Related Experiment Video

Updated: Sep 30, 2025

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

2.0K

Polycystin-1 regulates cell proliferation and migration through AKT/mTORC2 pathway in a human craniosynostosis cell

Maria A Katsianou1, Kostas A Papavassiliou1, Antonios N Gargalionis1

  • 1Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, Athens, Greece.

Journal of Cellular and Molecular Medicine
|March 14, 2022
PubMed

Insights

Polycystin-1 (PC1) plays a role in craniosynostosis by affecting cranial suture cell growth. Inhibiting PC1 increases cell proliferation and migration, potentially impacting this condition.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Biomedical Engineering

Background:

  • Craniosynostosis, the premature fusion of skull sutures, severely impacts children's lives.
  • Mechanical forces influence osteoblastogenesis in cranial sutures, potentially causing premature closure.
  • Mechanosensitive proteins polycystin-1 (PC1) and polycystin-2 (PC2) are crucial for craniofacial development.

Purpose of the Study:

  • To investigate the role of PC1 in the pathogenesis of non-syndromic craniosynostosis.
  • To elucidate the molecular mechanisms by which PC1 influences cranial suture development.

Main Methods:

  • Immunohistochemistry to detect PC1 and PC2 expression in human craniosynostosis tissues.
  • In vitro study using primary cranial suture cells treated with an anti-PC1 antibody (IgPKD1) to inhibit PC1 function.
  • Cell proliferation and migration assays to assess the effects of PC1 inhibition.
  • Western blot analysis to detect the activation of PI3K/AKT/mTOR pathway components.

Main Results:

  • PC1 and PC2 are expressed in human craniosynostosis tissues.
  • Inhibition of PC1 function using IgPKD1 led to increased proliferation and migration of primary cranial suture cells.
  • PC1 inhibition activated AKT signaling, evidenced by elevated phospho-AKT (Ser473) levels, but did not affect 4EBP1 or p70S6K.

Conclusions:

  • PC1 functions as a mechanosensing molecule in cranial sutures.
  • PC1 modulates osteoblastic cell proliferation and migration via the PC1/AKT/mTORC2 pathway.
  • These findings suggest PC1's potential involvement in the development of non-syndromic craniosynostosis.

Keywords:
cell migrationcell proliferationcraniosynostosismTOR signallingpolycystin-1

More Related Videos

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs10:47

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs

Published on: March 2, 2018

10.1K
Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

6.6K

Related Concept Videos

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...
4.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.9K
Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
3.2K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
7.0K
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
5.7K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.7K