Zhonghua xin xue guan bing za zhi · 2008
[Parathyroid hormone 1-34 induce cardiac myocytes hypertrophy via extracellular regulated protein kinase 1/2 pathway].
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Xiao-gang, An Hui-xia, Liu Su-yan, Ren Ye-ping, Zhang Wei-bing
Аннотация
OBJECTIVE: To investigate the role of mitogen activated protein kinase kinase 1 (MAPKK, MEK1) and regulated kinase1/2 (ERK1/2) on cardiac hypertrophy induced by rat parathyroid hormone1-34 (rPTH1-34).
METHOD: Neonatal rat cardiomyocytes was treated with or without 10(-7) mol/L rPTH1-34 in the absence or presence 2 x 10(-5) mol/L PD98059, a MEK1 inhibitor. Cellular diameter was measured by Motic Images Advanced 3.0 software and the synthetic rate of protein in cardiac myocytes was detected by 3H-leucine incorporation, mRNA expression of atrial natriuretic peptide (ANP) was measured by RT-PCR and protein expression of ERK1/2 and p-ERK1/2 was measured by Western blot.
RESULTS: rPTH1-34 (10(-7) mol/L) significantly increase cellular diameter (+13.6 microm), 3H-leucine incorporation (+898 cpm/well), ANP mRNA expression (+73.9%), and p-ERK1/2 protein expression (+15%) compared to control cells (all P < 0.05) and these effects could be significantly attenuated by PD98059: cellular diameter (-7.1 microm), 3H-leucin e incorporation (-644 cpm/well), ANP mRNA expression (-52.2%), and protein expression of p-ERK1/2 (-18%) (all P < 0.05 vs. PTH group). PD98059 did not affect control cells without PTH treatment (all P > 0.05).
CONCLUSIONS: PD98059 attenuates PTH induced cardiac hypertrophy in vitro via inhibiting the expression of ERK1/2 and p-ERK1/2.
METHOD: Neonatal rat cardiomyocytes was treated with or without 10(-7) mol/L rPTH1-34 in the absence or presence 2 x 10(-5) mol/L PD98059, a MEK1 inhibitor. Cellular diameter was measured by Motic Images Advanced 3.0 software and the synthetic rate of protein in cardiac myocytes was detected by 3H-leucine incorporation, mRNA expression of atrial natriuretic peptide (ANP) was measured by RT-PCR and protein expression of ERK1/2 and p-ERK1/2 was measured by Western blot.
RESULTS: rPTH1-34 (10(-7) mol/L) significantly increase cellular diameter (+13.6 microm), 3H-leucine incorporation (+898 cpm/well), ANP mRNA expression (+73.9%), and p-ERK1/2 protein expression (+15%) compared to control cells (all P < 0.05) and these effects could be significantly attenuated by PD98059: cellular diameter (-7.1 microm), 3H-leucin e incorporation (-644 cpm/well), ANP mRNA expression (-52.2%), and protein expression of p-ERK1/2 (-18%) (all P < 0.05 vs. PTH group). PD98059 did not affect control cells without PTH treatment (all P > 0.05).
CONCLUSIONS: PD98059 attenuates PTH induced cardiac hypertrophy in vitro via inhibiting the expression of ERK1/2 and p-ERK1/2.