Related Experiment Video

Updated: Aug 13, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

38.0K

Ac-SDKP suppresses epithelial-mesenchymal transition in A549 cells via HSP27 signaling

Haijing Deng1, Fang Yang2, Hong Xu3

  • 1Pathology Department, Hebei Medical University, Shi Jiazhuang, China.

Experimental and Molecular Pathology
|July 8, 2014
PubMed

Insights

The synthetic tetrapeptide N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) reduces fibrosis by inhibiting heat shock protein 27 (HSP27) in alveolar epithelial cells. This peptide therapy shows potential for treating fibrotic diseases.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Fibrosis involves the transformation of epithelial cells into myofibroblasts, a process modulated by TGF-β1.
  • Heat shock protein 27 (HSP27) plays a role in the molecular pathways of fibrosis.

Purpose of the Study:

  • To investigate the anti-fibrotic effects of N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) on human type II alveolar epithelial cells (A549).
  • To elucidate the role of HSP27 in TGF-β1-induced epithelial-mesenchymal transition (EMT) and myofibroblast differentiation.

Main Methods:

  • A549 cells were treated with TGF-β1 to induce EMT, and morphological changes were observed via phase-contrast microscopy.
  • Immunocytochemistry, western blot, and confocal microscopy were used to analyze the expression and localization of proteins including HSP27, SNAI1, CK8, α-SMA, and E-cad.
  • In vitro transfection experiments were performed to inhibit HSP27 expression.

Main Results:

  • TGF-β1 induced EMT in A549 cells, characterized by spindle-like morphology, decreased CK8 and E-cad, and increased vimentin and α-SMA expression.
  • TGF-β1 treatment led to increased levels of HSP27, SNAI1, and collagen types I and III.
  • Ac-SDKP inhibited TGF-β1-induced EMT and collagen synthesis.
  • Inhibition of HSP27 reduced SNAI1 and α-SMA expression, increased E-cad, and decreased collagen production.

Conclusions:

  • Ac-SDKP exhibits anti-fibrotic properties by modulating HSP27 expression in alveolar epithelial cells.
  • HSP27 is a key mediator in TGF-β1-induced EMT and subsequent collagen synthesis.
  • Ac-SDKP represents a potential therapeutic agent for fibrotic conditions by targeting the HSP27 pathway.
Keywords:
Epithelial–mesenchymal transitionHeat shock protein 27MyofibroblastsN-acetyl-seryl-aspartyl-lysyl-prolineType II alveolar epithelial cells

More Related Videos

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition11:48

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition

Published on: October 9, 2014

12.5K
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

13.1K

Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...