Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Przeglądasz jako GOŚĆ
Tytuł pozycji:

Autophagy-mediated cytoplasmic accumulation of p53 leads to apoptosis through DRAM-BAX in cadmium-exposed human proximal tubular cells.

Tytuł :
Autophagy-mediated cytoplasmic accumulation of p53 leads to apoptosis through DRAM-BAX in cadmium-exposed human proximal tubular cells.
Autorzy :
Lee HY; Department of Anesthesiology and Pain Medicine, South Korea.
Oh SH; School of Medicine, Chosun University, 309 Pilmundaero, Dong-gu, Gwangju, 61452, South Korea. Electronic address: .
Pokaż więcej
Źródło :
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2021 Jan 01; Vol. 534, pp. 128-133. Date of Electronic Publication: 2020 Dec 13.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Publication: <2002- >: San Diego, CA : Elsevier
Original Publication: New York, Academic Press.
MeSH Terms :
Apoptosis/*drug effects
Autophagy/*drug effects
Cadmium/*toxicity
Kidney Tubules, Proximal/*cytology
Tumor Suppressor Protein p53/*metabolism
Apoptosis/physiology ; Autophagy/physiology ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; Cell Line ; Epithelial Cells ; Humans ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/metabolism ; Membrane Proteins/metabolism ; Poly (ADP-Ribose) Polymerase-1/metabolism ; RNA Interference ; Tumor Suppressor Protein p53/genetics ; bcl-2-Associated X Protein/metabolism
Contributed Indexing :
Keywords: Autophagy*; BAX*; Cadmium*; DRAM*; Human proximal tubular cell*; p53*
Substance Nomenclature :
0 (ATG5 protein, human)
0 (Autophagy-Related Protein 5)
0 (BAX protein, human)
0 (DRAM1 protein, human)
0 (Membrane Proteins)
0 (TP53 protein, human)
0 (Tumor Suppressor Protein p53)
0 (bcl-2-Associated X Protein)
00BH33GNGH (Cadmium)
EC 2.4.2.30 (PARP1 protein, human)
EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
Entry Date(s) :
Date Created: 20201215 Date Completed: 20210413 Latest Revision: 20210413
Update Code :
20210414
DOI :
10.1016/j.bbrc.2020.12.019
PMID :
33321290
Czasopismo naukowe
The tumor suppressor p53 is involved in cadmium (Cd)-induced apoptosis and autophagy. However, the regulatory mechanisms of p53 in Cd-induced kidney injury are not well established. Here, we report the role of autophagy in Cd-induced p53 induction in human proximal tubular cells (HK-2). HK-2 cells treated with Cd induced the expression of p53, DNA damage autophagy modulator (DRAM), and Bcl-2-associated X protein (BAX), as well as caused poly [ADP-ribose] polymerase 1 (PARP-1) cleavage. Cd exposure also induced autophagy with the accumulation of monomeric p62 and multiple high molecular weight form (HMW)-p62. The expression levels of p53, p62, microtubule-associated protein 1A/1B-light chain 3 (LC3)-1, and LC3-II were similar in the sense that they increased up to 12 h and then gradually decreased. DRAM and BAX levels began to increase post autophagy induction and continued to increase, indicating that autophagy preceded apoptosis. While the genetic knockdown of p53 downregulated HWM-p62, DRAM, and BAX, the expression levels of these proteins were upregulated by p53 overexpression. The genetic knockdown of p62 downregulated p53, autophagy, DRAM, and BAX. The inhibition of autophagy through pharmacological and genetic knockdown reduced p53 and inhibited Cd-induced apoptosis. Collectively, Cd induces apoptosis through p53-mediated DRAM-BAX signaling, which can be regulated by autophagy.
(Copyright © 2020 Elsevier Inc. All rights reserved.)

Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies