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[Role of Bid protein in the mitochondria and Endoplasmic Reticulum associated apoptotic pathway]

Jie Hu1, Dong-Hua He, Liang Gao

  • 1Department of Hematology, First Affiliated Hospital of Medical College, Zhejiang University, Hangzhou 310003, China.

Zhonghua Xue Ye Xue Za Zhi = Zhonghua Xueyexue Zazhi
|December 13, 2007
PubMed
Abstract

Insights

Homoharringtonine (HHT) induces apoptosis in MUTZ-1 cells. Bid protein acts as a crucial link between endoplasmic reticulum (ER) stress and mitochondrial pathways in this cell death process.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Apoptosis is a critical cellular process.
  • Mitochondrial and endoplasmic reticulum (ER) pathways are key regulators of apoptosis.
  • Bid protein plays a role in mediating apoptosis.

Purpose of the Study:

  • To investigate the function of Bid protein in the ER and mitochondria-associated apoptotic pathways.
  • To elucidate the mechanism by which homoharringtonine (HHT) induces apoptosis in MUTZ-1 cells.

Main Methods:

  • Apoptosis was quantified using Fluorescence-Activated Cell Sorting (FACS).
  • ER and mitochondria-associated apoptotic pathways were analyzed via RT-PCR and Western blotting.
  • Bid protein translocation was visualized using laser scanning confocal microscopy (LSCM).

Main Results:

  • HHT treatment induced ER stress, Ca2+ release, and loss of mitochondrial membrane potential in MUTZ-1 cells.
  • HHT upregulated ER stress-associated proapoptotic factor mRNAs and activated caspase proteins.
  • Bid protein was observed to translocate from the ER to mitochondria following HHT exposure.

Conclusions:

  • HHT effectively induces apoptosis in MUTZ-1 cells.
  • Apoptosis is likely mediated by both ER stress and mitochondrial pathways.
  • Bid protein serves as a molecular bridge connecting these two apoptotic pathways.

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