Related Experiment Video

Updated: Feb 21, 2026

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
04:41

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue

Published on: July 28, 2023

3.6K

Mortalin deficiency suppresses fibrosis and induces apoptosis in keloid spheroids

Won Jai Lee1, Hyo Min Ahn2, Youjin Na2

  • 1Institute for Human Tissue Restoration, Department of Plastic & Reconstructive Surgery, Yonsei University College of Medicine, Seoul, Korea.

Scientific Reports
|October 13, 2017
PubMed

Insights

Blocking mortalin (Mot) in keloid fibroblasts reduces extracellular matrix proteins and promotes apoptosis. This suggests targeting mortalin is a promising therapeutic strategy for keloid treatment.

Area of Science:

  • Cell Biology
  • Dermatology
  • Molecular Biology

Background:

  • Mortalin (Mot), a mitochondrial chaperone, promotes cell proliferation and inhibits apoptosis, potentially contributing to keloid pathogenesis.
  • Elevated mortalin expression is observed in keloid tissues and activated keloid fibroblasts (KFs).

Purpose of the Study:

  • To investigate the therapeutic potential of mortalin knockdown in keloid treatment.
  • To examine the effects of mortalin knockdown on apoptosis and extracellular matrix (ECM) production in keloid spheroids.

Main Methods:

  • Generation of mortalin-specific small hairpin RNAs (shRNAs) (dE1-RGD/GFP/shMot).
  • Transduction of primary keloid spheroids with dE1-RGD/GFP/shMot to achieve mortalin knockdown.
  • Analysis of ECM components (collagens, fibronectin, elastin), signaling pathways (TGF-β1, EGFR, Erk1/2, Smad2/3), apoptosis markers (TUNEL, cytochrome C), and p53 localization via immunofluorescence.

Main Results:

  • Mortalin knockdown significantly reduced the expression of type I and III collagen, fibronectin, and elastin in keloid spheroids.
  • Knockdown of mortalin decreased the expression of TGF-β1, EGFR, Erk1/2, and Smad2/3 complex proteins.
  • Increased TUNEL activity and cytochrome C levels indicated enhanced apoptosis.
  • Mortalin knockdown led to the relocation of p53 to the nucleus in keloid spheroids.

Conclusions:

  • Knockdown of mortalin effectively induces apoptosis and reduces ECM production in keloid spheroids.
  • Targeting mortalin and its interaction with p53 presents a novel and potentially beneficial therapeutic strategy for keloid treatment.

More Related Videos

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates08:19

Evaluation of Keratinocyte Proliferation on Two- and Three-dimensional Type I Collagen Substrates

Published on: April 22, 2019

7.5K
In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding08:20

In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding

Published on: May 1, 2020

7.2K

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...
8.8K
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...
8.9K