Related Experiment Video

Updated: Jan 31, 2026

Author Spotlight: Exploring Heat Shock Proteins in Malaria and Tuberculosis Infections
07:14

Author Spotlight: Exploring Heat Shock Proteins in Malaria and Tuberculosis Infections

Published on: March 8, 2024

1.9K

Heat shock protein 70 is induced by pepsin via MAPK signaling in human nasal epithelial cells

Jing Wang1, Yu Zhao2, Jianjun Ren1

  • 1Department of Oto-Rhino-Laryngology, West China Medical School, West China Hospital, Sichuan University, No. 37 Guo Xue Alley, Chengdu, 610041, Sichuan, China.

European Archives of Oto-Rhino-Laryngology : Official Journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : Affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
|January 3, 2019
PubMed
Abstract

Insights

Pepsin activates the JNK/MAPK pathway in nasal cells, increasing heat shock protein 70 (HSP70) expression. This response may protect cells from pepsin damage, even at neutral pH.

Area of Science:

  • Otolaryngology
  • Molecular Biology
  • Cell Biology

Background:

  • Laryngopharyngeal reflux is linked to chronic rhinosinusitis.
  • Pepsin, a key reflux component, may injure nasal epithelial cells.
  • The precise mechanism of pepsin-induced nasal injury is not fully understood.

Purpose of the Study:

  • To investigate if the mitogen-activated protein kinase (MAPK) pathway regulates heat shock protein 70 (HSP70) expression in human nasal epithelial cells (HNEpCs) stimulated by pepsin.
  • To elucidate the role of MAPKs in pepsin-induced HSP70 expression and cellular responses.

Main Methods:

  • HSP70 expression and MAPK pathway activation (p38, ERK1/2, JNK1/2) were measured in HNEpCs treated with pepsin using Western blot.
  • Specific MAPK pathway inhibitors were employed to assess their role in the pepsin-HSP70 interaction.
  • Cellular apoptosis and viability were assessed after pepsin exposure.

Main Results:

  • Pepsin stimulation significantly increased HSP70 protein expression in HNEpCs.
  • Pepsin activated p38, ERK1/2, and JNK1/2 pathways.
  • Inhibition of JNK1/2 attenuated pepsin-induced HSP70 expression.
  • Pepsin exposure at neutral pH (7.0) increased HNEpC apoptosis and decreased cell viability.

Conclusions:

  • Pepsin, even at neutral pH, upregulates HSP70 in HNEpCs via JNK/MAPK pathway activation.
  • Elevated HSP70 expression likely represents a cellular defense mechanism against pepsin.
  • Findings suggest a potential role for pepsin in nasal pathology and cellular protection.
Keywords:
Chronic rhinosinusitisHeat shock protein 70Laryngopharyngeal refluxMitogen-activated protein kinasePepsin

More Related Videos

Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface10:38

Culturing of Human Nasal Epithelial Cells at the Air Liquid Interface

Published on: October 8, 2013

38.2K
RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing08:34

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing

Published on: September 27, 2016

7.9K

Related Concept Videos

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...
8.3K
What is Cell Signaling?02:03

What is Cell Signaling?

Despite the protective membrane that separates a cell from the environment, cells need the ability to detect and respond to environmental changes. Additionally, cells often need to communicate with one another. Unicellular and multicellular organisms use a variety of cell signaling mechanisms to communicate to respond to the environment.
130.3K
Cell-surface Signaling01:21

Cell-surface Signaling

Hormones—or any molecule that binds to a receptor, known as a ligand—that are lipid-insoluble (water-soluble) are not able to diffuse across the cell membrane. In order to be able to affect a cell without entering it, these hormones bind to receptors on the cell membrane. When a first messenger, a hormone, binds to a receptor, a signal cascade is set off, causing second messengers, proteins inside the cell, to become activated, resulting in downstream effects.
54.4K
Responses to Heat and Cold Stress02:45

Responses to Heat and Cold Stress

Every organism has an optimum temperature range within which healthy growth and physiological functioning can occur. At the ends of this range, there will be a minimum and maximum temperature that interrupt biological processes.
14.8K
Protein Digestion01:02

Protein Digestion

Protein digestion begins in the stomach, where the highly acidic environment can easily disrupt protein structure by exposing the peptide bonds of polypeptide chains. After polypeptide chains are broken into individual amino acids by a series of digestive enzymes, the amino acids are transported to the liver via the bloodstream to produce energy.
111.0K
Shock Waves01:16

Shock Waves

While deriving the Doppler formula for the observed frequency of a sound wave, it is assumed that the speed of sound in the medium is greater than the source's speed through it. When this condition is breached, a shock wave occurs.
When the source's speed approaches the speed of sound, constructive interference between successive wavefronts emitted by the source occurs immediately behind it. Initially, scientists believed that this constructive interference would result in such high...
2.5K