Related Experiment Videos

Down-regulation of programmed cell death 5 by insulin-like growth factor 1 in osteoarthritis chondrocytes

Chengqing Yi1, Chunhui Ma, Zongping Xie

  • 1Department of Orthopaedics, Shanghai First People's Hospital, No. 650 New Songjiang Road, Shanghai, 201620, China. chengqingyiyiyi@hotmail.com

International Orthopaedics
|January 17, 2013
PubMed
Abstract

Insights

Insulin-like growth factor (IGF)-1 down-regulation and programmed cell death 5 (PDCD5) up-regulation are linked to increased osteoarthritis chondrocyte apoptosis. IGF-1 may inhibit apoptosis by reducing PDCD5 expression.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Orthopedics

Background:

  • Osteoarthritis (OA) is a degenerative joint disease characterized by chondrocyte apoptosis.
  • Understanding the molecular mechanisms regulating chondrocyte apoptosis is crucial for developing OA treatments.

Purpose of the Study:

  • Investigate insulin-like growth factor (IGF)-1 and programmed cell death 5 (PDCD5) expression in OA chondrocytes.
  • Explore the correlation between IGF-1 and PDCD5 in OA chondrocyte apoptosis.

Main Methods:

  • Quantitative reverse transcriptase polymerase chain reaction (qPCR) and western blotting to measure mRNA and protein levels of IGF-1 and PDCD5.
  • Immunohistochemistry for protein expression analysis.
  • TUNEL staining to quantify apoptotic cells.

Main Results:

  • IGF-1 mRNA and protein levels were down-regulated in OA chondrocytes.
  • PDCD5 mRNA and protein levels were up-regulated in OA chondrocytes.
  • IGF-1 expression was negatively correlated with PDCD5 expression. Apoptosis rate positively correlated with PDCD5 and negatively with IGF-1.

Conclusions:

  • IGF-1 down-regulates PDCD5 expression.
  • IGF-1 inhibits apoptosis in osteoarthritis chondrocytes, potentially by modulating PDCD5 levels.

Related Concept Videos

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.
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...
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...