keyword(s):  
Pulmonary Hypertension ◽  
Endothelial Function ◽  
Protein Level ◽  
Chronic Hypoxia ◽  
Systolic Pressure ◽  
Vascular Complications ◽  
Hypoxic Exposure ◽  
Diabetic Mice ◽  
Type 2 Diabetic

Pulmonary hypertension (PH) is a progressive disease characterized by increased pulmonary vascular resistance. Increasing evidence shows that diabetes increases the risks of PH, and diabetic priming leads to severe PH. However, the molecular mechanism by which preconditioning of diabetes results in severe PH is still unknown. It has been shown that endothelium serves as a key regulator of vascular tone, and endothelial cell dysfunction is implicated in the development of PH and diabetes-related vascular complications. Therefore, we identified the genes that contribute to the development of severe PH in diabetic mice with a focus on endothelial function. We first determined the effect of chronic hypoxia (10% O 2 , 4 weeks) on hemodynamics in type 2 diabetic (T2D) mice. We used inducible T2D mice (generated by high-fat diet and a low-dose streptozotocin injection) and spontaneous T2D mice (TALLYHO/Jng). Diabetic mice exhibited a slight increase in right ventricular systolic pressure (RVSP), and chronic hypoxia led to a further rise in RVSP in both inducible and spontaneous T2D mice. We isolated pulmonary endothelial cells (MPEC) from normoxia-exposed control mice (CN), hypoxia-exposed control mice (CH), normoxia-exposed diabetic mice (DN), and hypoxia-exposed diabetic mice (DH) to examine the levels of 92 genes using real-time PCR. Nighty two genes were selected based on their functions, which are significantly related to endothelial function. We found that 27 genes were significantly changed among 4 groups. We then examined the protein levels of genes that were related to apoptosis and glycolysis. Western Blot data indicated that the protein level of GAPDH was significantly increased in CH and DH compared to CN and DN. In addition, hypoxic exposure in diabetic mice (DH) significantly increased HK2 protein level compare to hypoxia-exposed control mice (CH). These data suggest that precondition of diabetes increases susceptibility to developing PH due partly to altering gene expression of HK2 and Gapdh in MPECs. Since HK2 and GAPDH are a crucial regulator of glycolysis, alteration of glycolysis is expected in hypoxia-exposed diabetic mice. Our study revealed the key molecules which could be used for treating severe PH in diabetes.

AT2 receptor-mediated vasodilation in the heart: effect of myocardial infarction

2001 ◽  
Vol 281 (6) ◽  
pp. H2590-H2596 ◽  
Author(s):  
Martin P. Schuijt ◽  
Munesh Basdew ◽  
Richard van Veghel ◽  
René de Vries ◽  
Pramod R. Saxena ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Coronary Artery Ligation ◽  
Sham Operation ◽  
Ang Ii ◽  
Artery Ligation ◽  
Systemic Hemodynamic ◽  
Functional Consequences ◽  
Receptor Upregulation ◽  
Renal Vascular

To investigate the functional consequences of postinfarct cardiac angiotensin (ANG) type 2 (AT2) receptor upregulation, rats underwent coronary artery ligation or sham operation and were infused with ANG II 3–4 wk later, when scar formation is complete. ANG II increased mean arterial pressure (MAP) more modestly in infarcted animals than in sham animals. The AT1 receptor antagonist irbesartan, but not the AT2 receptor antagonist PD123319, decreased MAP and antagonized the ANG II-mediated systemic hemodynamic effects. Myocardial (MVC) but not renal vascular conductance (RVC) was diminished in infarcted versus sham rats. ANG II did not affect MVC and reduced RVC in all rats. MVC was unaffected by irbesartan and PD123319 in all animals. However, with PD123319, ANG II reduced MVC in sham but not infarcted animals, and, with irbesartan, ANG II increased MVC in infarcted but not sham animals. Irbesartan increased RVC and antagonized the ANG II-mediated renal effects in all animals. RVC, at baseline or with ANG II, was not affected by PD123319 in infarcted and sham animals. In conclusion, coronary but not renal AT2 receptor stimulation results in vasodilation, and this effect is enhanced in infarcted rats.

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