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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...

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Expression of progesterone receptor membrane component-1 in bovine reproductive system during estrous cycle.

European journal of histochemistry : EJH·2011
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Polymerase chain reaction : basic protocols.

Methods in molecular biology (Clifton, N.J.)·2011
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Progesterone inhibits apoptosis in part by PGRMC1-regulated gene expression.

Molecular and cellular endocrinology·2010
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Progesterone membrane receptor component 1 expression in the immature rat ovary and its role in mediating progesterone's antiapoptotic action.

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N-cadherin mediated cell contact inhibits germinal vesicle breakdown in mouse oocytes maintained in vitro.

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Progesterone regulates granulosa cell viability through a protein kinase G-dependent mechanism that may involve 14-3-3sigma.

Biology of reproduction·2004

Related Experiment Video

Updated: Jul 6, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Placing progesterone in the apoptotic pathway.

J J Peluso1

  • 1Department of Obstetrics and Gynecology, University of Connecticut Health Center, Farmington, CT 06030, USA.

Trends in Endocrinology and Metabolism: TEM
|April 15, 2008
PubMed
Summary

Progesterone supports reproductive cell survival. However, granulosa cells in ovarian follicles may use a non-genomic pathway, unlike other reproductive tissues, to maintain viability.

Area of Science:

  • Reproductive biology
  • Cellular signaling
  • Endocrinology

Background:

  • Progesterone is crucial for reproductive tissue viability, including the uterus, breast, corpus luteum, and ovarian granulosa cells.
  • Progesterone's antiapoptotic effects are generally attributed to its nuclear receptor, as evidenced by the progesterone antagonist RU 486.
  • While uterine, mammary, and luteal cells express the nuclear progesterone receptor, granulosa cells do not.

Purpose of the Study:

  • To review the mechanism by which progesterone maintains granulosa cell viability.
  • To explore the potential for a non-genomic progesterone signaling pathway in granulosa cells.

Main Methods:

  • Literature review of studies on progesterone action in reproductive tissues.
  • Analysis of data comparing progesterone receptor expression and function in different cell types.

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Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Related Experiment Videos

Last Updated: Jul 6, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
19:44

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Main Results:

  • Progesterone's antiapoptotic effects are well-established in the uterus, breast, and corpus luteum via the nuclear progesterone receptor.
  • Granulosa cells of developing and mature follicles lack the classic nuclear progesterone receptor.
  • Evidence suggests progesterone maintains granulosa cell viability through a non-genomic mechanism.

Conclusions:

  • Progesterone plays a vital role in maintaining the viability of various reproductive tissues.
  • Granulosa cells appear to utilize a non-genomic mechanism for progesterone signaling, distinct from the nuclear receptor pathway found in other reproductive tissues.