Related Experiment Video

Updated: Jun 8, 2026

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
14:48

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Deficiency of matrix metalloproteinase-13 increases inflammation after acute lung injury

Anita I Sen1, Takayuki Shiomi, Yasunori Okada

  • 1Department of Pediatrics, Columbia University, College of Physicians and Surgeons, New York, New York, USA. ais13@columbia.edu

Experimental Lung Research
|September 24, 2010
PubMed

Insights

Matrix metalloproteinase-13 (MMP-13) deficiency in mice with acute lung injury (ALI) increased inflammatory cells in the lungs. MMP-13 appears to regulate the lung

Area of Science:

  • Pulmonary Medicine
  • Biochemistry
  • Immunology

Background:

  • Matrix metalloproteinases (MMPs) are implicated in acute lung injury (ALI) pathogenesis.
  • The specific role of collagenase MMP-13 in ALI remains unclear despite its detection during the condition.

Purpose of the Study:

  • To investigate the function of MMP-13 in the context of hyperoxic lung injury.
  • To determine the impact of MMP-13 deficiency on inflammatory responses and lung pathology.

Main Methods:

  • Comparison of MMP-13 deficient (KO) mice and wild-type (WT) mice following induced hyperoxic lung injury.
  • Assessment of survival rates, lung fibrosis (hydroxyproline content, collagen expression via real-time PCR).
  • Analysis of inflammatory cell counts and chemokine levels (MCP-1) in bronchoalveolar lavage (BAL) fluid and lung tissue, including in vitro MMP-13 cleavage assays.

Main Results:

  • No significant differences in survival or lung fibrosis were observed between KO and WT mice.
  • MMP-13 KO mice showed a significant increase in inflammatory cells within the BAL fluid compared to WT mice.
  • Elevated levels of monocyte chemoattractant protein 1 (MCP-1) were detected in the lungs of KO mice, and MMP-13 was shown to cleave MCP-1 in vitro.

Conclusions:

  • MMP-13 plays a role in modulating the inflammatory response in the lung during ALI.
  • The absence of MMP-13 leads to increased inflammatory cell infiltration, potentially by allowing MCP-1 to remain active.
  • MMP-13 may regulate macrophage recruitment to the lung in ALI by cleaving MCP-1.

More Related Videos

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis07:52

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis

Published on: December 21, 2014

Related Concept Videos

Role of Matrix Metalloproteases in Degradation of ECM01:23

Role of Matrix Metalloproteases in Degradation of ECM

Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult body.
A...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation