Related Experiment Video

Updated: Apr 27, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.1K

Effect of Smad pathway activation on podocyte cell cycle regulation: an immunohistochemical evaluation

Konstantinos Koutroutsos1, Theodoros I Kassimatis, Alexandros Nomikos

  • 11st Department of Pathology, Medical School, University of Athens , Greece .

Renal Failure
|July 17, 2014
PubMed
Abstract

Insights

Glomerular Smad pathway activation, indicated by increased pSmad2/3 and P300, correlates with reduced p57 expression in human glomerulonephritis. This suggests a link between TGF-beta signaling, inflammation, and podocyte cell cycle deregulation in kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • Mature podocytes normally exist in cell cycle arrest.
  • p57 acts as a negative cell-cycle regulator, inhibiting podocyte proliferation.
  • Phosphorylated Smad2/3 (pSmad2/3) mediates TGF-beta signaling and regulates cell cycle proteins.

Purpose of the Study:

  • To investigate the relationship between Smad pathway activation and podocyte cell cycle regulation in glomerular injury.
  • To examine the expression of p57, pSmad2/3, and P300 in human glomerulonephritis (GN).

Main Methods:

  • Immunohistochemical analysis of p57, pSmad2/3, and P300 expression.
  • Study included 67 patients with various types of GN and 10 normal kidney tissue controls.

Main Results:

  • pSmad2/3 and P300 were significantly increased in glomerular cells of patients with GN compared to controls.
  • A significant reduction in p57-positive podocytes was observed in GN patients.
  • p57 expression inversely correlated with pSmad2/3, suggesting Smad pathway activation down-regulates p57 in proliferative GN.

Conclusions:

  • Increased pSmad2/3 and reduced p57 expression in GN biopsies suggest a link between TGF-beta/Smad signaling and podocyte cell cycle deregulation.
  • Interstitial inflammation may be associated with glomerular Smad pathway activation and podocyte cell cycle dysregulation.
Keywords:
GlomerulonephritisSmadimmunohistochemistryp57podocytes

More Related Videos

Author Spotlight: Generation of Patient-Derived Podocytes from Skin Biopsies08:52

Author Spotlight: Generation of Patient-Derived Podocytes from Skin Biopsies

Published on: May 26, 2023

4.7K
Guided Differentiation of Mature Kidney Podocytes from Human Induced Pluripotent Stem Cells Under Chemically Defined Conditions08:06

Guided Differentiation of Mature Kidney Podocytes from Human Induced Pluripotent Stem Cells Under Chemically Defined Conditions

Published on: July 2, 2020

4.3K

Related Concept Videos

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...
7.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.8K
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...
10.1K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
2.3K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
8.5K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
5.1K