Effect of selective inhibition or activation of PGE2 EP1 receptor on glomerulosclerosis

Autor: Zhi Qiu, Jun Yin, Jing Liu, Xu Chen, Xiaolan Chen, Yu-Yin Xu
Rok vydání: 2019
Předmět:
0301 basic medicine
Male
Cancer Research
17-phenyl- trinor-prostaglandin E2 ethyl amide
Apoptosis
Kidney
Biochemistry
Nephrectomy
TRPC1
Mice
eIF-2 Kinase
0302 clinical medicine
Glomerulonephritis
transient receptor potential channel 1
glucose-regulated protein 78
Receptor
Dibenz(b
f)(1
4)oxazepine-10(11H)-carboxylic acid
8-chloro-
2-acetylhydrazide

Endoplasmic Reticulum Chaperone BiP
Cells
Cultured

Heat-Shock Proteins
Chemistry
Articles
Receptor antagonist
Endoplasmic Reticulum Stress
Receptors
Prostaglandin E
EP1 Subtype

medicine.anatomical_structure
Oncology
030220 oncology & carcinogenesis
Mesangial Cells
Molecular Medicine
lipids (amino acids
peptides
and proteins)

glomerulosclerosis
Agonist
medicine.medical_specialty
endocrine system
Prostaglandin Antagonists
medicine.drug_class
Prostaglandin E2 receptor
Dinoprostone
Transforming Growth Factor beta1
03 medical and health sciences
Downregulation and upregulation
Internal medicine
Genetics
medicine
Animals
Molecular Biology
TRPC Cation Channels
SC-19220
Glomerulosclerosis
medicine.disease
prostaglandin E2 receptor 1
Mice
Inbred C57BL

Disease Models
Animal

030104 developmental biology
Endocrinology
Zdroj: Molecular Medicine Reports
ISSN: 1791-3004
Popis: Prostaglandin E2 (PGE2) is involved in numerous physiological and pathological processes of the kidney via its four receptors. A previous study has suggested that a defect in the PGE2 receptor 1 (EP1) gene markedly suppressed the transforming growth factor‑β1 (TGF‑β1)‑induced mesangial cell (MC) proliferation and extracellular matrix aggregation. Therefore, the present study aimed to adopt a pharmacological method of specifically suppressing or activating the EP1 receptor to further verify and demonstrate these results. The EP1 receptor antagonist SC‑19220 and EP1 receptor agonist 17‑phenyl‑trinor‑PGE2 ethyl amide (17‑pt‑PGE2) were selectively used to treat five‑sixths nephrectomy renal fibrosis model mice and TGF‑β1‑stimulated MCs. An Alpha screen PGE2 assay kit, flow cytometry, western blotting and immunohistochemical techniques were adopted to perform in vivo and in vitro experiments. The present results suggested that compared with the control group, the selective EP1 receptor antagonist SC‑19220 improved renal function, markedly reduced the plasma blood urea nitrogen and creatinine levels (P
Databáze: OpenAIRE