Related Experiment Video

Updated: Jun 23, 2026

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection
10:15

Identification of the Source of Secreted Proteins in the Kidney by Brefeldin A Injection

Published on: November 10, 2021

CTGF promotes inflammatory cell infiltration of the renal interstitium by activating NF-kappaB

Elsa Sánchez-López1, Sandra Rayego, Raquel Rodrigues-Díez

  • 1Cellular Biology in Renal Diseases Laboratory, Universidad Autónoma Madrid, Madrid, Spain.

Journal of the American Society of Nephrology : JASN
|May 9, 2009
PubMed

Insights

Connective tissue growth factor (CTGF) drives kidney inflammation by activating the nuclear factor-kappa B (NF-kappaB) pathway. Blocking NF-kappaB reduces CTGF-induced inflammatory cell recruitment and gene expression in the kidney.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Connective tissue growth factor (CTGF) is a key profibrotic factor in kidney disease.
  • CTGF influences cellular processes like adhesion, migration, proliferation, and the synthesis of inflammatory factors.

Purpose of the Study:

  • To investigate CTGF's role in kidney inflammation by examining its effect on the nuclear factor-kappa B (NF-kappaB) pathway.
  • To determine if CTGF activates NF-kappaB signaling and contributes to inflammatory cell recruitment in the kidney.

Main Methods:

  • Systemic administration of CTGF to mice and subsequent analysis of renal inflammatory cell infiltration and NF-kappaB activity.
  • Measurement of renal chemokine and cytokine expression following CTGF administration.
  • In vitro studies using cultured murine tubuloepithelial cells to assess CTGF's impact on NF-kappaB and mitogen-activated protein kinase (MAPK) pathways.
  • Evaluation of the effects of a NF-kappaB inhibitor (parthenolide) on CTGF-induced renal inflammation.

Main Results:

  • CTGF administration induced significant inflammatory cell infiltration (T lymphocytes, monocytes/macrophages) in the renal interstitium and elevated renal NF-kappaB activity.
  • CTGF increased the expression of inflammatory chemokines (MCP-1, RANTES) and cytokines (INF-gamma, IL-6, IL-4) in the kidney.
  • CTGF rapidly activated both the NF-kappaB and MAPK pathways in cultured renal cells, indicating pathway crosstalk.
  • Inhibition of NF-kappaB significantly reduced CTGF-induced inflammatory responses, including chemokine and cytokine upregulation.

Conclusions:

  • CTGF contributes to kidney inflammation by activating the NF-kappaB pathway.
  • CTGF promotes the recruitment of inflammatory cells into the kidney through NF-kappaB and MAPK signaling.
  • These findings highlight CTGF's dual role in kidney disease, encompassing both profibrotic and pro-inflammatory actions.

More Related Videos

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin10:21

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...