Leptin affects proliferation-, apoptosis- and protein kinase A-related peptides in human ovarian granulosa cells

Title:

Leptin affects proliferation-, apoptosis- and protein kinase A-related peptides in human ovarian granulosa cells

Creator:

Alexander V. Sirotkin, Miloš Mlynček, Alexander Makarevič, Iveta Konýčková, and Ladislav Hetényi

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:34ba36a4-b0a8-4c9e-be0c-1fba93de02f9
uuid:34ba36a4-b0a8-4c9e-be0c-1fba93de02f9
issn:0862-8408

Subject:

Biochemie. Molekulární biologie. Biofyzika, fyziologie, živočišná výroba, leptin, proteinové kinázy, vaječníky, physiology, animal industry, protein kinases, ovaries, accumulation of proliferation-related peptides (PCNA), cyclin B, Bax, 2, and 577

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The aim of our in vitro studies was to understand the role of leptin in controlling proliferation, apoptosis, and protein kinase A (PKA) in human ovarian cells. We analyzed the in vitro effects of leptin (0, 1, 10 or 100 ng/ml) on the accumulation of proliferation-related peptides (PCNA, cyclin B1), apoptosis-associated peptide (Bax) and the intracellular signaling molecule PKA in cultured human granulosa cells using immunocytochemistry and Western immunoblotting. It was observed that leptin stimulated in a dose-dependent manner the accumulation of PCNA (at doses 1-100 ng/ml), cyclin B1 (at doses 10 or 100 ng/ml), Bax (at doses 10 or 100 ng/ml) and PKA (at doses 1-100 ng/ml) in cultured human ovarian cells. These observations suggest the ability of leptin to control directly human ovarian cell functions: proliferation, apoptosis, and intracellular messenger PKA., A. V. Sirotkin, M. Mlynček, A. V. Makarevich, I. Florkovičová, L. Hetényi., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2008 Volume:57 | Number:3

Harvested from:

CDK

Metadata only:

false