Inactivated Pseudomonas aeruginosa inhibits hypoxia-induced pulmonary hypertension by preventing TGF-β1/Smad signaling

Autor: J.T. Wang, T. Liu, S.J. Ma, S.D. Chai, P.Z. Tang, M.F. Dong, Z.K. Li
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
Medicine (General)
Physiology
Smad Proteins
SMAD
Pharmacology
Biochemistry
Rats
Sprague-Dawley
Primary arterial smooth muscle cells
Biology (General)
General Pharmacology
Toxicology and Pharmaceutics
Hypoxia
lcsh:QH301-705.5
TGF-β/Smad
lcsh:R5-920
medicine.diagnostic_test
General Neuroscience
General Medicine
Flow Cytometry
Immunohistochemistry
Pseudomonas aeruginosa
α-smooth muscle actin
medicine.symptom
lcsh:Medicine (General)
Signal Transduction
QH301-705.5
Hypertension
Pulmonary
Immunology
Blotting
Western
Myocytes
Smooth Muscle
Biophysics
Ocean Engineering
Inflammation
Enzyme-Linked Immunosorbent Assay
Biology
Pulmonary hypertension
Transforming Growth Factor beta1
03 medical and health sciences
R5-920
Western blot
In vivo
medicine.artery
medicine
Animals
Inactivated Pseudomonas aeruginosa
Cell Proliferation
Biomedical Sciences
Reproducibility of Results
Cell Biology
Hypoxia (medical)
medicine.disease
Actins
030104 developmental biology
lcsh:Biology (General)
Pulmonary artery
Transforming growth factor
Zdroj: Brazilian Journal of Medical and Biological Research v.49 n.10 2016
Brazilian Journal of Medical and Biological Research
Associação Brasileira de Divulgação Científica (ABDC)
instacron:ABDC
Brazilian Journal of Medical and Biological Research, Vol 49, Iss 10 (2016)
Brazilian Journal of Medical and Biological Research, Volume: 49, Issue: 10, Article number: e5526, Published: 25 AUG 2016
Popis: Pseudomonas aeruginosa is one of the common colonizing bacteria of the human body and is an opportunistic pathogen frequently associated with respiratory infections. Inactivated P. aeruginosa (IPA) have a variety of biological effects against inflammation and allergy. Transforming growth factor-β (TGF-β) signaling plays a critical role in the regulation of cell growth, differentiation, and development in a wide range of biological systems. The present study was designed to investigate the effects of IPA on TGF-β/Smad signaling in vivo, using a hypoxia-induced pulmonary hypertension (PH) rat model. Sprague Dawley rats (n=40) were exposed to 10% oxygen for 21 days to induce PH. At the same time, IPA was administered intravenously from day 1 to day 14. Mean pulmonary artery pressure (mPAP) and the right ventricle (RV) to left ventricle plus the interventricular septum (LV+S) mass ratio were used to evaluate the development of PH. Vessel thickness and density were measured using immunohistochemistry. Primary arterial smooth muscle cells (PASMCs) were isolated and the proliferation of PASMCs was assayed by flow cytometry. The production of TGF-β1 in cultured supernatant of PASMCs was assayed by ELISA. The expression levels of α-smooth muscle actin (α-SMA), TGF-β1 and phospho-Smad 2/3 in PASMCs were assayed by western blot. Our data indicated that IPA attenuated PH, RV hypertrophy and pulmonary vascular remodeling in rats, which was probably mediated by restraining the hypoxia-induced overactive TGF-β1/Smad signaling. In conclusion, IPA is a promising protective treatment in PH due to the inhibiting effects on TGF-β1/Smad 2/3 signaling.
Databáze: OpenAIRE
Externí odkaz: